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patients | is with | severe COVID-19 (count: 18)
It has been demonstrated that serum urea, CREA and CysC could be potential biomarkers that could rapidly and specifically reflect severe COVID-19, and it is of great significance in the early diagnosis of COVID-19 to reduce the mortality and shorten the hospitalization period for patients with severe COVID-19.
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After adjusting for potential cofounders in separate modes, NT-proBNP presented as an independent risk factor of in-hospital death in patients with severe COVID-19. :
After adjusting for potential cofounders in separate modes, NT-proBNP presented as an independent risk factor of in-hospital death in patients with severe COVID-19.
Our data indicate that patients with severe COVID-19 exhibited an overall decline of lymphocytes including CD4+ and CD8+ T cells, B cells, and NK cells.
IL-2, IL-6, and IL-10 were remarkably up-regulated in patients with severe COVID-19.
In consistent with the train cohort, in validation cohort 1, AUC was 0.853 for patients with severe COVID-19 versus non-severe COVID-19 with a sensitivity of 77.5 % and specificity of 78.4% ( Figure 3D , Table 3 ).
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Such superimposed effects, however, would better reflect the features of patients with severe COVID-19.
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Although there was no clinical evidence to support the use of glucocorticoids [8] , whether early use of thymosin and gamma globulin for immunomodulation in patients with severe and critical COVID-19 can reduce cytokine storms, reduce clinical symptoms and improve prognosis requires further exploration.
The availability of recombinant ACE2 was the impetus to assemble a multinational team of intensivists, scientists, and biotech to rapidly initiate a pilot trial of rhACE2 in patients with severe COVID-19 (Clinicaltrials.gov #NCT04287686).
Pneumonia is always present in patients with severe COVID-19.
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Additional studies are compellingly needed to verify the putative bacterial origin of procalcitonin increase in patients with severe COVID-19.
Accumulating evidence suggests that a subgroup of patients with severe COVID-19 might have a cytokine storm syndrome.
In seven of the studies, patients with severe COVID-19 displayed a lower platelet count compared to those with milder forms (mean difference ranging between -3 to -5410 9 /L) [11, [13] [14] [15] [16] 18, 19] , whilst in the remaining two studies the platelet count was found to be lower in patients with non-severe forms of COVID-19 (mean difference ranging between 27 to 3110 9 /L) [12, 17] .
Additional research shall also be planned to clarify the precise mechanisms underlying the reduction of platelet count in patients with severe COVID-19, as well as their possible hyper-or hypo-activation.
In this letter, we explored the cardiac lesion biomarkers in patients with severe and very severe COVID-19.
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Further, higher serum levels of pro-inflammatory cytokines (i.e. TNF-α, IL-1 and IL-6) were found in patients with severe COVID-19 as compared to the non-severe ones [3] .
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Effective treatment interventions for patients with severe COVID-19 are still urgently needed.
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Here, fro m the perspective of clinical immunologists, we will discuss the clin ical and immunological characteristics of severe patients, and summarize the current evidence and share our experience in anti-inflammat ion treatment, including glucocorticoids, IL-6 antagonist, JAK inhibitors and choloroquine/hydrocholoroquine, of patients with severe COVID-19 that may have an impaired immune system.
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severe patients | is with | COVID-19 (count: 7)
Short-term (3 to 5 days) application of glucocorticoids is suggested for severe patients with COVID-19 in the protocol issued by NHC.
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Mean Difference (MD) in main laboratory index between severe and non-severe patients with COVID-19.
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155 It appears that liver dysfunction or damage in severe patients with COVID-19 is a 156 common but unignored phenomena.
However, severe patients with COVID-19 were likely to have neurological symptoms (such as headache, dizziness, hypogeusia, and neuralgia) and complications including acute cerebrovascular diseases, impaired consciousness and skeletal muscular injury 15 .
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The rates of co-infection, including other viruses, bacteria and fungus, were significantly increased in severe patients with COVID-19 than those in non-severe patients.
In the present study, we have focused on cardiac lesion biomarkers in severe and very severe patients with COVID-19.
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Considering their immunocompromised status, more intensive surveillance or individually tailored therapeutic approaches is needed for severe patients with COVID-19 with pre-existing conditions such as advanced liver disease, especially in older patients with other comorbidities.
-- Liver injury in COVID-19: management and challenges. The Lancet Gastroenterology & Hepatology. 2020-03-04.
patients | is with | severe COVID-19 pneumonia (count: 6)
Our data indicate that in patients with severe COVID-19 pneumonia, early, lowdose and short-term application of corticosteroid was associated with a faster improvement of clinical symptoms and absorption of lung focus.
To address this issue, we have performed a retrospective study on the clinical and radiographic outcomes of treatment with or without corticosteroid for a cohort of patients with severe COVID-19 pneumonia.
We studied patients with severe COVID-19 pneumonia from January 20 to February 25, 2020 at the isolation ward of Union Hospital of Huazhong University of Science and Technology.
In the present study, the patients with severe COVID-19 pneumonia had markedly increased inflammatory markers such as CRP, IL-6 and FER, which signified occurrence of the inflammatory reaction phase.
In our experience, once the secondary infection occurs in patients with severe COVID-19 pneumonia, sensitive and full-dose antibacterial drugs should be immediately added.
In conclusion, our data indicate that in patients with severe COVID-19 pneumonia, early, low-dose and short-term application of corticosteroid was associated with a faster improvement of clinical symptoms and absorption of lung focus. .
VeroE6/TMPRSS2 cells | were infected with | SARS-CoV-2 (count: 3)
VeroE6/TMPRSS2 cells(10) were infected with authentic SARS-CoV-2 in the presence of steroids or other inhibitors.
VeroE6/TMPRSS2 cells were infected with SARS-CoV-2 at MOI = 1 in the presence of 10 μ M compounds for 6 h. Cellular viral RNA was quantified by real-time PCR using the E gene primer/probe set. (
b) Culture Medium SARS-CoV-2 RNA (27 hpi).VeroE6/TMPRSS2 cells were infected with SARS-CoV-2 at MOI = 0.01 in the presence of ciclesonide for 27 h. Viral RNA in culture medium was quantified by real-time PCR using the E gene primer/probe set.
patients | is with | severe SARS-CoV-2 infection (count: 3)
Moreover, clinicians should constantly monitor the glomerular filtration function while treating patients with a severe SARS-CoV-2 infection.
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10 Nonetheless, what seems to emerge from our results is that cTnI values are significantly increased in patients with severe SARS-CoV-2 infection compared to those with milder forms of disease.
Cardiac troponin Ilevels are significantly increased in patients with severe SARS-CoV-2 infection compared to those with milder forms of disease 37 .
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severe illness | is with | COVID-19 (count: 3)
To aid clinical assessment, risk stratification, efficient resource allocation, and targeted public health interventions, future research must aim to further define those at high-risk of severe illness with COVID-19.
7) The primary aim of this study is therefore to conduct a systematic review and meta-analysis, aggregating all currently available data from published studies, of symptoms and comorbidities predictive for severe illness with COVID-19.
Though we are still learning what exactly puts someone at greater risk of developing a severe illness with COVID-19, early information indicates older patients and those with chronic medical conditions such as hypertension, diabetes and cardio-cerebrovascular diseases may be at higher risk (1) (2) (3) .
mild patients | is with | COVID-19 pneumonia (count: 3)
Comparison of age and cytokines among mild, severe and critical patients with COVID-19 pneumonia.
Comparison of inflammatory parametes among mild, severe and critical patients with COVID-19 pneumonia. (
Comparison of blood cell counts among mild, severe and critical patients with COVID-19 pneumonia.
SARS-CoV-2 | infects | cells (count: 3)
Previous studies have shown that SARS-CoV-2 infects cells by binding angiotensin-converting enzyme 2 (ACE2), which is the same as SARS-CoV. The expression and distribution of ACE2 in the pancreas are unknown.
SARS-CoV-2 infects ciliated cells of the human airway epithelium.
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Our results of SARS-CoV-2 RNA detection and intracellular staining of viral nucleocapsid protein in gastric, duodenal and rectal epithelia demonstrate that SARS-CoV-2 infects these gastrointestinal glandular epithelial cells.
cells | were infected with | SARS-CoV-2 (count: 3)
Then, the cells were infected with SARS-CoV-2 (100TCID 50 ) and the cell damage of Vero E6 and viral load were detected by crystal violet staining and quantitative PCR, respectively.
Vero E6 cells were cultured in a 96-well plate at 37ºC overnight, the supernatant was discard and 100 μl of medium (containing 3.125, 6.25, 12.5, 25, 50, 100, 150, 200 μg/mL Meplazumab) was added into the plates to incubate for 1 h. Then the cells were infected with SARS-CoV-2 (100TCID 50 ).
Vero-E6 cells were infected with SARS-CoV-2 (SARS-CoV-2-
Vero E6 cells | infected with | SARS-CoV-2 (count: 3)
To further determine the localization of CD147 and SP in the process of viral infection, the Vero E6 cells infected with SARS-CoV-2 were observed by immune-electron microscope.
Vero E6 cells infected with SARS-CoV-2 were harvested and treated with fixative at 4°C .
Vero E6 cells were treated with different doses of either compound or with PBS in the controls for 1 h and then infected with SARS-CoV-2 at MOIs of 0.01, 0.02, 0.2, and 0.8.
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patients | is with | mild COVID-19 (count: 3)
The number of immunosuppressive regulatory T cells was moderately increased in patients with mild COVID-19.
Compared with patients with mild and moderate COVID-19, those with severe or critically 209 disease presented with extensively and significantly different laboratory parameters, 210
Kaplan-Meier curves of cumulative survival probability for patients with mild and severe COVID-19 within 12-day after admission.
T cells | is in | COVID-19 patients (count: 3)
4] [5] [6] However, the factors which might cause the reduction in count, and the activation status of T cells in COVID-19 patients, remain uninvestigated.
12 We therefore examined whether T cells in COVID-19 patients have exhaustion phenotypes.
15, 16 Earlier studies have been unclear regarding the numbers and function of T cells in COVID-19 patients, albeit with suggestions of depressed lymphocyte counts.
COVID-19 | is caused by | severe syndrome coronavirus 2 (count: 3)
COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a new type of enveloped RNA coronavirus, which can be transmitted by personto-person via airborne and contact and caused epidemics in Wuhan, the capital of Hubei Province.
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COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
-- TH17 Responses in Cytokine Storm of COVID-19: An Emerging Target of JAK2 Inhibitor Fedratinib. Journal of Microbiology, Immunology and Infection. 2020-03-11.
1 Initially referred to as the 2019 novel coronavirus (2019-nCoV), COVID-19 is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
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SARS-CoV-2 | invade | cells (count: 2)
First, ACE2 expression is also found in the kidney, heart, and liver etc, therefore SARS-CoV-2 could invade the cells of above tissues, reproduce and damage these organ.
Researchers have found that the new SARS-CoV-2 and SARS coronaviruses invade human cells in target tissues in a similar manner via high-affinity binding to angiotensin-converting enzyme 2 (ACE2) [1] .
SARS-CoV-2 infection | is in | Vero E6 cells (count: 2)
In particular, as compared to the DMSO control group, both CVL218 and remdesivir showed potent antiviral activities during the full-time procedure of the SARS-CoV-2 infection in Vero E6 cells (Figure 2D ).
It has recently been demonstrated that, as a prodrug, FPV (half maximal effective concentration (EC 50 ) = 61.88 lmolÁL À1 , half-maximal cytotoxic concentration (CC 50 ) > 400-lmolÁL À1 , selectivity index (SI) > 6.46) effectively inhibits the SARS-CoV-2 infection in Vero E6 cells (ATCC-1586) [7] .
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severe patients | is with | SARS-CoV-2 infection (count: 2)
Recently published researches on the clinical characteristics of severe patients with SARS-CoV-2 infection showed that IL-6 was significantly elevated especially in those ICU patients, which caused excessive activated immune response [25, 26, 27, 28, 29] .
In order to identify the potential risks for intubation in severe patients with SARS-CoV-2 infection, Chi-square test showed that older (age > 60 years), higher SOFA (> 4), APACHE II (> 15) score and LDH (> 255U/L)and lower lymphocyte (< 0.8*10 9 /L) at ICU admission were at high risks for intubation.
severe patients | infected by | SARS-CoV-2 (count: 2)
Notably, current pathological studies have shown that the severe patients infected by SARS-CoV-2 generally have higher plasma levels of IL-2, IL-6, IL-10, TNFα, IFN-γ [25, 27, 28, 29] , implying a high risk of the inflammatory-associated cytokine storm after viral infection.
This finding indicates that CVL218 may also possess the IL-6 specific anti-inflammatory effect that is applicable to those severe patients infected by SARS-CoV-2.
COVID-19 patients | is with | mild diseases (count: 2)
Next, we examined the proportions of expanded clones between COVID-19 patients with mild and severe diseases.
Recent reports show that the lymphocyte counts are normal in COVID-19 patients with mild diseases.
patients | having | severe COVID-19 (count: 2)
All patients were diagnosed as having severe COVID-19 according to the WHO Interim Guidance (30) and the Guideline of Diagnosis and Treatment of COVID-19 of National Health Commission of China (version 5.0) (31), with confirmation by real-time RT-PCR assay.
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Because disease severity reportedly predicted poorer clinical outcomes of avian influenza [9], patients were classified as having severe or non-severe COVID-19 based on the American Thoracic Society guidelines for community-acquired pneumonia because of its global acceptance [26] .
severe patients | is with | 2019-nCoV infection (count: 2)
The severe or death patients with 2019-nCoV infection were mostly old age with comorbidities.
By analyzing the differences of lymphocyte subsets and 194 cytokines in peripheral blood between the mild and severe patients, we found that only CD4 + T, 195 CD8 + T, IL-6, IL-10 had statistical significance between the mild and severe groups, suggesting 196 that the immunosuppression of severe patients with 2019-nCoV infection was more obvious, which 197 was consistent with the opinions of many experts.
102 patients | is with | severe COVID-19 pneumonia (count: 2)
The study initially enrolled 102 patients with severe COVID-19 pneumonia from a continuous sample.
The study initially enrolled 102 patients with severe COVID-19 pneumonia from a continuous sample in Hubei General Hospital during the management by national medical team.
severe patient | is with | COVID-19 (count: 2)
This CT scan shows an enlarged pancreas with dilated pancreatic ducts in a severe patient with COVID-19.
Dynamic chest CT scan changes of a severe patient (a middle-aged female patient) with COVID-19.
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COVID-19 patients | is with | mild symptoms (count: 2)
The predictive values of selected parameters for distinguishing COVID-19 patients with mild and severe symptoms were evaluated by receiver operating characteristic (ROC) and area under the All rights reserved.
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COVID-19 patients with mild symptoms are easy to be overlooked, so it is necessary to take active and effective isolation measures for suspected patients or close contacts as early as possible.
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SARS-CoV-2 | gain | entry into host cells (count: 2)
SARS-CoV-2 utilizes glycosylated spike (S) protein to gain entry into host cells.
In similar fashion to SARS-CoV, SARS-CoV-2 also uses ACE2 to gain entry into host cells.
decrease | are indicators of | severe COVID-19 (count: 2)
In conclusion, our study shows that the comprehensive decrease of lymphocytes, and the elevation of IL-2 and IL-6 are reliable indicators of severe COVID-19.
IL-10 acts as an anti-inflammatory cytokine deriving from alternatively activated macrophages, Th2 cells, Tregs, etc 16 In conclusion, our study shows that the comprehensive decrease of lymphocytes, and the elevation of IL-2 and IL-6 are reliable indicators of severe COVID-19.
COVID-19 | induces | mild symptoms (count: 2)
While COVID-19 frequently induces mild symptoms common to other respiratory infections, it has also exhibited an ability to generate severe disease among certain groups including older populations and individuals with underlying health issues such as cardiovascular disease and diabetes (2) .
While COVID-19 frequently induces mild symptoms common to other respiratory infections, it has also exhibited an ability to generate severe disease among certain groups including older populations and individuals with underlying health issues such as cardiovascular disease and diabetes (Adler, 2020) .
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SARS-CoV-2 | enters | cells (count: 2)
Like other viruses, the SARS-CoV-2 enters cells through receptor-mediated endocytosis.
As previously described in detail, SARS-CoV-2 enters targeted cells through receptor-mediated endocytosis [12] .
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SARS-CoV-2 | infect | cells (count: 2)
26 Studies showed that the SARS-CoV-2 may infect alveolar epithelial cells in lung through the angiotensin-converting enzyme II (ACE2) receptor, which is also expressed in other tissues, such as kidney, blood vessels and heart.
SARS-CoV and SARS-CoV-2 have been shown to infect human respiratory epithelial cells through the interaction of viral S proteins and angiotensin-converting enzyme 2 receptors on human cells[26, 49] .
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men | is with | severe COVID-19 (count: 2)
These findings suggested that men with severe COVID-19 is susceptible to secondary infections with virus or bacteria, resulting in higher utilization rate of advanced antiviral therapy and antibiotics.
Our findings imply that physicians should pay more attention to cardiac function in men with severe COVID-19.
severe pneumonia patients | is with | COVID-19 (count: 2)
Laboratory characteristics of severe pneumonia patients with COVID-19
Treatment and outcomes for severe pneumonia patients with COVID-19
patients | progressed to | severe COVID-19 (count: 2)
Seven patients progressed to severe COVID-19; however, after treatment, their condition was stable.
Fifteen patients progressed to severe COVID-19 within a median follow-up time of 15 days.
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severe COVID-19 cases | have in | have adults (count: 2)
However, severe COVID-19 cases and deaths have mostly been in the middle-aged adults and the elderly with long smoking histories or other 45) [37] .
However, severe COVID-19 cases and deaths have mostly been in the middle-aged adults and the elderly with long smoking histories or other basic diseases, such as heart disease and hypertension [43, 44] .
they | designating 2019-nCoV as | severe syndrome coronavirus 2 (count: 2)
That same day, the Coronavirus Study Group (CSG) of the International Committee on Virus Taxonomy posted a manuscript on bioRxiv in which they suggested designating 2019-nCoV as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on the basis of a phylogenetic analysis of related coronaviruses.
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the Coronavirus Study Group (CSG) of the International Committee on Virus Taxonomy posted a manuscript on bioRxiv in which they suggested designating 2019-nCoV as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on the basis of a phylogenetic analysis of related coronaviruses.
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2019-nCoV | can | can found in cells (count: 2)
2019-nCoV can be found in human respiratory epithelial cells 96 h after in vitro isolation and culture, while it takes about 6 days in VeroE6 or Huh-7 cell lines [12] .
When cultured in vitro, 2019-nCoV can be found in human respiratory epithelial cells after about 96 hours, while it takes about 6 days to isolate and culture Vero E6 and Huh-7 cell lines.
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liver injury | is prevalent than | than mild cases of COVID-19 (count: 2)
4 Data suggest that liver injury is more prevalent in severe cases than in mild cases of COVID-19.
-- Implications of COVID-19 for patients with pre-existing digestive diseases. The Lancet Gastroenterology & Hepatology. 2020-03-11.
Therefore, liver injury is more prevalent in severe cases than in mild cases of COVID-19.
-- Liver injury in COVID-19: management and challenges. The Lancet Gastroenterology & Hepatology. 2020-03-04.
reporting | rate in | COVID-19 patients with definition of severe disease (count: 2)
The title, abstract and full text of all articles captured with the search criteria were evaluated, and those reporting the rate of COPD in COVID-19 patients with a clinically validated definition of severe disease were included in this meta-analysis.
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The title, abstract and full text of all documents captured with these search criteria were scrutinized, and those reporting the rate of active smokers in COVID-19 patients with clinically validated definition of severe disease were included in this meta-analysis.
patients | is with | more severe COVID-19 (count: 2)
The pooled results of these nine studies revealed that the platelet count was significantly lower in patients with more severe COVID-19 (WMD -3110 9 /L; 95% CI, -35 to -2910 9 /L).
The platelet count remained significantly 6 lower (WMD, -2210 9 /L; 95% CI, -26 to -1610 9 /L; I 2 , 91%; p<0.001) in patients with more severe COVID-19 after excluding the large study of Guan et al. [
None | developed | severe COVID-19 pneumonia (count: 2)
None of the patients developed severe COVID-19 pneumonia or died, as of Feb 4, 2020.
None of the patients developed severe COVID-19 pneumonia or died.
SARS-CoV-2 | causes | cluster of severe illness (count: 1)
SARS-CoV-2 causes a cluster of severe respiratory illness which is similar to another two fatal coronavirus infection caused by SARS-CoV and MERS-CoV. Death is more likely to occur in older male patients with comorbidity.
COVID-19 patients | is with | severe illness (count: 1)
/2020 We also depicted the immune status of COVID-19 patients with severe illness.
199 hospitalized adult patients | is with | severe COVID-19 (count: 1)
The results in our study are consistent with findings from a recent clinical trial of LPV/r in adults hospitalized with severe COVID-19 conducted in Wuhan, which recruited 199 hospitalized adult patients with severe COVID-19 and concluded that no benefit was observed with LPV/r treatment beyond standard care [20] .
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SARS-CoV-2 | is clade from | betacoronaviruses associated with severe syndrome (count: 1)
1,2 Full-genome sequencing and phylogenic analysis indicated that SARS-CoV-2 is a distinct clade from the betacoronaviruses associated with human severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS).
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Lymphocyte subsets | is in | COVID-19 pneumonia mild vs. severe rights reserved (count: 1)
Lymphocyte subsets in COVID-19 pneumonia mild vs. severe or critical All rights reserved.
mild cases | is with | COVID-19 (count: 1)
Representative chest radiographic manifestations in mild and severe cases with COVID-19
mild cases | were common in | patients with COVID-19 (count: 1)
Basically, mild cases were common in paediatric patients with COVID-19 [1] , presenting with acute upper respiratory tract infection or mild pneumonia.
2019-nCoV | was identified as | clade from severe syndrome coronavirus (count: 1)
The 2019-nCoV was identified as a diverse clade from the severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), and was reported as the cause of coronavirus disease-2019 (COVID-19)
% | were severe cases Of | COVID-19 patients (count: 1)
Of the total confirmed COVID-19 patients, about 19.9% were severe cases [1] , which have a mortality rate of about 20%.
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death | is in | severe COVID-19 patients (count: 1)
Furthermore, acute respiratory distress syndrome could lead to death in some severe COVID-19 patients, and this is often accompanied by heart failure, liver failure, and kidney failure [2, 4] .
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glomerular filtration function | is in | severe COVID-19 patients (count: 1)
Interestingly, the levels of serum biomarkers reflecting glomerular filtration function (including cystatin C (CysC), creatinine (CREA), and urea) in severe COVID-19 patients were significantly higher than those in mild patients.
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incidence | was higher in | severe COVID-19 patients (count: 1)
The incidence of liver or heart failure was higher in severe COVID-19 patients [2, 4] ; however, we found that most of the indicators, including liver and cardiac function biomarkers, except for serum DBIL, CHE and LDH, did not change significantly or directly in severe and mild patients.
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serum indicators | were higher than | than mild COVID-19 (count: 1)
Herein, we found that some serum indicators of glomerular function, including urea, CREA, and CysC, were observably higher in severe COVID-19 patients than in mild COVID-19
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confirmed | cases of | severe COVID-19 (count: 1)
The analysis included 4,166 test results from 28 COVID-19 patients, including 8 confirmed cases of severe COVID-19 (with a mean age of 66±22 years) and 20 confirmed cases of mild COVID-19 (with a mean age of 41±19 years), and the remaining baseline characteristics are shown in the Table 1.
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serum biochemical marker levels | is in | severe COVID-19 cases (count: 1)
Distributions showing serum biochemical marker levels in severe and mild COVID-19 cases.
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urea | LDH between | severe COVID-19 cases (count: 1)
Distributions and differences showing the concentration of serum urea, CREA, CysC, DBIL, CHE, LDH between severe and mild COVID-19 cases. ***
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monkey kidney Vero cells | were infected with | isolate SARS-CoV-2 (count: 1)
African green monkey kidney Vero cells (ATCC CCL-81) were infected with a clinical isolate SARS-CoV-2 (BetaCoV/Korea/KCDC03/2020 provided from Korea CDC).
COVID-19 | was severe in | Wuhan (count: 1)
On one hand, COVID-19 was more severe in Wuhan at its early stage, reaching approximately 32% of severe/critical types and 11% of fatality 8, 9 .
data | showed | mild type of COVID-19 (count: 1)
In contrast, data out of Wuhan showed more mild type of COVID-19, as presented in Zhejiang province 10 and nationwide 11 .
mild COVID-19 | is in | Zhejiang province (count: 1)
Based on these clinical findings, we performed in-depth bioinformatics analysis by comparing the virological features of previously reported 52 strains of SARS-CoV-2, including Bat coronavirus, SARS-CoV and SARS-CoV-2 in Wuhan and ZJ01 (SARS-CoV-2 we firstly reported in one patient with mild COVID-19 in Zhejiang province).
COVID-19 patient | is with | mild type in our hospital (count: 1)
One strain of SARS-CoV-2 was successfully isolated from the sputum of COVID-19 patient with mild type in our hospital, followed by whole genome sequencing with previously reported method 18 .
form mild COVID-19 patient | represents | potential branch (count: 1)
To sum up, ZJ01 isolated form mild COVID-19 patient of Zhejiang province represents a potential branch in virus evolution.
potential evolution direction | may promote | appearance of mild subtype of COVID-19 (count: 1)
Such potential evolution direction may promote the appearance of mild subtype of COVID-19.
one COVID-19 patient | is with | mild type (count: 1)
We selected one COVID-19 patient with mild type and isolated his virus (ZJ01) for comparative analysis.
SARS-CoV-2 | undergoing evolution towards | mild direction (count: 1)
Thereafter, we conclude that SARS-CoV-2 is undergoing evolution towards mild direction with increased furin cleavage sites.
we | characterize lung lavage fluid cells from | 6 COVID-19 patients (count: 1)
Here, we applied the emerging single-cell RNA sequence (scRNA-seq) and single-cell TCR-seq to comprehensively characterize the lung bronchoalveolar lavage fluid (BALF) cells from 6 of COVID-19 patients, including 3 severe and 3 mild cases.
lung cell compartments | differed between | mild COVID-19 patients (count: 1)
Together, our data showed an increased recruitment of immune cells to the lung in response to SARS-CoV-2 infection, and that the lung immune cell compartments differed between mild and severe COVID-19 patients.
lung macrophage population | was present in | severe COVID-19 patients (count: 1)
The increased lung macrophage population was present in severe COVID-19 patients.
composition | differed among | mild COVID-19 patients (count: 1)
We found that the composition of the macrophage groups differed significantly among controls, mild versus severe COVID-19 patients ( Figure 2C ).
SPP1 | were | expressed by severe COVID-19 patients (count: 1)
We further confirmed that FCN1 was preferentially expressed by individual controls and mild COVID-19 patients, while SPP1 and FABP4 were highly expressed by severe COVID-19 patients ( Figure 2E ).
severe COVID-19 patients | from population is | group 2 (count: 1)
Moreover, we identified a novel intermediate macrophage population (group 2), only from the severe COVID-19 patients.
infection | is in | severe COVID-19 (count: 1)
We assumed that it might be related to bystander activation induced by hyper inflammation, or a delayed response to the infection in severe COVID-19.
Perturbed CD68 compartments | is in | severe COVID-19 A (count: 1)
Perturbed CD68 + macrophage compartments in severe COVID-19 A. The UMAP presentation of the heterogenous clusters of lung macrophages B. The lung macrophages clusters were classified to 4 groups according to FCN1, SPP1 and FABP4 expression levels, indicated by red squares.
volcano plot | shows | DEGs between severe COVID-19 patients (count: 1)
Analysis of the BALF T and NK lymphocytes in COVID-19 patients A. The UMAP plot shows the clustering of lung T and NK cells B. The heatmap of showing the immune typing markers on different T and NK clusters C. The UMAP plots show comparison of the T and NK cell compartments across different groups D. The bar plot shows the percentages of T and NK clusters in each individual sample E. The volcano plot shows the DEGs of CD8 + T cells between severe vs. mild COVID-19 patients.
status | is in | BALFs of severe COVID-19 patients D (count: 1)
Analysis of the T cell clonal expansion in BALF of SARS-COV-2 infected patients A. The UMAP plot shows the T cell expansion status in COVID-19 patients B. The UMAP projection of expanded clonal T cells between severe and mild patient group C. The pie charts show the clonal expansion status of CD8 + T and proliferating T cells in BALFs of severe and mild COVID-19 patients D. The bar plots show clonal expansion status of CD8 + T and proliferating T cells in BALFs from each individual sample E. The volcano plot shows the DEGs of expanded vs. non-expanded CD8 + T cells in BALFs of COVID-19 patients.
cells | were scored by | immunofluorescence analysis with antibody specific for N protein of SARS-CoV-2 (count: 1)
At 24 h after the infection, the infected cells were scored by immunofluorescence analysis with an antibody specific for the viral N protein of SARS-CoV-2.
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SARS-CoV-2 | was propagated in | Vero cells (count: 1)
SARS-CoV-2 (βCoV/KOR/KCDC03/2020) was provided by Korea Centers for Disease Control and Prevention (KCDC), and was propagated in Vero cells.
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COVID-19 patients | is with | more severe NCP type (count: 1)
COVID-19 patients with more severe NCP type (OR, 2.896; 95CI% [1.266, 6.621]) may have a higher risk of AMI than other patients.
2019-nCoV genome | is identical with | two severe syndrome (count: 1)
Based on bioinformatics analyses, it has been shown that 2019-nCoV genome is 88% identical with two bat-derived severe acute respiratory syndrome (SARS)-like coronaviruses (bat-SL-CoVZC45 and bat-SL-CoVZXC21), 79% with SARS-CoV, and 50% with MERS- Single-cell RNA sequencing (scRNA-Seq) has been extensively applied in 2019-nCoV research, due to its capability to profile gene expressions for all cell types in multiple tissues unbiasedly at a high resolution.
teicoplanin | repress | entry of 2019-nCoV viruses into types of cells (count: 1)
Considering that ACE2 is a major receptor of 2019-nCoV, we have further analyzed the expression of ACE2 in different cell types from the GEO Profiles database and it was important to examine whether teicoplanin could repress the entry of 2019-nCoV viruses into different types of cells.
2019-nCoV | binds to | receptor ACE2 on surface of host cells (count: 1)
In this study, we identified that teicoplanin could inhibit the entry of HIV-1-2019-nCoV-S pseudoviruses with the IC 50 value of 1.66 uM. During the invasion phase, 2019-nCoV first binds to the receptor ACE2 on the surface of host cells.
cells | were infected with | HIV-luc/2019-nCoV pseudoviruses (count: 1)
After 24 h, the cells were infected with HIV-luc/2019-nCoV pseudoviruses.
cells | were infected with | HIV-luc/2019-nCoV (count: 1)
A549 cells were seeded in a 96-well plate, and 24 h later, the cells were infected with HIV-luc/2019-nCoV, HIVluc/SARS-nCoV or HIV-luc/VSVG pseudoviruses.
A549 cells | were infected with | HIV-luc/2019-nCoV pseudoviruses (count: 1)
C, A549 cells were infected with HIV-luc/2019-nCoV pseudoviruses and then incubated with teicoplanin at various concentrations.
HEK293T cells | were infected with | HIV-luc/2019-nCoV pseudoviruses (count: 1)
A, HEK293T cells were infected with HIV-luc/2019-nCoV pseudoviruses and then incubated with teicoplanin at various concentrations.
Huh7 cells | were infected with | HIV-luc/2019-nCoV pseudoviruses (count: 1)
B, Huh7 cells were infected with HIV-luc/2019-nCoV pseudoviruses and then incubated with teicoplanin at various concentrations.
2019-nCoV infection | causes damages to | most II type cells (count: 1)
Therefore, 2019-nCoV infection causes damages to most II type alveolar cells.
CP | serve as | rescue option for severe COVID-19 (count: 1)
These results indicate that CP can serve as a promising rescue option for severe COVID-19 while the randomized trial is warranted.
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we | explore feasibility in | 10 severe COVID-19 patients (count: 1)
Hence, we performed this pilot study in three participated hospitals to explore the feasibility of CPtreatment in 10 severe COVID-19 patients.
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enrolled severe COVID-19 patients | achieved | outcomes (count: 1)
All enrolled severe COVID-19 patients achieved primary and secondary outcomes.
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CP therapy | can | can rescue option for severe COVID-19 patients (count: 1)
Based on our preliminary results, CP therapy can be an easy-accessible, promising and safe rescue option for severe COVID-19 patients.
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effect | is in | treatment of severe COVID-19 patients (count: 1)
In conclusion, this pilot study on CP therapy showed a potential therapeutic effect and low risk in the treatment of severe COVID-19 patients.
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effects meta-analysis | identify | those associated with severe COVID-19 infection (count: 1)
Random effects meta-analysis was performed for selected symptoms and comorbidities to identify those most associated with severe COVID-19 infection or ICU admission.
comorbidities | predictive for | severe COVID-19 cases (count: 1)
The existing literature on COVID-19 fails to elucidate the specific symptoms and comorbidities most predictive for severe COVID-19 cases.
severe illness | is in | patients with 2019-nCoV infection (count: 1)
Results: The neutrophil-to-lymphocyte ratio (NLR) was identified as the independent risk factor for severe illness in patients with 2019-nCoV infection.
severe illness patients | is with | 2019-nCoV pneumonia (count: 1)
The NLR was the most useful prognostic factor affecting the prognosis for severe illness patients with 2019-nCoV pneumonia.
2019-nCoV | utilize ACE2 as | entry receptor in cells (count: 1)
A recent study showed that 2019-nCoV is able to utilize ACE2 as an entry receptor in ACE2-expressing cells [31] , suggesting potential drug targets for therapeutic development.
SARS-CoV-2 spike | expressed in | cells (count: 1)
The SARS-CoV-2 spike expressed in insect cells predominantly retains a unique 298 early prefusion conformation, which was repeatable in at least three batches of samples 299 and is ascribed to two possible reasons -native aa sequence used in the S ectodomain The copyright holder for this preprint (which was not peer-reviewed) is the .
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COVID-19 | mild types of were | 81 % (count: 1)
According to the Chinese epidemic data, the mild, severe, and critical types of COVID-19 were 81%, 14%, and 5% separately 6 .
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None | used for | progression prediction of mild COVID-19 patients (count: 1)
None of them used AI-based methods for progression prediction of mild COVID-19 patients up to date.
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133 patients | is with | mild COVID-19 pneumonia (count: 1)
133 patients with mild COVID-19 pneumonia at admission included 66 male and 67 female, age ranged from 18 to 82 (52.82 ± 12.59) years, the interval from symptoms onset to admission ranged from 1 to 20 (8.76 ± 4.05) days.
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patients | is with | potentially severe COVID-19 outcomes (count: 1)
The ability to identify patients with potentially severe and critical COVID-19 outcomes using an inexpensive, widely available, the point-of-care test has important practical implications for preventing mild patients from becoming severe, effectively improving cure rate, and reducing mortality.
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resources | can | can prioritized for those at risk of severe COVID-19 complications (count: 1)
Importance: Risk factors associated with COVID-19, the viral pneumonia originating in Wuhan, China, in Dec 2019, require clarification so that medical resources can be prioritized for those at highest risk of severe COVID-19 complications.
coinfection | lead to | development of severe COVID-19 symptoms (count: 1)
This data infers that coinfection of SARS-CoV-2 with MTB tends to lead to the development of more severe or critical COVID-19 symptoms.
B. Patients | developed | severe COVID-19 symptoms (count: 1)
B. Patients with MTB infection developed more severe COVID-19 symptoms.
B. COVID-19 patients | develop | severe complications (count: 1)
B. COVID-19 patients with MTB infection develop severe complications more rapidly.
lymphocytes counts | is in | most severe COVID-19 patients (count: 1)
Qin et al demonstrated that lymphocytes counts in most severe COVID-19 patients was reduced, which suggests that SARS-CoV2 might impaired immune system and mainly damaged lymphocytes, especially T lymphocytes (20) .
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SARS-CoV-2 | share | receptor protein expressed on cells (count: 1)
SARS-CoV-2 and SARS-CoV share a common host-cell receptor protein, angiotensin converting enzyme 2 (ACE2), expressed on epithelial cells in the respiratory track system and various human organs, such as the lung 9,10 .
SARS-CoV-2 | causing | severe COVID-19 symptoms (count: 1)
SARS-CoV-2 is spreading rapidly, causing severe COVID-19 symptoms and life-threatening diseases in some infected patients 6 .
SARS-CoV-2 virus | infects | cells (count: 1)
The above experimental results are consistent with our structure modeling analysis, which indicates that SARS-CoV-2 virus likely infects human cells through similar mechanisms as SARS-CoV virus by binding to human ACE2 with comparable affinities, and hence may possess similar transmissibility.
we | performed | RT-PCR analysis of SARS-CoV-2 in swab samples including residue cells (count: 1)
To explore the possibility of sexual transmission of this contagious virus, we performed RT-PCR analysis of SARS-CoV-2 in the anal swab samples and vaginal environment samples (including cervical or vaginal residue exfoliated cells, vaginal discharge) collected from 35 female patients with COVID-19 and inquired their recent sexual behavior.
RNA | was purified from | SARS-CoV-2 Vero cells (count: 1)
Total RNA was purified from SARS-CoV-2 infected Vero cells using the Qiagen RNA minikit following AVL inactivation.
2019-nCoV | can infect | Huh-7 cells (count: 1)
Similar to SARS-CoV and MERS-CoV, 2019-nCoV can infect ex vivo with the same range of cell culture lines, e.g. Vero E6, Huh-7 cells (Hoffmann et al.,
airway cells | be | cell type for 2019-nCoV (count: 1)
However primary human airway epithelial cells have been reported to be the preferential cell type for 2019-nCoV (Perlman, 2020; Zhu et al.,
SARS-CoV-2 RNA | were | In 12 patients with mild detected (count: 1)
In 12 patients with mild to moderately severe illness, SARS-CoV-2 RNA and viable virus were detected early, and prolonged RNA detection suggests the window for diagnosis is long.
SARS-CoV-2 | was cultured from | specimens of mild patients (count: 1)
SARS-CoV-2 was cultured from the initial respiratory specimens of mild and moderately ill patients.
SARS-CoV-2 replication | is in | non-human cells (count: 1)
29, 30 In vitro studies have demonstrated that remdesivir inhibits SARS-CoV-2 replication in non-human cells.
severe acute respiratory infection | is with | suspected COVID-19 (count: 1)
WHO interim guidance for clinical management of severe acute respiratory infection with suspected COVID-19 advises against use of corticosteroids unless indicated for another reason.
relationship | is in | severe COVID-19 patients (count: 1)
The present study for the first time showed the relationship between plasma NT-proBNP level and risks of in-hospital death in severe COVID-19 patients.
plasma NT-proBNP elevation | is in | severe COVID-19 patients (count: 1)
Further understanding of physiological and pathological significance of plasma NT-proBNP elevation in severe COVID-19 patients might help clinicians make corresponding decisions to reduce the risks of adverse outcome.
non-survivors | is with | severe COVID-19 pneumonia (count: 1)
Font-line doctors pointed that some non-survivors with severe COVID-19 pneumonia died without warning.
it | investigating | effect of NP-proBNP level of severe COVID-19 patients (count: 1)
By investigating the prognostic effect of NP-proBNP level of severe COVID-19 patients at admission, it might be helpful to identifying patients with poor prognoses early.
coronavirus disease 2019 | caused by | severe acute respiratory syndrome coronavirus 2 (count: 1)
The coronavirus disease 2019 , caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged in Wuhan, China in the end of 2019, and spread to over 40 foreign countries in a short period of time [1] [2] [3] .
screening | prevent | proportion of SARS-CoV-2 travellers (count: 1)
Syndromic screening of air travellers at departure and/or arrival is unlikely to prevent a sufficient proportion of SARS-CoV-2 infected travellers from entering a yet unaffected country and thereby prevent a local outbreak.
aim | explore | characteristics of 5 severe pneumonia caused by 2019-nCoV (count: 1)
4 Objectives: The aim of this study was to explore the clinical characteristics and risk factors of the 5 severe pneumonia caused by the 2019-nCoV in Wuhan, China.
level | was | correlated with 2019-nCoV severe pneumonia (count: 1)
These results suggested that the level of D-dimer was 158 significantly positively correlated with the 2019-nCoV severe pneumonia, which was also shown in 159 another study [13] .
blood cells | elevated in | COVID-19 patients (count: 1)
The white blood cells and C-reactive protein level elevated in severe COVID-19 patients may be accompanying bacterial infection.
SARS-CoV-2 infected patients | is with | severe diseases (count: 1)
https://doi.org/10.1101/2020.02.28.20028514 doi: medRxiv preprint of SARS-CoV-2 infected patients with severe diseases have lymphopenia and the low level of lymphocyte counts in patients is associated with mortal outcome 8, 18 .
2019-nCoV | is clade from | beta coronaviruses associated with severe syndrome (count: 1)
Full-genome sequencing and phylogenic analysis indicated that 2019-nCoV is a distinct clade from the beta coronaviruses associated with human severe acute respiratory syndrome (SARS) and
COVID-19 | poses | severe threat (count: 1)
6 As the epidemic spreads to many countries, COVID-19 poses a severe threat to global health.
SARS-CoV-2 | infects | host cells (count: 1)
Research has confirmed that SARS-CoV-2 infects host cells by binding to angiotensin converting enzyme II (ACE2), 10-12 and ACE2 is highly expressed in nasopharyngeal cells.
CD8 T cells counts | contribute to | severity of COVID-19 (count: 1)
Reduced CD3 and CD8 T cells counts in the context of excessive activation of these cells have been shown to contribute to the severity and mortality of COVID-19 by causing severe immune damage.
mild patients | is with | COVID-19 (count: 1)
And further, clinical data including mild and severe patients with COVID-19 demonstrated there existed mild pancreatitis.
mild pancreatic injury | is in | patients with COVID-19 (count: 1)
Our study revealed the phenomenon and possible cause of mild pancreatic injury in patients with COVID-19.
mild pancreatic lesions | is in | patients with COVID-19 (count: 1)
These clinical data show that there exist mild pancreatic lesions in some patients with COVID-19, mainly in severe cases.
damage | is in | proportion of patients with SARS-CoV-2 infection (count: 1)
In this study, we focused on the expression of ACE2 in pancreas and the damage to the pancreas in a proportion of patients with SARS-CoV-2 infection.
attention | should | should paid in patients with SARS-CoV-2 infection in severe cases (count: 1)
Therefore, increased attention should be paid to the pancreas in patients with SARS-CoV-2 infection, especially in severe cases.
systemic inflammatory response | is in | severe COVID-19 patients (count: 1)
At the same time, the systemic inflammatory response in severe COVID-19 patients might also cause mild damage to the pancreas.
severe COVID-19 patients | is in | early stage (count: 1)
ESR can be used as a valuable indicator for distinguishing severe COVID-19 patients in early stage, so as to increase the survival of severe patients.
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severe COVID-19 patients | for factor is | 12 (count: 1)
suggest that lymphocytopenia can be used as an useful prognostic factor for severe COVID-19 patients [12] .
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COVID-19 patients | were enrolled including | 29 mild patients (count: 1)
A total of 43 COVID-19 patients were enrolled in this study, including 29 mild patients (67.4%) and 14 sever patients (32.6%) according to above mentioned conditions.
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studies | have reported | increase in COVID-19 patients in severe patients (count: 1)
Recent studies have reported an increase in serum cytokine levels in COVID-19 patients, especially in severe patients, and suggest that cytokine storm is associated with disease severity [6, 13] .
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Our study | identify | severe COVID-19 patients (count: 1)
Our study may help to identify severe COVID-19 patients in early stage, in order to provide supportive treatment and reduce the mortality.
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mild cases | indicating | COVID-19 (count: 1)
18 Our findings showed that CD4 and CD8 T lymphocytes have significant difference (p < 0.01) between mild (Non-ICU) and severe or critical (ICU) cases without glucocorticoid treatment indicating COVID-19 directly effected on immune system is possible.
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syncytium | was formed after | coincubation similar to syncytium formed by 154 SARS-CoV-2-infected Huh-7 cells (count: 1)
Their syncytium 153 was obviously formed after coincubation for 48 h, similar to the syncytium formed by 154 live SARS-CoV-2-infected Huh-7 cells (Fig.
SARS-CoV-2 S protein | mediating entry into | 159 target cells 14 (count: 1)
Therefore, compared to SARS-CoV, SARS-CoV-2 S 158 protein showed much more efficiency in mediating viral surface-fusion and entry into 159 target cells 14 .
SARS-CoV-2 | enter inside | host cells (count: 1)
SARS-CoV, live SARS-CoV-2-infected cells were found to form typical359 syncytium, suggesting that SARS-CoV-2 may mainly utilize the plasma membrane to enter and replicate inside host cells.
SARS-CoV-2 | caused | severe 446 changes (count: 1)
However, SARS-CoV-2 mainly infected and caused severe 446 pathological changes in human lung tissue 4 .
target cells 542 | 293T/ACE2 for | SARS-CoV-2 (count: 1)
To 541 detect the inhibitory activity of a peptide on infection of coronavirus PsV, target cells 542 (293T/ACE2 for SARS-CoV-2, SARS-CoV and SL-CoVs; RD cells for HCoV-OC43; 543 Huh-7 for other CoVs) were plated at a density of 10 4 cells per well in a 96-well plate 544 one day prior to infection 14 .
COVID-19 patients | may develop | mild symptoms (count: 1)
COVID-19 patients may develop mild or severe symptoms after infection.
SARS-CoV-2 | infect | bile duct cells (count: 1)
11 All these findings suggest that SARS-CoV-2 may infect the bile duct cells and cause the abnormal liver function in these patients.
SARS-CoV-2 | invaded | host cells (count: 1)
Here, we reported a research finding that SARS-CoV-2 invaded host cells via a novel route of CD147-spike protein (SP).
localization | was observed in | SARS-CoV-2 Vero E6 cells (count: 1)
Finally, the localization of CD147 and SP was observed in SARS-CoV-2 infected Vero E6 cells by immuno-electron microscope.
possible function | is in | invasion for host cells by SARS-CoV-2 (count: 1)
Owing to the similar characteristics of SARS-CoV and SARS-CoV-2, we conduct the present study to investigate the possible function of CD147 in invasion for host cells by SARS-CoV-2.
possible function | is in | SARS-CoV-2 invasion for host cells (count: 1)
The antiviral tests were performed to investigate the possible function of CD147 in SARS-CoV-2 invasion for host cells.
CD147 | is associated with | SARS-CoV-2 invasion for host cells (count: 1)
CD147 is closely associated with SARS-CoV-2 invasion for host cells, and SP binds to cellular receptors to mediate infection of host cells [7] , leading to the question whether there is some author/funder.
route | facilitated | SARS-CoV-2 invasion for host cells (count: 1)
The route of CD147-SP facilitated SARS-CoV-2 invasion for host cells.
SARS-CoV-2 fragments | reduce | replication in lung cells (count: 1)
We demonstrated the ability of our approach to cleave SARS-CoV-2 fragments and to reduce the replication of IAV in human lung epithelial cells.
SARS-CoV-2 | infect | tract cells (count: 1)
As SARS-CoV-2 appears to mainly infect respiratory tract cells in patients 5 , we chose to use human lung epithelial A549 cells as a model cell line.
we | transfected SARS-CoV-2 reporters into | Cas13d A549 cells (count: 1)
To do this, we transfected or transduced the SARS-CoV-2 reporters into Cas13d A549 cells that had been transduced with pools of four crRNAs targeting either RdRP or N gene regions (Fig.
SARS-CoV-2 sequences | is in | human cells (count: 1)
These data together suggest: 1) Cas13d PAC-MAN can be an effective system to target and degrade SARS-CoV-2 sequences in human cells and 2) proper design of crRNAs are important for obtaining a high efficiency of SARS-CoV-2 inhibition.
H1N1 IAV | virus as | SARS-CoV-2 for respiratory tract epithelial cells (count: 1)
Since we do not yet have access to live SARS-CoV-2 virus, as a proof-of-concept we elected to test the CRISPR-Cas13d strategy on inhibiting H1N1 IAV, a RNA virus with a similar tropism as SARS-CoV-2 for respiratory tract epithelial cells.
cells | were challenged with | SARS-CoV-2 reporter plasmids (count: 1)
On day 3, cells were switched to fresh medium with Puromycin at 2 ug/mL. Twenty-four hours after Puromycin selection, cells with transfected crRNAs were challenged with SARS-CoV-2 reporter plasmids or SARS-CoV-2 reporter lentivirus.
SARS-CoV-2 virions | bind to | ACE2 receptor on surface of cells (count: 1)
SARS-CoV-2 virions bind to the ACE2 receptor on the surface of cells via interactions with the Spike protein.
D Workflow | challenge Cas13d A549 lung cells with | SARS-CoV-2 reporters (count: 1)
D) Workflow used to challenge Cas13d A549 lung epithelial cells with SARS-CoV-2 reporters.
Lenti-X 293T cells | were transfected with | 27.18 μg of SARS-CoV-2 reporter (count: 1)
The following day, Lenti-X 293T cells were transfected with 27.18 μg of SARS-CoV-2 reporter, 23.76 μg of dR8.91 and 2.97 μg of pMD2.G (Addgene) in 4.5 mL of Opti-MEM reduced serum media (Gibco) with 150 μL of Mirus TransIT-LT1 reagent.
SARS-CoV-2 | enter | host target cells (count: 1)
Both SARS-CoV and SARS-CoV-2 interact directly with angiotensin-converting enzyme 2 (ACE2) to enter host target cells (Hoffmann et al.,
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ACE2 | receptor for | entry into target cells by SARS-CoV-2 (count: 1)
ACE2, the receptor for entry into the target cells by SARS-CoV-2, was found to abundantly express in testes, including spermatogonia, Leydig and Sertoli cells.
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cells | were disturbed under | COVID-19 (count: 1)
Therefore, it seemed that Sertoli cells were less disturbed than Leydig cells under COVID-19.
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increase | was | In COVID-19 observed in severe cases (count: 1)
In COVID-19, rapid and dramatic increase of CRP was observed more often in severe cases than in non-severe cases [19] .
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2019-nCoV | cause | severe illness (count: 1)
Like SARS-CoV and MERS-CoV, 2019-nCoV can spread from the human to human and cause fever, severe respiratory illness, and a series of unidentified pneumonia disease (Chan et al.,
2019-nCoV | entering into | cells (count: 1)
2019-nCoV utilizes cell membrane receptor for entering into cells and causes infection diseases.
we | see | severe COVID-19 (count: 1)
If more generalised outbreaks occur outside China, we may start to see severe COVID-19 presenting to UK healthcare services.
school breaks | contributed to | proportion of COVID-19 cases (count: 1)
It is unclear whether nationwide school breaks could have contributed to the low proportion of confirmed COVID-19 cases among school-age individuals, and whether schools reopening will lead to a change in the transmission patterns of COVID-19.
patients | were diagnosed with | severe COVID-19 pneumonia (count: 1)
Three patients were diagnosed with severe COVID-19 pneumonia.
Tongji hospital | was assigned | responsibility for treatments of severe COVID-19 patients (count: 1)
Tongji hospital was assigned responsibility for the treatments of severe COVID-19 patients by Wuhan government on January 31 th .
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studies | focused on | characteristics of patients with COVID-19 in mild cases (count: 1)
Previous studies focused on the epidemiologic, clinical characteristics and outcomes of patients with COVID-19 in mild and severe cases [5] [6] .
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severe cases | is with | COVID-19 (count: 1)
Organ dysfunction including acute respiratory distress syndrome, shock, acute cardiac injury, and acute renal injury, could occur in severe cases with COVID-19, which lead to poor clinical outcome.
ratio | was identified as | indicator for severe COVID-19 (count: 1)
Increasing clinical data indicated that the neutrophil-to-lymphocyte ratio (NLR) was identified as a powerful predictive and prognostic indicator for severe COVID-19.
overall exaggerated immune activation | is in | severe SARS-CoV-2 infection (count: 1)
5 Here, we evaluated antibody response within 35 days after symptom onset in laboratory-confirmed case with COVID-19 as one component of an overall exaggerated immune activation in severe SARS-CoV-2 infection, and developed an immune phenotyping based on late IgG response and NLR that could help determine disease severity and clinical outcome of COVID-19 patients.
NLR | was identified as | factor for severe COVID-19 (count: 1)
3, 11, 12 Recent data indicated that the NLR was identified as a powerful predictive and prognostic factor for severe COVID-19.
severe COVID-19 | was | associated (count: 1)
Nevertheless, our findings indicate that severe COVID-19 was associated with a more robust IgG response that can be developed as an acquired immunity-related marker to predictive disease severity, along with other innate immunity-relate makers such as NLR.
Median anti-SARS-CoV-2 IgG | is in | patients with severe illness within 35 days after symptom onset (count: 1)
Median anti-SARS-CoV-2 IgG and IgM levels in patients with severe or nonsevere illness within 35 days after symptom onset. (
severe patients | had P/F ratio Among | 101 patients with COVID-19 (count: 1)
Among 101 hospitalized patients with confirmed COVID-19, 23 severe patients had P/F ratio less than 300mmHg, 9 critical patients had P/F ratio less than 150mmHg, accompanied by elevated lactate level.
COVID-19 patients | had | had treated for 22 severe patients (count: 1)
Depended on rich experience of respiratory specialist on treatment of viral pneumonia, COVID-19 patients had been treated well, particularly for 22 severe and critical patients.
rapid spread | is in | severe COVID-19 patients (count: 1)
At the beginning of this new epidemic crisis, the missing or insufficient hospital emergency responsive plan caused rapid spread of COVID-19 and high mortality in severe COVID-19 patients.
SARS-CoV-2 | is related to | group of severe coronaviruses (count: 1)
[1] As the name suggests, SARS-CoV-2 is closely related to a group of severe acute respiratory syndrome-related coronaviruses (SARSr-CoV), namely subgenus Sarbecovirus, showing 96% identity to a bat coronavirus [2, 3] .
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SARS-CoV-2 | of protein is | type I transmembrane glycoprotein expressed on epithelial cells (count: 1)
12 Our current published data showed a direct interaction between spike protein of SARS-CoV-2 and CD147, a type I transmembrane glycoprotein expressed on epithelial cells.
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meplazumab treatment | make | recovery from COVID-19 pneumonia for severe cases (count: 1)
These results indicated that meplazumab treatment accelerated the improvement and make a rapid recovery from COVID-19 pneumonia, especially for the severe and critical cases.
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COVID-19 pneumonia patients | had | counts of blood cells (count: 1)
Compared to the controls, COVID-19 pneumonia patients had lower counts of white blood cells (WBC), neutrophils, C-reactive protein (CRP), and alanine aminotransferase (ALT) on admission.
SARS-CoV-2 infection | caused | mild symptoms (count: 1)
We found that SARS-CoV-2 infection caused generally mild respiratory symptoms in pregnant women.
COVID-19 pneumonia | causes | severe complications (count: 1)
In this study, we did not find any evidence to suggest that COVID-19 pneumonia causes severe maternal and neonatal complications among pregnant women who had vaginal All rights reserved.
2019-nCoV | use civet as | entry receptor in cells (count: 1)
had experimentally confirmed that 2019-nCoV is able to use human, Chinese 18 horseshoe bats, civet, and pig ACE2 as an entry receptor in the ACE2-expressing cells(2), 19 suggesting the RBD of 2019-nCoV mediates infection to human and other animals.
severe COVID-19 patients | were | admitted (count: 1)
More severe COVID-19 patients were admitted to Tongji Hospital.
b | is in | Vero cells infected with SARS-CoV-2 (count: 1)
b, NHC 637 antiviral activity and cytotoxicity in Vero cells infected with SARS-CoV-2.
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Vero cells | duplicate with | SARS-CoV-2 isolate virus (count: 1)
Vero cells were infected in 638 duplicate with SARS-CoV-2 clinical isolate virus at an MOI of 0.05 in the presence of a dose response of 639 drug for 48 hours, after which replication was measured through quantitation of cell viability by Cell-Titer-640 Glo assay.
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We | proportion of | COVID-19 patients (count: 1)
Interpretation: We reported a large proportion of COVID-19 patients with coinfection of seasonal respiratory pathogens in Qingdao, northeast China, which differed greatly from the patients in Wuhan, central China.
COVID-19 patients | had | mild symptoms (count: 1)
A study conducted in Zhejiang Province, China revealed that COVID-19 patients outside of Wuhan had relatively mild symptoms as compared with those initially reported in Wuhan.
2019-nCoV | causes | severe pneumonia (count: 1)
2019-nCoV invades the lungs through the respiratory tract and causes severe pneumonia, which is the main pathogenesis mode.
2019-nCoV | bind on | surface of cells (count: 1)
It was found that 2019-nCoV was able to bind to ACE2 receptor on the surface of epithelial cells.
cells | infected by | 2019-nCoV (count: 1)
further confirmed that ACE2 was necessary for the cells infected by 2019-nCoV(4).
patients | diagnosed as | mild cases of COVID-19 pneumonia (count: 1)
Chinese experts recommend that patients diagnosed as mild, moderate and severe cases of COVID-19 pneumonia and without contraindications to chloroquine, be treated with 500 mg chloroquine twice a day for ten days [11] .
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severe patients | be | COVID-19 (count: 1)
Factors predicting progressive diseaseDuring hospital stay, 1 case with common-type COVID-19 progressed to be severe COVID-19, 4 severe patients progressed to be extremely severe COVID-19.
2019-nCoV | During | infection of host cells (count: 1)
During the 2019-nCoV's infection of host cells, a critical virion protein is the Spike surface glycoprotein, also known as the S protein.
SARS-CoV-2 | enters body on | surface of cells (count: 1)
Researchers have confirmed that SARS-CoV-2 enters the human body through ACE2 receptors on the surface of human cells and causes disease 5 .
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SARS-CoV-2 | enter body on | surface of cells (count: 1)
Moreover, recent study showed that SARS-CoV-2 could enter the human body through ACE2 receptors on the surface of human cells and causes disease 5 .
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2019-nCoV RBD | entering | cells (count: 1)
The 2019-nCoV RBD was capable of entering cells expressing human ACE2, but not any of the other receptors tested (figure 3d; s3).
patients | is with | 2 9 4 severe COVID-19 (count: 1)
T lymphocytes, CD4 + T cells and CD8 + T cells decreased in the majority of patients with either 2 9 4 severe (100%, 100% and 87.5%) or moderate COVID-19 (83.3%, 100% and 83.3%), and 2 9 5 total T lymphocytes, CD4 + T cells and CD8 + T cells counts were reduced more profoundly in author/funder, who has granted medRxiv a license to display the preprint in perpetuity.
CD4 cells | is in | patients infected with 2019-nCoV (count: 1)
These CD4 + T cells in patients infected with 2019-nCoV have 77 higher expression of CD69, CD38, and CD44 compared with healthy controls (Fig.1a, b) , 78 indicating their activated status.
Activated T cells | is in | severe pulmonary syndrome patients of 2019-nCoV (count: 1)
Activated T cells in severe pulmonary syndrome patients of 2019-nCoV. (a, b) Representative density plots and MFI statistics calculated for CD69, CD38, CD44 and OX40 expressions in gated CD45 + CD3 + CD4 + T cells (Gating strategy showing in Extended Data Figure 2a) isolated from peripheral blood in healthy controls, ICU and non-ICU patients of 2019-nCoV. (c, d) Representative density plots and MFI statistics calculated for CD69, CD38, CD44 and 41BB expressions in gated CD45 + CD3 + CD8 + T cells isolated from peripheral blood in healthy controls, ICU and non-ICU patients of 2019-nCoV. (e, f) Representative density plots and percentage statistics calculated for Tim-3 and PD-1 co-expressions in gated CD45 + CD3 + CD4 + T cells isolated from peripheral blood in healthy controls, ICU and non-ICU patients of 2019-nCoV. (g, h) Representative density plots and percentage statistics calculated for Tim-3 and PD-1 co-expressions in gated CD45 + CD3 + CD8 + T cells isolated from peripheral blood in healthy controls, ICU and non-ICU patients of 2019-nCoV. Data represent the mean ± SEM.
Pathogenic Th1 cells | is in | severe pulmonary syndrome patients of 2019-nCoV (count: 1)
Pathogenic Th1 cells with high expression of GM-CSF in severe pulmonary syndrome patients of 2019-nCoV. (a) Representative density plots showing an analysis of GM-CSF and IL-6 expressions in gated CD45 + CD3 + CD4 + T cells (Gating strategy showing in Extended Data Figure 1a) isolated from peripheral blood in healthy controls, ICU and non-ICU patients of 2019-nCoV. (b) Representative density plots showing an analysis of co-expression of GM-CSF and IFN- in gated CD45 + CD3 + CD4 + T cells isolated from peripheral blood in healthy controls, ICU and non-ICU patients of 2019-nCoV. (c) Statistics calculated by the percentage of GM-CSF+ or IL-6+ cells from CD4 + T cells. (
high expression | is in | severe pulmonary syndrome patients of 2019-nCoV (count: 1)
Inflammatory monocytes with high expression of IL-6 in severe pulmonary syndrome patients of 2019-nCoV. (a) Representative density plots showing an analysis of CD14 and CD16 expressions in gated CD45 + monocytes (Gating strategy showing in Extended Data Figure 1a) isolated from peripheral blood in in healthy controls, ICU and non-ICU patients of 2019-nCoV. (b) Representative density plots showing an analysis of GM-CSF and IL-6 expressions in gated CD45 + CD14 + monocyte cells isolated from peripheral blood in healthy controls, in ICU and non-ICU patients of 2019-nCoV. (c) Statistics calculated by the percentage of CD14 + CD16 + subsets from monocytes.
prophylactic anti-coagulation therapy | mollifying damage during | severe 91 COVID-19 (count: 1)
2,19 Given that angiotensin II levels were highly elevated in the HCoV-19 89 infected patients, 20 RAS was likely activated in HCoV-19 infected patients, Thus, prophylactic 90 anti-coagulation therapy should be considered for mollifying the multi-organ damage during severe 91 COVID-19.
531 represented severe COVID-19 patient | of images is | right panel (count: 1)
Chest CT images in the axial (left panel) and coronal view (right panel) of 531 represented severe COVID-19 patient before and after receiving DIP adjunctive therapy. (
non-severe case | is with | COVID-19 (count: 1)
Clinical data is limited up to now regarding the risk factors in favor of severe conversion of non-severe case with COVID-19.
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20.5 % | is with | non-severe course of COVID-19 suffered from acute hepatic injury (count: 1)
In this study, there were about 20.5% of cases with non-severe course of COVID-19 suffered from acute hepatic injury, needed liver protection treatment.
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RNA sequencing | characterised | transcriptome of SARS-CoV-2 grown in Vero E6 cells (count: 1)
Direct RNA sequencing using an Oxford Nanopore MinION characterised the transcriptome of SARS-CoV-2 grown in Vero E6 cells.
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SARS-CoV-2 stock | infecting | Vero E6 cells (count: 1)
A SARS-CoV-2 stock was produced by infecting Vero E6 cells at a multiplicity of infection (MOI) of 0.01 and incubating the cells for 72 hours.
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severe cases | is in | COVID-19 patients (count: 1)
Next, we examined the possibilities of using above-mentioned parameters as prognostic factors for identifying severe cases in COVID-19 patients.
favorable outcome | is in | severe COVID-19 patients (count: 1)
All these severe patients included in our study survived the disease, and thus we speculate this course is associated with a favorable outcome in severe COVID-19 patients.
we | identified N8R as | factors for identification of severe COVID-19 cases (count: 1)
Importantly, we identified N8R and NLR as powerful prognostic factors for early identification of severe COVID-19 cases.
NLR | is with | our patient cohort as predictive factors for severe COVID-19 (count: 1)
The results were obtained for NLR (OR: 143, 95% Cl: 11.72-1745.3), N8R (OR: 68.75, 95% Cl: 8.55-552.68), NE (OR: 22, 95% Cl: 3.646-132.735) and WBC (OR: 55, 95% Cl: 6.779-446.23) with our patient cohort as predictive factors for severe COVID-19.
severe COVID-19 patients | have | concentrations (count: 1)
Our results also demonstrate that severe COVID-19 patients have higher concentrations of IL6, IL10, IL2 and IFN-γ in the serum than mild cases, suggesting that the magnitude of1 6 cytokine storm is associated with the disease severity.
kinetic changes | is in | severe COVID-19 patients (count: 1)
In line with this hypothesis, we observed that the kinetic changes of T cell counts are reversely correlated with the kinetic changes of most examined cytokine levels in the peripheral blood in severe COVID-19 patients.
2019-nCoV infection | activity of | NK cells (count: 1)
The reduction ratio of NK cells accounted for 172 34.31% in the mild group and 47.62% in the severe group, which suggested that 2019-nCoV 173 infection limited the activity of NK cells to a certain extent, and in view of the fact that immune 174 adjuvant IL-2 can improve the activity of NK cells, the above research results may provide new 175 .
trend | is in | mild COVID-19 patients (count: 1)
We found that in comparison with the control group, there was a trend of decrease in B cell cellularity in mild COVID-19 patients, and a notable reduction in B cells of severe COVID-19 patients ( Figure 2B) .
COVID-19 patients | ' cells is | Figure 2C (count: 1)
A similar decrease was also seen in COVID-19 patients' NK cells ( Figure 2C ).
Tregs | were increased in | mild COVID-19 patients (count: 1)
We found that Tregs were increased in mild COVID-19 patients as compared with controls ( Figure 3B ).
lymphopenia | is indicator of | severe COVID-19 (count: 1)
Whatever the case, lymphopenia is an indicator of severe COVID-19.
CD8 | is in | lung microenvironment of mild COVID-19 patients (count: 1)
unpublished data indicate highly expanded clonal CD8+ T cells in the lung microenvironment of mild COVID-19 patients, suggesting a robust adaptive immune response connected to a better control of COVID-19 (https://www.medrxiv.org/content/10.1101/2020.02.23.20026690v1.full.pdf).
NK cells | is in | COVID-19 patients at hospital admission (count: 1)
Cellularity of blood B cells, NK cells and NKT cells in COVID-19 patients at hospital admission. (
COVID-19 | presents | mild symptoms (count: 1)
Despite in most of the cases (80%) COVID-19 presents mild symptoms, in some cases the admission to intensive care units (ICU) and the use of mechanical ventilation are necessary.
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SARS-CoV-2 spike protein | precluding | virus entry into cells (count: 1)
This peptide binder to SARS-CoV-2-RBD provides new avenues for 44 COVID-19 treatment and diagnostic modalities by blocking the SARS-CoV-2 spike protein 45 interaction with ACE2 and thus precluding virus entry into human cells.
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SARS-CoV-2 | causes | severe problems (count: 1)
Similar to the SARS-CoV outbreak in 2002, SARS-CoV-2 56 causes severe respiratory problems.
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structures | have identified PPI as | step for entry of SARS-CoV-2 to cells (count: 1)
Recently published cryo-EM and co-crystal structures of the RBD of SARS-CoV-2 with 121 human ACE2 have identified this PPI as key step for the entry of SARS-CoV-2 to human cells.
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world | severe outbreak of | COVID-19 (count: 1)
This sharp increase in number of new cases and cumulative cases indicated that the world is experiencing a severe epidemic outbreak of COVID-19 with little evidence of mitigation.
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world | was in | severe situation of COVID-19 outbreak (count: 1)
The world was in a severe situation of the COVID-19 outbreak.
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world | experiencing | severe COVID-19 pandemic (count: 1)
We found the sharp increasing trends in new cases and cumulative cases and the expanding number of epidemic centers, indicating that the world is experiencing a severe COVID-19 pandemic with little evidence of mitigation.
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22 patients | is with | severe COVID-19 (count: 1)
There were 22 patients with severe COVID-19, and the proportion of severe Table 2 for the detailed data. .
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areas | is with | severe SARS-CoV-2 infection (count: 1)
All countries have adopted isolation measures for imported populations from areas or countries with severe SARS-CoV-2 infection, and treated patients with symptoms who have a history of contact with this imported population 1 .
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2019-nCoV | may cause failure in | severe pneumonia patients (count: 1)
In a recent clinical report, 2019-nCoV may cause cytokine storm and multi-organ failure in severe pneumonia patients(8).
SARS-CoV-2 S1 subunit | were | expressed in 293T cells (count: 1)
Likewise, the SARS-CoV-2 S1 subunit or its subdomains (S;S1, residues 1-682; S1 A , residues 1-294; RBD, residues 329-538; GenBank: QHD43416.1) were expressed in 293T cells as
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SARS-CoV-2 specific antibody responses | is in | severe cases (count: 1)
We evaluated SARS-CoV-2 specific antibody responses in severe and mild cases using serum samples collected at different times post-disease onset from three French PCR-confirmed CoVID-19 patients.
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We | tested | two mild SARS-CoV-2 patients (count: 1)
We tested one severe (red) and two mild (green and black) SARS-CoV-2 patients for antibody responses against the (A) Spike (S), (B) spike S1 subunit, (C) spike N-terminal (S1 A ) domain, (D) receptor binding domain, (E) nucleocapsid proteins using ELISAs. (
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COVID-19 patients | lead to | severe state (count: 1)
Previous report indicated that Mycoplasma fermentans enhanced the cytotoxicity against Vero E6 cells infected with SARS-CoV. 20 This indicate COVID-19 patients co-infected with the two types of pathogens may lead to more severe state, thus clinicians need pay attention to the screening of these two pathogens in these patients.
COVID-19 | is | severe disease (count: 1)
COVID-19 is a novel severe respiratory disease.
SARS-CoV-2 infection | induces | severe necrosis (count: 1)
Collectively, these results demonstrated that SARS-CoV-2 infection mainly induces severe acute tubular necrosis and lymphocyte infiltration.
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risk | is in | severe COVID-19 (count: 1)
Higher serum hs-CRP could also be used to predict the risk of death in severe COVID-19
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2019-nCoV | infect | host cells (count: 1)
Since the receptor-binding of S-protein is the major driving force for the viral transmission to the human host cells, such a strength order supports that 2019-nCoV is able to infect the human host cells like SARS-CoV .
we | determined at | risk of severe COVID-19 (count: 1)
Because individuals with chronic obstructive pulmonary disease (COPD) are at increased risk of severe COVID-19, we determined whether ACE-2 expression in the lower airways was related to COPD and cigarette smoking.
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COVID-19 | is caused by | severe syndrome coronavirus-2 (count: 1)
COVID-19 is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2).
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severe inflammatory cascade | is in | patients with COVID-19 (count: 1)
In the present study, CRP and SAA were elevated before death in 85% and 100% of patients, suggesting that there is a severe inflammatory cascade in patients with COVID-19.
COVID-19 remains | severe At | time (count: 1)
At the time of this writing, the COVID-19 epidemic remains very severe.
SARS-CoV-2 | is similar to | severe syndrome (count: 1)
SARS-CoV-2 is very similar to the severe acute respiratory syndrome (SARS) coronavirus broke out 17 years ago.
we | have performed | exploration of characteristics of 221 patients with COVID-19 including 55 severe patients (count: 1)
14 In this study, we have performed a comprehensive exploration of the epidemiological, clinical, laboratory and radiological characteristics of 221 hospitalized patients with laboratory-confirmed COVID-19, including 55 severe patients and 166 non-severe patients of Zhongnan Hospital of Wuhan University, Wuhan, China, from January 2 to February 10, 2020.
severe COVID-19 patients | were | defined (count: 1)
The severe or critical COVID-19 patients were defined according to the following criteria: fever plus one of these conditions, including respiratory rate ≥ 30 breaths/min, severe respiratory distress, SpO2 ≤ 93% on room air, occurrence of respiratory failure requiring mechanical ventilation, shock and other organ failure.
remdesivir | shown in | one severe COVID-19 pneumonia patient 29 (count: 1)
4 28 In addition, a case report showed that remdesivir, an adenosine analogue, has shown survival benefits in one severe COVID-19 pneumonia patient 29 .
72-year-old man | is with | severe COVID-19 (count: 1)
Case A:Transverse chest CT images from a 72-year-old man with severe COVID-19.
44-year-old man | is with | mild COVID-19 (count: 1)
Case B: Transverse chest CT images from a 44-year-old man with mild COVID-19.
2019-nCoV-S-and SARS-S-92 | driven into | BHK-21 cells (count: 1)
In agreement with these findings, directed expression 90 of human and bat ACE2 but not human DPP4, the entry receptor used by MERS-CoV (20), or 91 human APN, the entry receptor used by HCoV-229E (21), allowed 2019-nCoV-S-and SARS-S-92 driven entry into otherwise non-susceptible BHK-21 cells (Fig.
ammonium chloride treatment | inhibited | 2019-nCoV-S-105 entry into TMPRSS2 -293 T cells (count: 1)
Moreover, ammonium chloride treatment strongly inhibited 2019-nCoV-S-105 and SARS-S-driven entry into TMPRSS2 -293T cells while inhibition of entry into TMPRSS2 + 106 Caco-2 cells was less efficient, which would be compatible with 2019-nCoV-S priming by 107 TMPRSS2 in Caco-2 cells.
target cells | has | implications for our understanding of 2019-nCoV transmissibility (count: 1)
120 target cells has important implications for our understanding of 2019-nCoV transmissibility and 121 pathogenesis.
2019-nCoV | targets | cells (count: 1)
Thus, one can expect that 2019-nCoV targets the same cells as SARS-CoV and that 122 the previously documented modest ACE2 expression in the upper respiratory tract (23, 28) might 123 limit 2019-nCoV transmissibility.
addressing | search for | 2019-nCoV receptor cells (count: 1)
For 44 experiments addressing the search for the 2019-nCoV receptor cells were transfected with 45 expression plasmids 24 h in advance.
293T cells | tagged | 2019-nCoV-S (count: 1)
51 52 Analysis of 2019-nCoV-S expression and particle incorporation by SDS-PAGE and 53 immunoblot 54 Preparation of whole cell lysates: 293T cells were transfected with expression vectors for HA-55 tagged 2019-nCoV-S or SARS-S , or empty expression vector (negative control).
patients | is with | severe coronavirus disease 2019 (count: 1)
To compare the sex differences in the clinical findings among patients with severe coronavirus disease 2019 .
Conclusion | exist in | COVID-19 patients of severe type (count: 1)
Conclusion: Sex differences may exist in COVID-19 patients of severe type.
men | is with | severe type of COVID-19 (count: 1)
In this study, we aim to compare clinical findings between men and women with severe type of COVID-19, and hope to contribute to the prevention and treatment.
COVID-19 patients | were classified as | severe pneumonia (count: 1)
From February 8 to February 11, 2020, 47 laboratory-confirmed COVID-19 patients were classified as severe pneumonia at the area, 28 (59.6%) cases were men.
we | analyzed | data from 47 patients with COVID-19 of severe type (count: 1)
In this retrospective study, we analyzed data from 47 patients with laboratory-confirmed COVID-19 of severe type.
those | had outcomes in | severe COVID-19 patients (count: 1)
19] found that in severe COVID-19 patients, those with cancer had poorer outcomes from COVID-19.
severe COVID-19 | was | defined (count: 1)
According to the diagnostic and treatment guidelines for COVID-19 issued by the Chinese National Health Committee, severe COVID-19 was defined as All rights reserved.
COVID-19 | severe patients of were | 18.4 % (count: 1)
The death toll and severe patients of COVID-19 were 18.4% and 2.5%.
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COVID-19 | is caused by | severe 40 syndrome coronavirus 2 (count: 1)
COVID-19 is caused by a novel coronavirus, severe 40 acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (2).
cells | Sprotein of | 2019-nCoV (count: 1)
According to the evolutionary analysis of coronavirus, 2019-nCov is probably originated from bat, and the Sprotein of 2019-nCoV may enter human cells by interacting with human ACE2 receptor, which revealed the pathopoeia mechanism of 2019-nCoV 1 .
2 | were severe patients Of | 12 patients with COVID-19 (count: 1)
Of the 12 patients with COVID-19, 2 were severe patients, 8 were general patients, and 2 were light patients.
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case study | reported | 59 patients infected by 2019-nCoV including 28 severe cases (count: 1)
Previously, an ongoing case study reported 59 patients infected by 2019-nCoV, including 28 severe cases and 3 death.
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2019-nCoV | is similar to | severe syndrome (count: 1)
Notably, the 2019-nCoV is highly similar to the severe acute respiratory syndrome 54 coronavirus (SARS-CoV), which is characterized by high mortality and infectivity.
mild infection | is In | 34 COVID-19 cases with inconsistent results (count: 1)
In 34 COVID-19 cases with inconsistent results, 94.1% (n=32) are mild infection, 62.5% of which (20/32) showed positive RT-PCR.
we | pay attention in | severe COVID-19 patients (count: 1)
It should be noted that we have to pay great attention on the tachycardia in the severe and critical COVID-19 patients.
COVID-19 patients | is in | severe cases (count: 1)
https://doi.org/10.1101/2020.02.24.20027052 doi: medRxiv preprint those COVID-19 patients in severe and critical cases.
COVID-19 patients | be in | severe cases (count: 1)
COVID-19 patients with cardiacrelated chronic diseases could be more prone to be in the severe or critical cases.
three mild cured patients | is with | COVID-19 (count: 1)
To further validate this finding, we performed quantitative real-time reverse transcriptase polymerase chain reaction (RT-PCR) testing to detect the expressions of IRF27, BST2, and FOS in another cohort of three critical, three server, 19 moderate, three mild and 10 cured patients with COVID-19 and five normal controls (Fig.
COVID-19 | enters | cells (count: 1)
Studies revealed that COVID-19 enters cells mainly through angiotensin converting enzyme 2.
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International Committee | announced | classification of 2019-nCoV as severe syndrome coronavirus 2 (count: 1)
In addition, the International Committee on Taxonomy of Viruses (ICTV) announced the official classification of 2019-nCoV as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1] [2] [3] [4] .
SARS-CoV-2 S glycoprotein | mediates | entry into host cells (count: 1)
The SARS-CoV-2 S glycoprotein mediates viral entry into host cells and therefore represents a prime target for drug and vaccine development (17, 18) .
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severe SARS-CoV-2 disease | corresponded to | age (count: 1)
In addition, the most severe SARS-CoV-2 disease corresponded to old age (>50 35 years old), health status, and health care workers, similar to both SARS and MERS-CoV 5 .
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severe SARS-CoV-2 cases | have | have observed (count: 1)
Notably, less severe SARS-CoV-2 cases have also been observed and were 44 not captured in the original SARS-CoV outbreak.
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Vero E6 cells | explore | replication kinetics of SARS-CoV-2 (count: 1)
Our initial studies infected Vero E6 cells using a low multiplicity of infection (MOI) to 75 explore the viral replication kinetics of SARS-CoV-2 relative to SARS-CoV. Following infection, 76
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we | examined protein production in | 96 nucleocapsid protein production in IFN-I cells following SARS-CoV-2 infection (count: 1)
Finally, we examined viral protein production finding a major deficit in 96 nucleocapsid protein production in IFN-I treated cells following SARS-CoV-2 infection (Fig.
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SARS-CoV-2 | is in | untreated cells (count: 1)
In contrast, viral proteins were robustly expressed for SARS-CoV-2 in untreated cells and for 98 SARS-CoV in both conditions.
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IFN-I cells | infected with | SARS-CoV-2 (count: 1)
Examining Vero cell protein lysates, we found that IFN-I treated cells infected with 104 SARS-CoV-2 induced phosphorylated STAT-1 by 48 hours post infection (Fig.
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STAT1 phosphorylation | was absent in | cells infected with SARS-CoV-2 (count: 1)
STAT1 105 phosphorylation was absent in untreated cells infected with SARS-CoV-2 and suggest the novel 106
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115 COVID-19 patients | are classified as | mild to cases (count: 1)
All 115 COVID-19 patients are classified as mild to critically ill cases at admission, according to 116
We | construct model at | risk of progression to severe COVID-19 (count: 1)
We aimed to construct an effective model for early identifying cases at high risk of progression to severe COVID-19.
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RDW | predicting | severe COVID-19 (count: 1)
The RDW plays an important role in predicting severe COVID-19, implying that the role of RBC in severe disease is underestimated.
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severe illnesses | colds such as | cause of COVID-19 1 (count: 1)
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a member of coronaviruses known to cause common colds and severe illnesses such as , is the cause of COVID-19 1 .
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COVID-19 patients | have | mild disease course (count: 1)
Most COVID-19 patients have a mild disease course, while some patients experience rapid deterioration (particularly within 7-14 days) from onset of symptoms into severe COVID-19 with or without acute respiratory distress syndrome (ARDS) 3 .
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mortality rate | is higher than | that of non-severe COVID-19 patients (count: 1)
Current epidemiological data suggests that the mortality rate of severe COVID-19 patients is about 20 times higher than that of non-severe COVID-19 patients 4, 5 .
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we | developed | nomogram with sensitivity for assessment of incidence of severe COVID-19 (count: 1)
Based on these indexes, we developed and validated an effective prognostic nomogram with high sensitivity and specificity for accurate individualized assessment of the incidence of severe COVID-19.
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non-severe COVID-19 group | consisted with | age (count: 1)
In the train cohort, the non-severe COVID-19 group consisted of 159 (86.41%) patients, with a median age of 45 years of age (range 33-61 years) while 25 patients (13.59%), with a median age of 64 years of age (range 55-72 years) progressed to severe COVID-19.
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individuals | is with | severe COVID-19 (count: 1)
In the train cohort, the nomogram had a significantly high AUC 0.912 (95% CI 0.846-0.978) to discriminate individuals with severe COVID-19 from non-severe COVID-19, with a sensitivity of 85.71 % and specificity of 87.58% ( Figure 3C , Table 2 ).
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severe patients | is with | SARS-CoV-2 infection 3 6 7 (count: 1)
Among of them, age, NLR and LDH has been reported to be risk factors for severe patients with SARS-CoV-2 infection 3, 6, 7 .
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medRxiv preprint | might at | might risk for severe COVID-19 (count: 1)
17.20037515 doi: medRxiv preprint with higher levels of inflammation at admission might be at higher risk for severe COVID-19 as well.
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RDW | was predictor for | severe COVID-19 (count: 1)
Interestingly, we found RDW was also an important prognostic predictor for severe COVID-19.
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372 patients | is with | non-severe COVID-19 (count: 1)
First, this is a retrospective study, including 372 patients with non-severe COVID-19 on admission.
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our nomogram | identify | severe COVID-19 patients (count: 1)
In summary, our data suggest that our nomogram could early identify the severe COVID-19 patients, and RDW was vaulable for prediction of severe diseases.
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severe COVID-19 | is in | train cohort (count: 1)
The calibration curve and ROC for performance to distinguish individuals with severe COVID-19 from non-severe COVID-19 in the train cohort (A, C) and validation cohort 1 (B, D), respectively.
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severe COVID-19 | is in | train group (count: 1)
one patient with severe COVID-19 in the train group died.
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severe COVID-19 | is with | maximal Area Under Curve (count: 1)
The results of the 189 patients showed that age, DBIL, RDW, BUN, CRP, LDH and ALB were predictive factors for severe COVID-19 with maximal Area Under Curve (AUC) (Figure 2B and 2C).
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researches | reported | risk factors for severe COVID-19 (count: 1)
So far, several researches reported some risk factors for severe COVID-19.
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nomogram | could present | predictor tool for risk stratification of non-severe COVID-19 patients (count: 1)
However, the nomogram could present a quantitive and practical predictor tool for risk stratification of non-severe COVID-19 patients at admission.
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severe COVID-19 probability | is in | patients with COVID-19 infection (count: 1)
C) Nomogram predicting the severe COVID-19 probability in patients with COVID-19 infection was plotted.
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D Decision curve | predicting | severe COVID-19 probability (count: 1)
D) Decision curve compares the net clinical benefits of three scenarios in predicting the severe COVID-19 probability: a perfect prediction model (grey line), screen none (horizontal solid black line), and screen based on the nomogram (blue line). (
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severe infections | being treated in | COVID-19 patients (count: 1)
The majority of COVID-19 deaths reported so far have occurred in patients with underlying health conditions or at older ages (5-7); this situation is changing (SH personal communication) with severe infections being treated in younger COVID-19 patients without underlying conditions.
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2019-nCoV viral RNA detection | is in | mild cases (count: 1)
Giving the priority of 2019-nCoV detection to severe cases because of shortness of test kits in our hospital initially and potential false negative results of 2019-nCoV viral RNA detection in mild cases might account for this discrepancy.
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COVID-19 case | counts for | severe cases (count: 1)
We extracted and estimated confirmed COVID-19 case counts for severe and critical cases from Wuhan and Guangzhou from situation updates from Chinese national and local health commissions.
patients | is with | mild COVID-19 disease (count: 1)
Unlike Wuhan, where patients with mild COVID-19 disease were isolated in quarantine centers and not in designated hospitals, all confirmed patients in Guangzhou were hospitalized until cure.
COVID-19 patients | were hospitalized with | 10,000 in severe conditions (count: 1)
During the peak of the Wuhan epidemic in February, nearly 20,000 COVID-19 patients were hospitalized simultaneously, with 10,000 in severe or critical conditions.
RNA | extracted from | Vero cells 107 infected with SARS-CoV-2 (count: 1)
To delineate the SARS-CoV-2 transcriptome, we first performed DRS runs on 106 a MinION nanopore sequencer using total RNA extracted from Vero cells 107 infected with SARS-CoV-2 (BetaCoV/Korea/KCDC03/2020).
non-severe patients | is with | SARS-CoV-2 infection (count: 1)
Comparisons of characteristics between severe patients and non-severe patients with SARS-CoV-2 infection.
SARS-CoV-2 | cause | severe illness (count: 1)
Of all included patients, 37 (82.2%) had developed ARDS, 20 (44.4%) required invasive mechanical ventilation and 9 (20.0%) required ECMO, suggesting that the SARS-CoV-2 can cause severe illness.
patients | is with | severe SARS-CoV-2 (count: 1)
Demographics and baseline characteristics of patients with severe SARS-CoV-2
patients | is with | severe SARS-CoV-2All rights (count: 1)
Comorbidities during ICU and treatments of patients with severe SARS-CoV-2All rights reserved.
suspected COVID-19 patients | is with | mild symptoms (count: 1)
Furthermore, in cases of insufficient hospitalization conditions, safety or medical resources, alternative quarantine methods, including home care and isolation, should be considered for suspected COVID-19 patients with mild symptoms.
evaluation | is needed under | severe threat of COVID-19 epidemics (count: 1)
However, to pick out a reliable predictable model/method is far from simple, a rational evaluation of various possible choices is eagerly needed, especially under the severe threat of COVID-19 epidemics which is spreading worldwide right now.
death | can occur in | severe COVID-19 cases (count: 1)
Recent clinical research found that dyspnea might occur on the fifth day and acute respiratory distress syndrome on the eighth day from first symptom of COVID-19 in median, organ dysfunction and death can also occur in severe COVID-19 cases [5, 6] .
patients | is in | severe COVID-19 condition (count: 1)
Severe hypokalemia of under 3 mmol/L plasma K + can trigger ventricular arrhythmia and respiratory muscle dysfunction, both conditions being life-threatening in patients in severe COVID-19 condition.
severe COVID-19 | is in | age (count: 1)
14] [15] [16] There were significant differences between severe and nonsevere COVID-19 in age, clinical manifestations, imaging findings, levels of inflammatory cytokines and myocardial enzymes, and distribution of lymphocytes and their subsets, consistent with previous studies.
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nonsevere patient | is with | COVID-19 (count: 1)
Dynamic chest CT scan changes of a nonsevere patient (a young male patient) with COVID-19.
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efficacy | is in | treatment of severe COVID-19 pneumonia (count: 1)
We aimed to evaluate the definite efficacy and safety of corticosteroid in the treatment of severe COVID-19 pneumonia.
Forty-six hospitalized patients | is with | severe COVID-19 pneumonia (count: 1)
Methods: Forty-six hospitalized patients with severe COVID-19 pneumonia hospitalized at Wuhan Union Hospital from January 20 to February 25, 2020, were retrospectively reviewed.
severe COVID-19 pneumonia | process of is | inflammation reaction (count: 1)
The pathological process of severe COVID-19 pneumonia is the inflammation reaction characterized by destruction of deep airway and alveolar [6] .
aggravation | occurs For | patients of severe COVID-19 pneumonia (count: 1)
For the patients of severe COVID-19 pneumonia, aggravation of symptoms always occurs during 5-7 days after onset [13] .
hospitalization | is in | severe COVID-19 pneumonia patients with methylprednisolone treatment (count: 1)
https://doi.org/10.1101/2020.03.06.20032342 doi: medRxiv preprint Figure 3 Images of chest CT scan on day 1, 7 and 14 after hospitalization in severe COVID-19 pneumonia patients with and without methylprednisolone treatment .
46 hospitalized patients | is with | severe COVID-19 pneumonia (count: 1)
A total of 46 hospitalized patients with severe COVID-19 pneumonia were diagnosed and included in this study, the age, sex, comorbidities, clinical and laboratory parameters on admission for the are shown inTable 1.
46 patients | is with | severe COVID-19Data (count: 1)
Clinical characters and main laboratory parameters of 46 patients with severe COVID-19Data are n (%), or median (interquartile range).
COVID-19 patients | developed pneumonia with | plasma levels of cytokines in severe cases (count: 1)
Clinically, several papers showed that most COVID-19 patients developed lymphopenia as well as pneumonia with higher plasma levels of pro-inflammatory cytokines in severe cases [6] [7] [8] , suggesting that the host immune system is involved in the pathogenesis 9, 10 .
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coronavirus disease 2019 | ongoing pandemic of is | disease caused by severe syndrome coronavirus 2 (count: 1)
The ongoing pandemic of the coronavirus disease 2019 is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV2).
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COVID-19 | cause death in | severe cases (count: 1)
COVID-19 is clinically manifests as fever, cough, muscle pain, fatigue, diarrhea and pneumonia, and can cause death in severe cases. [
reduction | was | observed in COVID-19 patients with T cells (count: 1)
These patients were further categorized into three groups based on age (<20 years old, 20~60 years and ≥60 years), and an age-dependent reduction of T cell numbers was observed in COVID-19 patients, with the lowest T cells numbers found in patients ≥60 years old (Figure 1C) , suggesting a potential cause for increased susceptibility in elderly patients.
result | decrease of | T cells seen in COVID-19 patients (count: 1)
The phenomena suggests that the decrease of T cells seen in COVID-19 patients is likely the result of high serum concentration of TNF-α, IL-6 and IL-10 negatively regulating T cell survival or proliferation.
T cells | decrease in | COVID-19 patients (count: 1)
Interestingly, the numbers of total T cells, CD4 + T and CD8 + T cells are negatively correlated to levels of TNF-α, IL-6 and IL-10, respectively (Figure 2B) , suggesting these cytokines promote T cells decrease in COVID-19 patients.
T cells | are decreased in | patients with COVID-19 (count: 1)
35, 36 Taken together, we conclude that T cells are decreased and exhausted in patients with COVID-19.
focal SARS-CoV-2 antigen expression | is in | epithelial cells of mucous glands (count: 1)
In the upper respiratory tract, there was focal or locally extensive SARS-CoV-2 antigen expression in epithelial cells of mucous glands in the 5 nasal cavity (septum or concha) of all four macaques, without any associated histological lesions ( fig.
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cells | expresses | SARS-CoV-2 antigen (count: 1)
I) Epithelial cells of mucous glands in nasal cavity expresses SARS-CoV-2 antigen (IHC for SARS-CoV-nucleocapsid, 40X objective).
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severe condition | is in | COVID-19 patients (count: 1)
The underlined mechanism of SARS-CoV-2 inflicted harmful effects leading to severe condition or death in COVID-19 patients is the over response against the virus by immune system and large amount of cytokines production (cytokine storm) [13] .
Th cells | was | reduced irrespective of SARS-CoV-2 infection (count: 1)
The results showed that compared with the general population, the T cells, Th cells, killer T cells, as well as NK cells was reduced remarkably in PBMCs of HD patients, irrespective of SARS-CoV-2 infection.
2019-nCoV | utilizes cell entry receptor ACE2 as | severe syndrome coronavirus (count: 1)
As 2019-nCoV utilizes the same cell entry receptor ACE2 as severe acute respiratory syndrome coronavirus (SARS-CoV) and ACE2 tightly controls intestinal inflammation, to trace the route of infection mediated by 2019-nCoV, we used the single-cell RNA sequencing data for analysis.
epithelium cells | be vulnerable to | 2019-nCoV infection (count: 1)
Thus, we suspect that ACE2-expressing small intestinal epithelium cells might be vulnerable to 2019-nCoV infection when people eat infected wild animals and diarrhea may serve as an indicator for infection, suggesting that clinicians should pay more attention to patients with diarrhea during the outbreak of pneumonia.
epithelium cells | be | vulnerable to attack by 2019-nCoV (count: 1)
To sum up, we proposed that ACE2-expressing small intestinal epithelium cells might be are more vulnerable to attack by 2019-nCoV and clinicians should be careful when their patients complain of diarrhea since the incidence of diarrhea may be underestimated.
epithelium cells | might | might vulnerable by 2019-nCoV (count: 1)
Based on the current findings, we proposed that:(1) The incidence of diarrhea may be underestimated in previous investigations, and it is an easily neglected symptom at an early stage; (2) ACE2-expressing small intestinal epithelium cells might be are more vulnerable to attack by 2019-nCoV.
SARS-CoV-2 | infects | 159 cells (count: 1)
Our 157 results of viral RNA detection and intracellular staining of NP in gastric, duodenal and 158 rectal epithelia demonstrate that SARS-CoV-2 infects these gastrointestinal glandular 159 epithelial cells.
2019-nCoV infection | clusters of | 194 severe illness (count: 1)
Tis article point the 2019-nCoV infection caused clusters of 194 severe respiratory illness similar to severe acute respiratory syndrome coronavirus 195 and was associated with ICU admission and high mortality.
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SARS-CoV-2 stocks | were propagated on | VeroE6 cells (count: 1)
SARS-CoV-2 (BetaCoV/Wuhan/IVDC-HB-01/2019, GISAID Accession ID: EPI_ISL_402119) stocks were propagated on VeroE6 cells.
severe disease | was defined According to | COVID-19 prevention (count: 1)
According to the Chinese COVID-19 prevention and control program (6th edition), severe disease was defined as meeting one of the following criteria:
COVID-19 | can present as | mild tract illness (count: 1)
COVID-19 can present as a mild upper respiratory tract illness.
cells | expressing | protein of SARS-CoV-2 (count: 1)
Seroconversion was detected by IgG and IgM immunofluorescence using cells expressing the spike protein of SARS-CoV-2 and a virus neutralization assay using SARS-CoV-2 ( Table 3 ).
SARS-CoV-2 virus | causes | severe disease (count: 1)
The SARS-CoV-2 virus causes severe respiratory disease that can quickly spread from person to person and in some cases lead to death.
SARS-CoV-2 | enters | host cells (count: 1)
After binding to ACE2 via its Spike protein, SARS-CoV-2 undergoes membrane fusion and enters the host cells by endocytosis.
COVID-19 | is in | severe cases (count: 1)
In general, COVID-19 in severe cases progresses rapidly to lethal complications (ARDS, septic shock, acute cardiac injury, refractory metabolic acidosis and so on), even leading to death.
severe COVID-19 | is in | Chongqing (count: 1)
Additionally, Figure1-3 demonstrates the representative radiologic images of patients with non-severe and a patient with severe COVID-19 in Chongqing.
discharged COVID-19 patients | donate plasma for | severe patients ' treatment (count: 1)
Two discharged COVID-19 patients promised to donate convalescent plasma for critically severe patients' further treatment.
COVID-19 patients | donate plasma for | severe patients ' treatment (count: 1)
And, two discharged COVID-19 patients promised to donate convalescent plasma for critically severe patients' further treatment.
COVID-19 severe outbreaks | were | reported (count: 1)
Almost two months after the first report, COVID-19 severe outbreaks were reported in numerous countries and became a public health priority in the world (World Health Organization, Situation Report 48).
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2019-nCoV genome | is close to | that of severe syndrome (count: 1)
Study shows that 2019-nCoV genome is very close to that of the severe acute respiratory syndrome (SARS)-CoV [11] .
SARS-CoV-2 infection | cause | syndrome ranging from cold to severe pneumonia (count: 1)
In the human host, SARS-CoV-2 infection may be asymptomatic or may cause a syndrome (named COVID-19) ranging from common cold to a severe pneumonia with acute respiratory syndrome and need of mechanical ventilation in intensive care unit (ICU).
ACE2 | mediates | 2019-nCoV infection of type II cells (count: 1)
It also has been linked to 2019-nCoV infection; ACE2 interacts with the Spike protein and mediates 2019-nCoV infection of the type II alveolar cells of the lung [7] .
hypertension | is common in | severe 2019-nCoV pneumonia (count: 1)
Given that hypertension is common in severe 2019-nCoV pneumonia [1] , it is highly likely that the RAS is activated in the lungs of patients with severe pneumonia.
examination | shows | proportion between COVID-19 (count: 1)
Our genome-level analyses show that the spike protein, which is responsible for receptor binding, has undergone significant Darwinian selection along the branches related to 2019-nCoV and SARS-CoV. Further examination shows an unusually high proportion of evolutionary convergent amino acid sites in the receptor binding domain (RBD) of the spike protein between COVID-19 and SARS-related CoV clades, leading to the phylogenetic uniting of their RBD protein sequences.
Relative | developed | severe COVID-19 pneumonia (count: 1)
Among the 3 infected family members, Relative 1 developed severe COVID-19 pneumonia and was admitted to the ICU on Feb 6, 2020.
airport screening | detect | proportion of 2019-nCoV travellers (count: 1)
While this is likely to be an effective strategy, we find that airport screening for initial symptoms, via thermal scanners or similar, on either exit or entry is unlikely to detect a sufficient proportion of 2019-nCoV infected travellers in order to avoid entry of infected travellers and therefore the potential for seeding of local transmission.
phenomenon | may | may indicative of immunosuppression in COVID-19 patients in severe subgroup (count: 1)
This phenomenon may be indicative of the immunosuppression in COVID-19 patients with CNS symptoms, especially in the severe subgroup.
SARS-CoV-2 | infects | muscle cells (count: 1)
Therefore, whether SARS-CoV-2 infects skeletal muscle cells by binding with ACE2 requires to be further studied.
COVID-19 patients | of proportion is | 64.8 % (count: 1)
Similarly, a large proportion (64.8%) of COVID-19 patients had an increase level of CRP.
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non-survivors | proportion in | patients with COVID-19 44 (count: 1)
Yang et al also found that non-survivors have a higher proportion of CRRT in patients with COVID-19 44 .
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cells | are potential targets of | 2019-nCoV (count: 1)
These results indicate that testicular cells are the potential targets of 2019-nCoV.
EC50 | is in | SARS-CoV-2-infected cells (count: 1)
Notably, S416 is reported to be the most potent inhibitor with an EC50 of 17nM and SI value >5882 in SARS-CoV-2-infected cells so far.
ICU patients | had plasma levels in | severe COVID-19 cases (count: 1)
Similarly, in severe COVID-19 cases, ICU patients had higher plasma levels of IL-2, IL-7, IL-10, GSCF, MCP1, MIP1A, and TNFα compared to non-ICU patients 44 .
patients | suffering from | severe COVID-19 (count: 1)
We hope our study may quickly and finally benefit the patients now suffering from severe COVID-19 and other infectious diseases caused by emerging and reemerging viruses.
Vero E6 cells | were infected with | SARS-CoV-2 (count: 1)
Vero E6 cells were infected with SARS-CoV-2 under the same procedure of C. Cells were fixed and permeabilized for staining with anti-viral NP antibody, followed by staining with Alexa 488-labeled secondary antibody.
We | grouped | patients into severe 2019-nCoV ARD (count: 1)
We grouped patients into severe and non-severe 2019-nCoV ARD .
two patients | is with | severe 2019-nCoV ARD (count: 1)
Figure E1 in the Supplementary Appendix demonstrates the representative radiologic findings of two patients with non-severe 2019-nCoV ARD and another two patients with severe 2019-nCoV ARD.
our cohort | severe end of | 2019-nCoV ARD (count: 1)
Third, we might have missed asymptomatic or mild cases managed at home, and hence our cohort might represent the more severe end of 2019-nCoV ARD.
2019-nCoV | was detected In | case with severe ulcer (count: 1)
In a case with severe peptic ulcer after symptom onset, 2019-nCoV was directly detected in the esophageal erosion and bleeding site (Hong Shan and Jin-cun Zhao, personal communication).
SARS-CoV-2 | was detected in | case with severe ulcer symptom (count: 1)
Similarly, SARS-CoV-2 was also directly detected in the oesophageal erosion and bleeding site in a case with severe peptic ulcer symptom reported by Zhong et al.
we | need for | infection like COVID-19 with proportion of cases (count: 1)
A particularly important point to raise is that for an infection like COVID-19 with a relatively high proportion of severe cases, we need to think carefully about an intervention before we decide that it is not sustainable.
2019-nCoV infection | is in | Vero E6 cells (count: 1)
8, 9 Chloroquine is known to block virus infection by increasing endosomal pH required for virus/ cell fusion, as well as interfering with the glycosylation of cellular receptors of SARS-CoV. 10 Our time-of-addition assay demonstrated that chloroquine functioned at both entry, and at postentry stages of the 2019-nCoV infection in Vero E6 cells (Fig.
cells | were | For experimental groups infected with 2019-nCoV (count: 1)
For all the experimental groups, cells were infected with 2019-nCoV at an MOI of 0.05, and virus yield in the infected cell supernatants was quantified by qRT-PCR c and NP expression in infected cells was analyzed by Western blot d at 14 h p.i.
Vero E6 cells | were infected with | 2019-nCoV (count: 1)
a Vero E6 cells were infected with 2019-nCoV at an MOI of 0.05 in the treatment of different doses of the indicated antivirals for 48 h. The viral yield in the cell supernatant was then quantified by qRT-PCR.
2019-nCoV | have | incubation period than severe syndrome (count: 1)
8] , 2019-nCoV appears to have a shorter incubation period than severe acute respiratory syndrome (SARS), and a higher rate of asymptomatic infections [11] .
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2019-nCoV pneumonia | symptoms of are | for severe patients fever (count: 1)
Clinically, for those severe patients, the main symptoms of 2019-nCoV pneumonia are fever, decreased white blood cell and lymphocyte count, increased C reaction protein and abnormally expressed cytokines [6] .
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mild symptoms | be frequent in | cases of COVID-19 (count: 1)
Increasing evidence suggests that mild clinical symptoms could be more frequent in cases of COVID-19 than with SARS-CoV and MERS-CoV [5] .
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COVID-19 ranges | of spectrum is | mild cases (count: 1)
The full clinical spectrum of COVID-19 ranges from asymptomatic cases, mild cases that do not require hospitalization, to severe cases that require hospitalization and ICU treatment, and those with fatal outcomes.
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2019-nCoV | is agent for | severe infection (count: 1)
2019-nCoV is the causative agent for severe respiratory infection in humans termed as novel coronavirus-infected pneumonia (NCIP) [10] .
severe patients | is with | 2019-nCoV (count: 1)
Along with an increasing number of confirmed cases, the cumulative total of severe patients with 2019-nCoV is growing (Fig.
severe cases | is with | 2019-nCoV infection in Wuhan (count: 1)
Over the past month, we collaborated with front-line ICU physicians and firstly evaluated the efficacy of corticosteroids treatment for severe or fatal cases with 2019-nCoV infection in Wuhan.
COVID-19 | was mild for | 81 % (count: 1)
Their findings show that COVID-19 was mild for 81% of patients and had an overall case fatality rate of 2.3%.
knowledge gap | is efficiency of | community transmission of 2019-nCoV including contribution of mild cases (count: 1)
A key knowledge gap is the efficiency of community transmission of 2019-nCoV, including the contribution of mild or asymptomatic cases.
2019-nCoV | belongs as | severe syndrome coronavirus (count: 1)
2019-nCoV belongs to the same family of viruses as the well-known severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), which have killed hundreds of people in the past 17 years.
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2019-nCoV | may infect | cells (count: 1)
Considering the predominant expression of ACE2 in intestines and kidney, 2019-nCoV may infect cells in these tissues and find its way into feces and urine.
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2019-nCoV/SARS-CoV | utilize ACE2 as | entry receptor in cells 33 (count: 1)
A recent study showed that 2019-nCoV/SARS-CoV-2 is able to utilize ACE2 as an entry receptor in ACE2-expressing cells 33 , suggesting potential drug targets for therapeutic development.
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severe distress syndrome | patients with | COVID-19 (count: 1)
Inter-hospital transfer may be required for extracorporeal membrane oxygenation (ECMO) if patients with COVID-19 develop severe acute respiratory distress syndrome within hospitals with only basic ventilation facilities.
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2019-nCoV | have caused | severe pneumonia (count: 1)
Unlike the above four human CoVs, SARS-CoV, MERS-CoV, and 2019-nCoV have caused severe pneumonia and/or failure of other organs, even death, among infected populations (Nicholls et al.,
2019-nCoV | enters | cells Fig (count: 1)
We show that 2019-nCoV is able to use all ACE2 proteins, except for mouse ACE2, as an entry receptor to enter ACE2expressing cells, but not cells that did not express ACE2, indicating that ACE2 is probably the cell receptor through which 2019-nCoV enters cells (Fig.
2019-nCoV | grown in | Vero E6 cells (count: 1)
2019-nCoV grown in Vero E6 cells was used for infection at a MOI of 0.5.
1b | increase in | incidence of severe COVID-19 (count: 1)
1b , a step-wise increase in the incidence of severe COVID-19 at admission was observed with the increment of the host risk score (P < 0.001).
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trend | analyzing | correlation between host risk score of severe COVID-19 (count: 1)
A similar trend to the above was confirmed when analyzing the correlation between host risk score and occurrence of severe COVID-19 (P = 0.014) (see Fig.
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study | identifying | host risk factors associated with severe COVID-19 (count: 1)
In summary, by identifying host risk factors associated with severe COVID-19, this study shed light on the underlying mechanisms of disease progression.
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hypertension | is | host risk factor for severe COVID-19 (count: 1)
In particular, the major finding that hypertension is a host risk factor for severe COVID-19 may underscore the involvement of renin-angiotensin system (RAS) in the pathogenesis of this disease.
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likely | severe symptoms of | COVID-19 (count: 1)
However, from their published data we can calculate that the smokers were 1.4 times more likely (RR=1.4, 95% CI: 0.98-2.00) to have severe symptoms of COVID-19 and approximately 2.4 times more likely to be admitted to an ICU, need mechanical ventilation or die compared to non-smokers (RR=2.4, 95% CI: 1.43-4.04).
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we | elucidate proportion along with | time of infection among COVID-19 cases (count: 1)
In this study, we conducted statistical modelling analyses on publicly available data to elucidate the asymptomatic proportion, along with the time of infection among the COVID-19 cases on board the Diamond Princess cruise ship.
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2019-nCoV | can bind to | ACE2 receptor from cells (count: 1)
Although there are four amino acid variations of S protein between 2019-nCoV and SARS-CoV, 2019-nCoV can also bind to the human angiotensinconverting enzyme 2 (ACE2), the same host receptor for SARS-CoV, as 2019-nCoV can bind to the ACE2 receptor from the cells from human, bat, civet cat, and pig, but it cannot bind to the cells without ACE2 11, [33] [34] [35] .
-- Transmission routes of 2019-nCoV and controls in dental practice. International Journal of Oral Science. 2020.
COVID-19 | involves | mild infections (count: 1)
Although COVID-19 involves mostly mild infections among the majority of the general population, the risk of death among young adults is higher than that of seasonal influenza, and elderly with underlying comorbidities require additional care.
increase | range of | host cells of 2019-nCoV (count: 1)
Together with the structure modelling analysis, the authors speculated that these motif insertions sharing similarity with HIV-1 proteins could provide an enhanced affinity towards host cell receptors and increase the range of host cells of 2019-nCoV. This study implies that 2019-nCoV might be generated by gaining gene fragments from the HIV-1 genome.
-- HIV-1 did not contribute to the 2019-nCoV genome. Emerg Microbes Infect. 2020 Feb 14.
we | provide | process of treatment case of severe 2019-nCoV pneumonia (count: 1)
This guideline includes the guideline methodology, epidemiological characteristics, disease screening and population prevention, diagnosis, treatment and control (including traditional Chinese Medicine), nosocomial infection prevention and control, and disease nursing of the 2019-nCoV. Moreover, we also provide a whole process of a successful treatment case of the severe 2019-nCoV infected pneumonia and experience and lessons of hospital rescue for 2019-nCoV infections.
total | confirmed cases with | 2019-nCoV infection from 30 provinces including 461 severe cases (count: 1)
At 24:00 on 26 January 2020, the National Health Commission of the People's Republic of China has recorded a total of 2744 confirmed cases of pneumonia with 2019-nCoV infection from 30 provinces (districts and cities), including 461 severe cases and 80 deaths.
2019-nCoV | caused | severe illness (count: 1)
The 2019-nCoV has impacted multiple countries, caused severe illness, and sustained person-to-person transmission making it a concerning and serious public health threat.
% | are severe Of | COVID-19 cases (count: 1)
Of the diagnosed COVID-19 cases, less than 20% are severe.
1-year-old infant | is with | severe COVID-19 (count: 1)
A 1-year-old infant with severe COVID-19 was reported by Chen et al.
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2019-nCoV | severe illness like | SARS (count: 1)
Since 2019-nCoV can cause a severe respiratory illness like SARS and MERS and was found to be adept at human-to-human transmission, China launched an emergency response at an early stage of the outbreak.
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COVID-19 | induce | mild symptoms (count: 1)
In addition, despite mild symptoms of COVID-19 in his case, isolation in the negative pressure room during treatment might be one This case shows that the COVID-19 may induce relatively mild symptoms and a patient can recover when early diagnosis of pneumonia was made.
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COVID-19 serial interval | is shorter than | serial interval of severe syndrome (count: 1)
The COVID-19 serial interval is also shorter than the serial interval of severe acute respiratory syndrome (SARS), indicating that calculations made using the SARS serial interval may introduce bias.
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SARS-CoV-2 | causes | disease ranging from mild illness (count: 1)
2, 3 SARS-CoV-2 Often causes a respiratory disease, similar to SARS and MERS, ranging from mild upper respiratory illness to a severe interstitial pneumonia, also requiring intensive care.
-- COVID-19 R0: Magic number or conundrum?. Infectious Disease Reports. 2020.
Information | collected from | practice for severe COVID-19 (count: 1)
Information collected from the practice of ECMO for severe COVID-19 must be compiled and shared.
COVID-19 outbreak | is similar to | severe syndrome (count: 1)
The COVID-19 outbreak is highly similar to the severe acute respiratory syndrome (SARS) outbreak that occurred in 2003; both outbreaks were caused by new coronaviruses during time periods overlapping with the Chinese Spring Festival. [
Genome sequencing | found | sequence of 2019-nCoV homologous to that of severe coronavirus (count: 1)
Genome sequencing found the genetic sequence of 2019-nCoV homologous to that of severe acute respiratory syndrome-associated coronavirus.
airway cells | provide | growth conditions for 2019-nCoV (count: 1)
16, 17 It has also been hypothesized that the novel virus might use angiotensin converting enzyme 2 as a receptor similar to SARS-CoV. 18 Unlike SARS-CoV or MERS-CoV, primary human airway epithelial cells provide better growth conditions for 2019-nCoV than standard tissue culture cells.
-- The Novel Coronavirus: A Bird's Eye View. Int J Occup Environ Med. 2020.
SARS-CoV-2 | be associated with | severe syndrome coronavirus 2 (count: 1)
Keywords: SARS-CoV-2; incubation period; cluster; COVID-19An emerging infectious disease, 2019 novel coronavirus disease, was identified to be associated with a novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which was initially reported in December 2019 in Wuhan City, China[1].
-- Transmission of COVID-19 in the terminal stage of incubation period: a familial cluster. International Journal of Infectious Diseases. 2020-03-16.
TMPRSS2 usage | is required for | SARS-CoV-2 infection of lung cells (count: 1)
We next analyzed whether TMPRSS2 usage is required for SARS-CoV-2 infection of lung cells.
SARS-CoV-2 | blocks | SARS-CoV-2 infection of lung cells (count: 1)
Collectively, SARS-CoV-2 can use TMPRSS2 for S protein priming and camostat mesylate, an inhibitor of TMPRSS2, blocks SARS-CoV-2 infection of lung cells.
presence | is required for | SARS-CoV-2 entry into cells (count: 1)
It will thus be interesting to determine whether the presence of a multibasic cleavage site is required for SARS-CoV-2 entry into human cells and how this cleavage site was acquired.
Infection | is with | authentic SARS-CoV-2 BHK-21 cells (count: 1)
Infection with authentic SARS-CoV-2 BHK-21 cells (1.6 x10 5 cells/mL) were transfected with ACE2 and DsRed as a negative control.
C BHK-21 cells | were infected with | SARS-CoV-2 (count: 1)
C) BHK-21 cells transfected with ACE2-encoding plasmid or control transfected with DsRed-encoding plasmid were infected with SARS-CoV-2 and washed, and genome equivalents in culture supernatants were determined by quantitative RT-PCR.
D Calu-3 cells | infected with | SARS-CoV-2 (count: 1)
D) Calu-3 cells were pre-incubated with camostat mesylate and infected with SARS-CoV-2.
COVID-19 | result in | severe syndrome (count: 1)
1 , 2 COVID-19 could induce symptoms including fever, dry cough, dyspnea, fatigue and lymphopenia in patients, and might result in severe acute respiratory syndrome (SARS) and even death in severe cases. [
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SARS-CoV-2 reactivation | developed in | proportion of COVID-19 patients (count: 1)
We confirmed that in a significantly proportion of COVID-19 patients, SARS-CoV-2 reactivation developed after discharging from hospital (9%).
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SARS-CoV-2 | infected | airway cells (count: 1)
The virus propagated on monkey and human cells and, notably, parallel investigations by others demonstrated that SARS-CoV-2 also productively infected primary human airway epithelial cells [3] .
-- SARS Coronavirus Redux. Trends in Immunology. 2020-03-12.
severe cases | attributed to | SARS-CoV-2 infections (count: 1)
In the Hubei province, where the outbreak originated, severe cases or deaths attributed to SARS-CoV-2 infections are predominantly arising from patients suffering from one or more previous pathological conditions such as diabetes, cardiovascular and cerebrovascular disease leading to sequelae, sometimes fatal, such as cellular immune deficiency, coagulation activation, myocardia injury, hepatic and kidney injury, and secondary bacterial infection [4, 6] .
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2019-nCoV | infect | lung cells (count: 1)
The receptor that 2019-nCoV uses to infect lung cells might be ACE2, a cellsurface protein on cells in the kidney, blood vessels, heart, and, importantly, lung AT2 alveolar epithelial cells (figure).
COPD | may | may associated with odds of severe COVID-19 (count: 1)
In this article, we analyze if COPD may be associated with increased odds of severe COVID-19
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results | was found | associated with severe COVID-19 (count: 1)
However, when the data of the individual studies was pooled, COPD was found to be significantly associated with severe COVID-19 In conclusion, the results of this concise meta-analysis demonstrate COPD is associated with a significant, over five-fold increased risk of severe CODID-19 infection.
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association | is with | severe COVID-19 disease (count: 1)
Forest plot demonstrating association of Chronic Obstructive Pulmonary Disease with severe COVID-19 disease.
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SARS-CoV-2 infection | is in | Huh-7 cells (count: 1)
Pro-inflammatory cytokine expression levels upon SARS-CoV-2 infection in Huh-7 cells were measured by real-time quantitative PCR assays.
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SARS-CoV-2 replication | is in | Vero E6 cells (count: 1)
Results: LH significantly inhibited SARS-CoV-2 replication in Vero E6 cells and markedly reduced pro-inflammatory cytokines (TNF-α, IL-6, CCL-2/MCP-1 and CXCL-10/IP-10) production at the mRNA levels.
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SARS-CoV-2 | caused | severe illness (count: 1)
Like the other two highly pathogenic coronaviruses SARS-CoV and MERS-CoV, SARS-CoV-2 also caused severe respiratory illness and even death.
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SARS-CoV-2 virus replication | is in | cells (count: 1)
To further confirm the efficacy of LH in inhibiting SARS-CoV-2 virus replication in cells, we detected the viral particles in ultrathin sections of infected cells under electron microscopy.
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Abundant virus particles | is in | SARS-CoV-2 infected cells (count: 1)
Abundant virus particles assembled at the surface of membrane, cytoplasm, and plasma vesicles in the SARS-CoV-2 infected cells, decreased in the treatment of LH at 600ug/mL. Notably, slight deformation of virus particles was seen in the LH treatment, which required us to make further studies.
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SARS-CoV-2 | is in | Vero E6 cells (count: 1)
Antiviral activity of LH and remdesivir against SARS-CoV-2 in Vero E6 cells. (
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severe limitations | are in | supplies deal with SARS-CoV-2 outbreak (count: 1)
As there are severe limitations in the medical supplies available in the Iranian public health system to deal with the current SARS-CoV-2 outbreak, international support, additionally to be provided from the World Health Organization, is needed in the country to mitigate the impacts of this epidemic, and to avoid additional spreading.
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2019-nCoV severe acute respiratory syndrome coronavirus -2 likely experienced adaptive evolution | is in | intermediate hosts (count: 1)
Originated in bats, 2019-nCoV/ severe acute respiratory syndrome coronavirus (SARS-CoV)-2 likely experienced adaptive evolution in intermediate hosts before transfer to humans at a concentrated source of transmission.
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chloroquine | preventing | SARS-CoV-2 binding to target cells (count: 1)
Since SARS-CoV-2 was found a few days ago to utilise the same cell surface receptor ACE2 (expressed in lung, heart, kidney and intestine) as SARS-CoV-1 [85, 86] (Table 1) , it may be hypothesised that chloroquine also interferes with ACE2 receptor glycosylation thus preventing SARS-CoV-2 binding to target cells.
chloroquine | be used on | line for treatment of severe SARS-CoV-2 infections (count: 1)
As a result, chloroquine is probably the first molecule to be used in China and abroad on the front line for the treatment of severe SARS-CoV-2 infections.
patients | had | severe COVID-19 (count: 1)
Ten patients had severe COVID-19, of whom all required oxygen supplementation, and 13 patients had mild disease.
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patients | had comorbidities with | severe COVID-19 (count: 1)
Chronic comorbidities were more common among patients with severe COVID-19 (seven [70%] patients with severe disease had chronic comorbidities vs four [31%] with mild disease), although this difference was not significant (table).
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symptoms | include shock In | severe 2019-nCoV infection cases (count: 1)
In severe 2019-nCoV infection cases, the symptoms include acute respiratory distress syndrome, septic shock, metabolic acidosis, and bleeding and coagulation dysfunction.
esophagus cells | may contribute to | infection of 2019-nCoV (count: 1)
ACE2, a receptor for 2019-nCoV, is necessary for the viral entry of 2019-nCoV. The ubiquitous expression of ACE2 in various cells, such as lung AT2 cells, esophagus upper, stratified epithelial cells, and absorptive enterocytes of ileum and colon may contribute to the multi-tissue infection of 2019-nCoV [22] .
COVID-19 infection | is associated in | severe cases (count: 1)
Recent literature indicates that in severe cases, COVID-19 infection is associated with a cytokine-storm, which is characterized by increased plasma concentrations of interleukins 2 (IL-2), IL-7, IL-10, granulocyte-colony stimulating factor, interferon-γ-inducible protein 10, monocyte chemoattractant protein 1, macrophage inflammatory protein 1 alpha, and tumor necrosis factor α (TNF-α) (Huang et al.,
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patient | is with | severe COVID-19 (count: 1)
showed that peripheral blood of a patient with severe COVID-19 had a strikingly high number of CCR4+CCR6+ TH17 cells 2 , further supporting a TH17 type cytokine storm in this disease.
-- TH17 Responses in Cytokine Storm of COVID-19: An Emerging Target of JAK2 Inhibitor Fedratinib. Journal of Microbiology, Immunology and Infection. 2020-03-11.
COVID-19 infection | pathogenesis of was | severe pneumonia (count: 1)
The main pathogenesis of COVID-19 infection as a respiratory system targeting virus was severe pneumonia, RNAaemia, combined with the incidence of ground-glass opacities, and acute cardiac injury [6] .
bind | inhibit | SARS-CoV-2 entry into cells (count: 1)
Highlights d SARS-CoV-2 uses ACE2 to enter target cells d SARS-CoV-2 and SARS-CoV bind with similar affinities to ACE2 d Structures of SARS-CoV-2 spike glycoprotein in two conformations d SARS-CoV polyclonal antibodies inhibit SARS-CoV-2 spikemediated entry into cells
SARS-CoV-2 S | enter | cells (count: 1)
We show that SARS-CoV-2 S uses ACE2 to enter cells and that the receptor-binding domains of SARS-CoV-2 S and SARS-CoV S bind with similar affinities to human ACE2, correlating with the efficient spread of SARS-CoV-2 among humans.
SARS-CoV-2 S | entry into | cells (count: 1)
Finally, we demonstrate that SARS-CoV S murine polyclonal antibodies potently inhibited SARS-CoV-2 S mediated entry into cells, indicating that cross-neutralizing antibodies targeting conserved S epitopes can be elicited upon vaccination.
We | determined | cryoelectron microscopy structures of Entry pseudotyped with SARS-CoV-2 S in VeroE6 cells (count: 1)
We determined cryoelectron microscopy (cryo-EM) structures of (A) Entry of MLV pseudotyped with SARS-CoV-2 S, SARS-CoV S and SARS-CoV-2 S fur/mut in VeroE6 cells.
we | compared | transduction of SARS-CoV-2 S-MLV into VeroE6 cells (count: 1)
To assess the ability of SARS-CoV-2 S to promote entry into target cells, we first compared transduction of SARS-CoV-2 S-MLV and SARS-CoV S-MLV into VeroE6 cells, that are known to express ACE2 and support SARS-CoV replication (Drosten et al.,
SARS-CoV-2 S | was processed during | biosynthesis in HEK293T cells (count: 1)
Using western blot analysis, we observed that SARS-CoV-2 S was virtually entirely processed at the S 1 /S 2 site during biosynthesis in HEK293T cells, presumably by furin in the Golgi compartment ( Figure 1D ).
SARS-CoV S | neutralizing | SARS-CoV-2 entry into cells (count: 1)
This resemblance is further strengthened by our finding that SARS-CoV S elicited polyclonal Ab responses, potently neutralizing SARS-CoV-2 S-mediated entry into cells.
SARS-CoV-2 2P S ectodomain | was produced in | 500mL HEK293F cells (count: 1)
The SARS-CoV-2 2P S (GenBank: YP_009724390.1) ectodomain was produced in 500mL HEK293F cells grown in suspension using FreeStyle 293 expression medium (Life technologies) at 37 C in a humidified 8% CO2 incubator rotating at 130 rpm The culture was transfected using 293fectin (ThermoFisher Scientific) with cells grown to a density of 1 million cells per mL and cultivated for three days.
COVID-19 | has | affinity for cells (count: 1)
6 COVID-19 also has affinity for cells in the lower respiratory tract and can replicate there, causing radiological evidence of lower respiratory tract lesions in patients who do not present with clinical pneumonia.
-- COVID-19: what is next for public health?. The Lancet. 2020-02-28.
women | could at | could risk of severe course of COVID-19 (count: 1)
We should note, though, that this evidence is based on limited data, while reports from SARS-CoV, MERS-CoV and from other respiratory infections suggest these conclusions are premature and pregnant women could be at risk of a severe course of COVID-19 (Rasmussen et al.,
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COVID-19 severe complications | included | injury (count: 1)
The COVID-19 severe complications in such patients included respiratory distress syndrome 29%, RNAaemia 15%, acute cardiac injury 12%, and other secondary infections.
-- COVID-19: Zoonotic aspects. Travel Medicine and Infectious Disease. 2020-02-27.
Wuhan City | Province into | makeshift hospitals for patients in coronavirus disease 2019 with mild symptoms (count: 1)
As of February 19 th , the Chinese government has converted 13 large-scale public places in Wuhan City, Hubei Province into makeshift hospitals for patients in the coronavirus disease 2019 (COVID-19) with mild symptoms and such conversion will continue to contain the spread of the COVID-19 (Table I) .
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both | severe outcomes | lack on consequences of 2019-nCoV infection (count: 1)
Considering that the 2019-nCoV seems to have a similar pathogenic potential as SARS-CoV and MERS-CoV, 4 pregnant women are at increased risk of severe infections, there are no specific clinical signs of coronavirus infections preceding severe complications, 5 coronaviruses have the potential to cause severe maternal or perinatal adverse outcomes, or both, 2,3 and the current lack of data on the consequences of a 2019-nCoV infection during pregnancy, we recommend systematic screening of any suspected 2019-nCoV infection during pregnancy.
mild disease 1 | % of | people with COVID-19 (count: 1)
However, it is important to bear in mind that the current best estimate is that about 81% of people with COVID-19 have mild disease 1 and never require hospitalisation.
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adults | is with | COVID-19 severe enough require (count: 1)
In The Lancet, Fei Zhou and colleagues 2 provide further insight into the clinical course and mortality risk for adults with COVID-19 severe enough to require hospitalisation.
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severe events | is in | COVID-19 disease (count: 1)
A recent study from Prof He and colleagues shows that the risk of developing severe events in COVID-19 disease is statistically significant higher in patients with cancer, with a hazard ratio of 3.56 [4] .
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We | provided | proportion of COVID-19 infection (count: 1)
We reported the characteristics of 262 cases infected with COVID-19 from 57 hospitals across Beijing and provided the proportion of the COVID-19 infection on the severe cases to mild, asymptomatic and non-pneumonia cases.
-- Characteristics of COVID-19 infection in Beijing. Journal of Infection. 2020-02-27.
we | provided | proportion of cases of COVID-19 infection (count: 1)
On the basis of this study, firstly we provided the proportion of severe versus common cases of the COVID-19 infection, which was approximately 1:4, the ratio of severe to mild, non-pneumonia and asymptomatic cases were 18%, 73%, 4% and 5% respectively, the changes and prognosis of those four categories should be future observed in hospitals.
-- Characteristics of COVID-19 infection in Beijing. Journal of Infection. 2020-02-27.
COVID-19 | may present distress syndrome In | severe cases (count: 1)
In severe cases, COVID-19 may present as pneumonia, the acute respiratory distress syndrome (ARDS), with or without both distributive and cardiogenic shock, to which elderly populations with preexisting medical comorbidities are the most vulnerable (1, 6, 19, 20) .
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severe COVID-19 | are | summarized (count: 1)
A number of studies in the available literature suggest an association between preexisting CVD and severe COVID-19, which are summarized in Tables 1 and 2 .
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it | is likely in | setting of severe infection due to COVID-19 (count: 1)
With severe respiratory infection and hypoxia, especially in the setting of severe infection and ARDS due to COVID-19, it is likely that a number of patients will develop such injury.
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hospitalized patients | is with | severe COVID-19 disease (count: 1)
Though there are no published case series thus far, there are reports of abnormal coagulation parameters in hospitalized patients with severe COVID-19 disease(59,60).
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patients | is with | mild of COVID-19 pneumonia (count: 1)
They showed that chloroquine could reduce the length of hospital stay and improve the evolution of COVID-19 pneumonia [4, 6] , leading to recommend the administration of 500 mg of chloroquine twice a day in patients with mild, moderate and severe forms of COVID-19 pneumonia.
-- Chloroquine and hydroxychloroquine as available weapons to fight COVID-19. International Journal of Antimicrobial Agents. 2020-03-04.
data | is in | COVID-19 patients with severe disease (count: 1)
The title, abstract and full text of all documents identified according to these search criteria were scrutinized by the authors, and those reporting data in COVID-19 patients with or without severe disease (defined as needing admission to intensive care unit or use of mechanical ventilation), were finally included in our meta-analysis.
procalcitonin values | are associated with | risk of severe SARS-CoV-2 infection (count: 1)
The pooled OR of these studies is summarized in figure 1 , which shows that increased procalcitonin values are associated with a nearly 5-fold higher risk of severe SARS-CoV-2 infection (OR, 4.76; 95% CI, 2.74-8.29).
COVID-19 infection | causes | mild disease (count: 1)
At the time of writing this editorial the figures suggest that COVID-19 infection causes mild disease (i.e. non-pneumonia or mild pneumonia) in about 80 % of cases and most cases recover, 14 % have more severe disease and 6% experience critical illness; the latter being more likely amongst high-risk groups such as the elderly and those with other chronic underlying conditions [4] .
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particular importance | is in | treatment of severe cases of COVID-19 (count: 1)
Such drugs are predicted to be of particular importance in the treatment of severe cases of COVID-19, when the host inflammatory response becomes a major cause of lung damage and subsequent mortality.
-- COVID-19: combining antiviral and anti-inflammatory treatments. The Lancet Infectious Diseases. 2020-02-27.
tests | identify | severe cases of COVID-19 (count: 1)
In two recent articles from Huang C et al and Yang X in The Lancet Biomarkers / tests assessing endothelial function could also help to early identify severe cases of COVID-19.
lymphocyte | counts observed in | severe cases of COVID-19 3 8 (count: 1)
In their works, Yang X et al and Chen N et al propose a direct cytotoxic action of the virus to explain the low lymphocyte counts observed in the severe cases of COVID-19 3 8 .
extravasation | explain | lymphopenia observed in severe COVID-19 patients 9 (count: 1)
As we recently reviewed in J Clin Med, endothelial dysfunction induces disassembly of intercellular junctions, endothelial cell death and blood-tissue barrier disruption, along with enhanced leukocyte adhesion and extravasation, which could contribute to explain the lymphopenia observed in severe COVID-19 patients 9 .
factors | presenting | severe failure following COVID-19 infection (count: 1)
In aged individuals with chronic diseases, these features could represent predisposing factors for presenting a severe respiratory failure following COVID-19 infection.
mild patients | were negative Among | 50 patients infected with SARS-CoV-2 (count: 1)
Among 50 patients infected with SARS-CoV-2, nine mild patients were negative in CT pulmonary imaging ( Fig.
Background | has experienced | outbreak of coronavirus disease 2019 caused by severe syndrome coronavirus 2 (count: 1)
Background Since December, 2019, Wuhan, China, has experienced an outbreak of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
Interpretation 2019-nCoV infection | caused | clusters of severe illness (count: 1)
Interpretation The 2019-nCoV infection caused clusters of severe respiratory illness similar to severe acute respiratory syndrome coronavirus and was associated with ICU admission and high mortality.
2019-nCoV | known as | severe syndrome coronavirus 2 (count: 1)
The 2019 novel coronavirus (2019-nCoV, officially known as severe acute respiratory syndrome coronavirus 2) was detected in Wuhan at the end of 2019 in cases of unexplained pneumonia.
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SARS-CoV-2 infected patients | have developed | mild symptoms (count: 1)
To date, most SARS-CoV-2 infected patients have developed mild symptoms such as dry cough, sore throat, and fever.
10 patients | is with | severe COVID-19 (count: 1)
10 All patients with severe COVID-19 should be screened for hyperinflammation using laboratory trends (eg, increasing ferritin, decreasing platelet counts, or erythrocyte sedimentation rate) and the HScore 11 (table) to identify the subgroup of patients for whom immunosuppression could improve mortality.
50-year-old male patient | is in | severe stage of COVID-19 (count: 1)
G, H, I): Images from a 50-year-old male patient in the severe stage of COVID-19.
cTnT | is in | COVID-19 patients with severe disease i.e. included (count: 1)
The title, abstract and full text of all documents identified with these search criteria were assessed, and those reporting information on cTnT or cTnI values in COVID-19 patients with or without severe disease (i.e., those needing mechanical ventilation, ICU admission or those who died), were included in a metaanalysis.
standardized mean difference | is in | COVID-19 patients with severe disease (count: 1)
A meta-analysis was finally carried out, with calculation of standardized mean difference (SMD) and 95% confidence interval (95% CI) of cTnI or cTnT values in COVID-19 patients with or without severe disease.
COVID-19 patients | is with | severe disease (count: 1)
Although the heterogeneity was considerably high (i.e., I 2 , 98%; p b 0.001), the values of cTnI were found to be significantly increased in COVID-19 patients with severe disease than in those without (SMD, 25.6 ng/L; 95% CI, 6.8-44.5 ng/L).
COVID-19 infection symptoms | range from | mild symptoms (count: 1)
Because COVID-19 infection symptoms range from unspecific mild respiratory symptoms to acute respiratory distress [3] and because these symptoms are very similar to those of many seasonal viruses [11] [12] [13] , we implemented an outpatient rapid diagnosis for mildly affected patients which operated ten hours a day, seven days a week.
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death | severe presentation of | COVID-19 infection (count: 1)
We need to develop a hypothesis to explain the causal path underlying the more severe clinical presentation of COVID-19 infection and subsequent death in diabetic patients.
COVID-19 patients | is with | mild illness (count: 1)
The prolonged duration of SARS-CoV-2 detection in naso-oropharyngeal specimens of the COVID-19 patients with mild illness is of concern in epidemic areas.
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mild illness | increase | potential of COVID-19 (count: 1)
The long duration of SARS-CoV-2 shedding and the transmission in patients asymptomatic or with mild illness drastically increase the pandemic potential of COVID-19.
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2 COVID-19 patients | is with | mild illness (count: 1)
Owing to the early wave of SARS-CoV-2 transmission in Taiwan, our study was limited by the small number of cases for screening and included 2 COVID-19 patients with mild illness.
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infection-protection experience | severe diseases such as | COVID-19 (count: 1)
This article describes the emergency management procedure of our radiology department for situations involving severe infectious diseases, such as COVID-19, and the infection-protection experience of the department staff.
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2019-nCoV | is with | mild symptoms (count: 1)
By This prescription is suitable for patients who is diagnosed with 2019-nCoV with mild symptoms, ordinary patients and severely ill patients.
-- New thinking in the treatment of 2019 novel coronavirus pneumonia. Complementary Therapies in Clinical Practice. 2020-05-31.
SARS-CoV-2 | was isolated from | airway cells (count: 1)
SARS-CoV-2 was recently isolated from human airway epithelial cells, characterized by next-generation sequencing in January 2020, and identified to be a new member of β-CoVs [16] .
-- Coronavirus Disease 2019: Coronaviruses and Blood Safety. Transfusion Medicine Reviews. 2020-02-21.
2019-nCoV | belongs as | severe syndrome (count: 1)
The 2019-nCoV belongs to the same coronavirus group as the severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS) viruses that caused two of the more severe epidemics in recent years.
SARS-CoV-2 Spike cells | called | I-cells (count: 1)
Our approach entails utilizing SARS-CoV-2 Spike antigen-expressing, non-replicating cells as carriers and presenters of immunogenic antigens, so called "I-cells".
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decoy cells | will | will developed as vaccine protect against COVID-19 disease (count: 1)
Utilizing this innovative strategy, these viral antigen-displaying decoy cells will be developed as a vaccine to protect against COVID-19 disease.
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we | assess | may associated with severe COVID-19 (count: 1)
In the present study, we aim to investigate whether platelet count could differentiate between COVID-19 patients with or without severe disease, and assess if thrombocytopenia may be associated with severe COVID-19.
severe COVID-19 | for ratio is | OR (count: 1)
A meta-analysis was performed, with calculation of weighted mean difference (WMD) and 95% confidence interval (95% CI) of platelet number in COVID-19 patients with or without severe disease, as well as the odds ratio (OR) of thrombocytopenia for severe COVID-19.
1779 COVID-19 patients | 399 with | severe disease (count: 1)
Therefore, 9 studies could finally be included in our metaanalysis, totaling 1779 COVID-19 patients, 399 of whom (22.4%) with severe disease [11] [12] [13] [14] [15] [16] [17] [18] [19] .
mean difference | is in | platelet count between COVID-19 patients with severe disease (count: 1)
The mean difference in platelet count between COVID-19 patients with or without severe disease in the nine individual studies is shown in Figure 1 .
thrombocytopenia | is associated with | risk of severe COVID-19 (count: 1)
Moreover, we observed that thrombocytopenia is also associated with threefold enhanced risk of severe COVID-19.
limited data | is | available on clinically useful biomarkers for severe COVID-19 (count: 1)
Outside findings from the early small, retrospective studies on this emerging pathogen, limited data is available on clinically useful biomarkers for severe COVID-19.
mean difference | is in | platelet count between COVID-19 patients with severe disease .13 (count: 1)
Forest plot of mean difference in platelet count between COVID-19 patients with or without severe disease.13
severe COVID-19 respiratory disease | with patients is | 13 (count: 1)
Another ongoing phase 3 randomized, double-blind, placebo-controlled, multicenter study is evaluating the efficacy and safety of remdesivir in 452 hospitalized adult patients with severe COVID-19 respiratory disease [13] .
-- Remdesivir as a possible therapeutic option for the COVID-19. Travel Medicine and Infectious Disease. 2020-03-05.
COVID-19 | grew in | airway cells (count: 1)
Notably, COVID-19 grew more readily in primary human airway epithelial cells than in standard tissue culture cells, unlike SARS-CoV or MERS-CoV, suggesting the potential for increased infectivity.
Vero E6 cells | infected by | SARS-CoV-2 (count: 1)
The research letter, written by a group of Chinese researchers, studied the effect of chloroquine in vitro, using Vero E6 cells infected by SARS-CoV-2 at a multiplicity of infection (MOI) of 0.05.
2019-nCoV RT-PCR negativity | to time is | five outcomes for severe type (count: 1)
stay, composite events, score of clinical symptoms, and time to 2019-nCoV RT-PCR negativity), five outcomes for the severe type (composite events, length of hospital stay, arterial oxygen partial pressure (PaO 2 )/fraction of inspired oxygen (FiO 2 ), duration of mechanical ventilation, and time to 2019-nCoV RT-PCR negativity), one outcome for critical type (all-cause mortality), and one outcome for rehabilitation period (pulmonary function).
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could distinct feature | is in | very severe COVID-19 (count: 1)
Thus, the consistently high cTnI levels in very severe group point to the importance that the heart injury could be a distinct, or even lethal feature in very severe COVID-19.
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severe COVID-19 | present with | injury 2-4 (count: 1)
Previous studies suggest that severe COVID-19 may present with acute cardiac injury 2-4 .
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injury-SARS-CoV-2 | enters | cells (count: 1)
Direct myocardial injury-SARS-CoV-2 enters human cells by binding to angiotensinconverting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in heart and lungs.
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SARS-CoV-2 | gain | entry into cells (count: 1)
Since SARS-CoV-2 binds to ACE2 to gain entry into human cells, there is a potentially increased risk of developing COVID-19 or developing more severe disease in patients who are already on background treatment with ACEi/ARB.
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higher prevalence | is in | severe COVID-19 disease (count: 1)
2 Close inspection of the available data supports a higher prevalence of abnormal aminotransferase levels in severe COVID-19 disease, but these studies actually suggest that clinically significant liver injury is uncommon, even when data for the most severely ill patients are selected (table) .
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mild liver test derangement | is | present at baseline in many patients with COVID-19 before significant medication use (count: 1)
Drug-induced liver injury is a possible contributing factor to the observed abnormal liver blood test abnormalities after therapeutics begin and should be considered by clinicians, but mild liver test derangement is present at baseline in many patients with COVID-19 before significant medication use.
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COVID-19 infection | might induce | myositis similar to that observed in severe influenza infections (count: 1)
It is therefore possible that aminotransferase elevations do not necessarily arise from the liver alone and that COVID-19 infection might induce a myositis similar to that observed in severe influenza infections.
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Hepatic dysfunction | is in | severe COVID-19 (count: 1)
Hepatic dysfunction in severe COVID-19 is accompanied by greater activation of coagulative and fibrinolytic pathways, relatively depressed platelet counts, climbing neutrophil counts and neutrophil to lymphocyte ratios, and high ferritin levels.
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meta-analysis | was performed with | estimation of odds ratio in patients without severe forms of COVID-19 (count: 1)
A meta-analysis was then performed, with estimation of the odds ratio (OR) and its 95% confidence interval (95% CI) in patients with or without severe forms of COVID-19.
1399 COVID-19 patients | 288 with | severe disease (count: 1)
Therefore, 5 studies could finally be included in our meta-analysis, totaling 1399 COVID-19 patients, 288 of whom (20.6%) with severe disease [6] [7] [8] [9] [10] .
smoking | be associated with | risk progressing towards severe disease in COVID-19 (count: 1)
Despite a trend towards higher risk was appreciable, no significant association could neither be found between active smoking and severity of COVID-19 when data of individual studies were pooled (OR, In conclusion, the results of this preliminary meta-analysis based on Chinese patients suggest that active smoking does not apparently seem to be signicantly associated with enhanced risk of progressing towards severe disease in COVID-19.
patients | is with | moderate to severe COVID-19 infection (count: 1)
In view of good tolerability of HCQ and low cost, it could be offered as an off-label treatment to the patients with moderate to severe COVID-19 infection.
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Patients | are among | risk individuals for severe COVID-19 disease (count: 1)
Patients with underlying cardiovascular disease are among the highest risk individuals for severe COVID-19 disease and death 36 .
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paving appearance | reflecting | interstitial In severe phase of COVID-19 (count: 1)
The "crazy paving appearance" was apparent, suggesting the thickened interlobular and intralobular septae, and reflecting interstitial In the severe phase of COVID-19, the pulmonary lesions generally reached peaked around 14 days after the onset of the disease, but a few cases developed rapidly, with the lesions appearing bilaterally with diffuse infiltration of all segments of the lungs, and manifesting as "white lung."
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3 Our clinical findings | is in | severe case of COVID-19 (count: 1)
3 Our clinical and pathological findings in this severe case of COVID-19 can not only help to identify a cause of death, but also provide new insights into the pathogenesis of SARS-CoV-2-related pneumonia, which might help physicians to formulate a timely therapeutic strategy for similar severe patients and reduce mortality.
patient | is with | severe pneumonia caused by SARS-CoV-2SARS-CoV-2 = (count: 1)
Pathological manifestations of right (A) and left (B) lung tissue, liver tissue (C), and heart tissue (D) in a patient with severe pneumonia caused by SARS-CoV-2SARS-CoV-2=severe acute respiratory syndrome coronavirus 2.
we | Combining | model of severe SARS-CoV-2 transmission (count: 1)
Combining a mathematical model of severe SARS-CoV-2 transmission with four datasets from within and outside Wuhan, we estimated how transmission in Wuhan varied between December, 2019, and February, 2020.
Patients | is with | severe COVID-19 (count: 1)
Patients with severe COVID-19 seem to have higher rates of liver dysfunction.
-- Liver injury in COVID-19: management and challenges. The Lancet Gastroenterology & Hepatology. 2020-03-04.
Liver damage | is in | mild cases of COVID-19 (count: 1)
Liver damage in mild cases of COVID-19 is often transient and can return to normal without any special treatment.
-- Liver injury in COVID-19: management and challenges. The Lancet Gastroenterology & Hepatology. 2020-03-04.
ACE2 | promoted | entry of SARS-CoV-2 into cells (count: 1)
Recently, it has been found that human ACE2 promoted the entry of SARS-CoV-2 into the cells [3, 10] .
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SARS-CoV-2 | is | related to severe syndrome-like could possible reservoir (count: 1)
Genomic analysis revealed that SARS-CoV-2 is phylogenetically related to severe acute respiratory syndrome-like (SARS-like) bat viruses, therefore bats could be the possible primary reservoir.
mild manifestations | caused by | COVID-19 (count: 1)
The mild manifestations caused by COVID-19 should be distinguished from respiratory infections caused by other viruses.
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COVID-19 cases | suggesting | proportion of cases (count: 1)
Of note, in Wuhan, 48,557 COVID-19 cases with 2,169 deaths were confirmed on that same day, suggesting a much higher proportion of severe cases and mortality rate in Wuhan than in other provinces of China.
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patients | had improved | function including one severe COVID-19 pneumonia case (count: 1)
Detailed follow-up over 14 days post-transplantation showed no adverse effects, and within 2 days, all patients had significantly improved pulmonary function, including the one severe COVID-19 pneumonia case who was well enough for discharge by day 10.
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severe pneumonia | caused by | COVID-19 (count: 1)
30] have confirmed that the patient has severe pneumonia caused by COVID-19 according to pathological characteristics, and this patient died from severe infection with ARDS obtaining biopsy samples at autopsy.
COVID-19 outbreak | creates sense with | 2003 outbreak of severe syndrome (count: 1)
The COVID-19 outbreak "creates a sense of déjà vu" with the 2003 outbreak of severe acute respiratory syndrome (SARS).
-- COVID-19 and the anti-lessons of history. The Lancet. 2020-03-20.
SARS-CoV-2 | expressing | cells (count: 1)
SARS-CoV-2 can enter angiotensin converting enzyme II (ACE2)-expressing cells.
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drugs | included in | severe case management protocols COVID-19 (count: 1)
Consequently, lopinavir-ritonavir and remdesevir are currently the only anti-viral drugs included in the more severe case management protocols of COVID-19 [10] .
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ARDS | occurring in | severe case of COVID-19 infection (count: 1)
As already described, ARDS occurring in most severe case of COVID-19 infection is mainly produced by the massive release of pro-inflammatory mediators (CRS) associated with viral replication and lung injury, leading to multiorgan failure [22] .
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baricitinib | produce | dampening of host response due to CRS responsible for severe forms during COVID-19 (count: 1)
Moreover, as a selective inhibitor of JAK 1 and 2, baricitinib is also able to produce an important dampening of host inflammatory response due to CRS (including IL-6 and interferon gamma) responsible for the more severe forms of interstitial pneumonia during COVID-19 [107, 108] .
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patients | is with | severe 2019-nCoV infection (count: 1)
15 Expansion of anti-2019-nCoV-specific T cells, as cellular drugs, could aid to prepare T-cell products for the adjunct treatment of patients with severe 2019-nCoV infection.
SARS-CoV-2 | can | can detected in airway cells (count: 1)
The gene features of SARS-CoV-2 are significantly different from those of SARS-CoV and MERS-CoV. During in vitro culture, SARS-CoV-2 can be detected in human airway epithelial cells within 96 hours
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patients | is with | severe COVID-19 infection (count: 1)
Second, investigations are needed regarding the key pathways and immune cell types involved in cytokine storm onset in COVID-19; these will benefit the understanding of artificial-liver support system treatment for alleviating cytokine storm to reverse the disease process in patients with severe COVID-19 infection by rebalancing the immune system.
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death | is in | severe cases of SARS-CoV-2 infection (count: 1)
The cytokine storm will trigger a violent attack by the immune system to the body, cause ARDS and multiple organ failure, and finally lead to death in severe cases of SARS-CoV-2 infection, just like what occurs in SARS-CoV and MERS-CoV infection [31] .
-- Molecular immune pathogenesis and diagnosis of COVID-19. Journal of Pharmaceutical Analysis. 2020-03-05.
preliminary acquired favorable results | is in | acute severe SARS-CoV-2 patients (count: 1)
It has preliminary acquired favorable results in acute, severe SARS-CoV-2 patients.
-- Molecular immune pathogenesis and diagnosis of COVID-19. Journal of Pharmaceutical Analysis. 2020-03-05.
ACE2 protein | supporting | entry of SARS-CoV-2 into host cells (count: 1)
Our immunofluorescent data showed that ACE2 protein, which has been proved to be a cell receptor for SARS-CoV-2, is abundantly expressed in the glandular cells of gastric, duodenal and rectal epithelia, supporting the entry of SARS-CoV-2 into the host cells.
people | is with | severe COVID-19 (count: 1)
The partnership has six work streams: laboratory diagnosis and subtyping; surveillance, including screening at points of entry and cross-border activities; infection prevention and control in healthcare facilities; clinical management of people with severe COVID-19; risk communication; and supply-chain management and stockpiles.
2019-nCoV | causes | severe disease (count: 1)
While it is expected that the 2019-nCoV causes more severe disease in those with underlying medical conditions, the first published case series (n = 99) reports that only 50% had co-morbidities, while the first two fatal cases had none, other than being smokers [10] .
-- Coronavirus 2019-nCoV: Is the genie already out of the bottle?. Travel Medicine and Infectious Disease. 2020-02-07.
severe patients | are susceptible to | COVID-19 (count: 1)
Aged people and severe patients are more susceptible to COVID-19, this may be associated with a higher frequency of comorbidities 9 .
SARS-CoV-2 | use horseshoe bat as | entry receptor in cells (count: 1)
experimentally confirmed that SARS-CoV-2 is able to use human, Chinese horseshoe bat, civet, and pig ACE2 proteins as an entry receptor in ACE2-expressing cells [3] , suggesting that the RBD of SARS-CoV-2 mediates infection in humans and other animals.
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our experience | is in | treatment of severe COVID-19 (count: 1)
Here, fro m the perspective of clin ical immunologist and rheu matologists, we would like to d iscuss and share our experience in the treatment of severe COVID-19.
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ly mphocytes | were activated In | severe COVID-19 (count: 1)
In severe COVID-19, although patients have lymphcytopenia, the ly mphocytes were activated.
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severe COVID-19 patients | is in | our ICU ward (count: 1)
Consistent with others, most of severe COVID-19 patients in our ICU ward had persistent very high level of erythematosus sedimentation rate (ESR), CRP, and h igh level of IL-6,TNF, IL-1, IL-8, IL2R, etc, and were associated with ARDS, hypercoagulation and disseminated intravascular coagulation (DIC), manifested as thrombosis, thrombocytopenia, gangrene of extremit ies.
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cells | is in | patients with COVID-19 (count: 1)
Both T cells and NK cells in patients with COVID-19 were reduced.
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prominent clinical man ifestation | is in | severe COVID-19 patients (count: 1)
Another prominent clinical man ifestation in severe COVID-19 patients is endothelium damage.
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Mimicry | could | could seen in severe COVID-19 patients (count: 1)
Mimicry of vasculitis could be seen in severe COVID-19 patients.
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TCZ | be treatment in | severe patients of COVID-19 (count: 1)
Their data suggests TCZ might be an effective treatment in severe patients of COVID-19.
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trials | have | have registered in treatment of severe COVID-19 pneumonia (count: 1)
Till now, several clinical trials have been registered on safety and efficacy of tocilizu mab in the treatment of severe COVID-19 pneumonia in adult inpatients , including a mult icenter, rando mized controlled trial for the efficacy and safety of tocilizu mab in the treat ment of novel coronary pneumonia (NCP) (Ch iCTR2000029765), a single arm open mu lticenter study on tocilizu mab (Ch iCTR2000030796), and comb ination of tocilizu mab and other drugs (Ch iCTR2000030442 and ChiCTR2000030894).
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antibody | block SARS-CoV-2 | entering into target cells (count: 1)
Besides, a recent study showed that neutralizing antibody from a convalescent SARS patient could block the SARS-CoV-2 from entering into target cells in vitro 1 , which implies the potential cross-protective epitode between the two viruses.
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we | risk for | severe COVID-19 (count: 1)
In this study, we analysed the risk for severe COVID-19 in patients with cancer for the first time, to our knowledge; only by nationwide analysis can we follow up patients with rare but important comorbidities, such as cancer.
Interpretation 2019-nCoV infection | result in | severe diseases (count: 1)
Interpretation The 2019-nCoV infection was of clustering onset, is more likely to affect older males with comorbidities, and can result in severe and even fatal respiratory diseases such as acute respiratory distress syndrome.
2019-nCoV infection | result in | severe diseases (count: 1)
The 2019-nCoV infection was of clustering onset, is more likely to affect older men with comorbidities, and could result in severe and even fatal respiratory diseases such as acute respiratory distress syndrome.
COVID-19 | is characterised for | patients with mild disease (count: 1)
Radiologically, COVID-19 is characterised by multifocal ground-glass opacities, even for patients with mild disease.
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severe acute respiratory syndrome coronavirus 2-which results | is in | COVID-19-people with mental disorders (count: 1)
Second, once infected with severe acute respiratory syndrome coronavirus 2-which results in COVID-19-people with mental disorders can be exposed to more barriers in accessing timely health services, because of discrimination associated with mental ill-health in health-care settings.
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2019-nCoV | use ACE2 as | entry receptor in ACE2expressing cells (count: 1)
found that the 2019-nCoV just like SARS-Cov may also use ACE2 as an entry receptor in the ACE2expressing cells, and the majority of which are type II alveolar cells (AT2) in human lung.
patients | is with | laboratory-confirmed non-severe COVID-19 (count: 1)
By day three of admission the patient had lymphocytopenia, which was found in 80.4% of patients with laboratory-confirmed non-severe COVID-19 in mainland China (3).
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SARS-CoV-2 infection | characterised by | severe hypoxaemia (count: 1)
We report on 52 critically ill patients with con firmed SARS-CoV-2 infection, characterised by severe hypoxaemia.
Study flow diagram SARS-CoV-2 | = | severe syndrome coronavirus 2 (count: 1)
Study flow diagram SARS-CoV-2=severe acute respiratory syndrome coronavirus 2.
patients | is with | severe SARS-CoV-2 pneumonia (count: 1)
Demographics and baseline characteristics of patients with severe SARS-CoV-2 pneumonia
International Committee | has renamed 2019-nCoV as | severe syndrome coronavirus-2 (count: 1)
Regarding the virus itself, the International Committee on Taxonomy of Viruses has renamed the previously provisionally named 2019-nCoV as severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) [3] .
2019-nCoV results | is in | clusters of severe respiratory illness similar to that caused by severe acute respiratory syndrome coronavirus (count: 1)
Infection with 2019-nCoV results in clusters of severe respiratory illness similar to that caused by severe acute respiratory syndrome coronavirus (SARS-CoV) and is associated with high mortality .
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2019-nCoV | showed | mild infectivity (count: 1)
Similar to the beginning of the SARS-CoV pandemic, 2019-nCoV showed mild infectivity.
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our rehabilitation patients | are at | risk of severe 2019-nCoV infections (count: 1)
Other common conditions needing 111 rehabilitation like chronic respiratory disease and cancer are also associated with higher risk of mortality from 112 2019-nCoV. Hence, our rehabilitation patients are at higher risk of severe and fatal 2019-nCoV infections.
-- How Should the Rehabilitation Community Prepare for 2019-nCoV?. Archives of Physical Medicine and Rehabilitation. 2020-03-16.
COVID-19 | is proving | infectious than severe syndrome (count: 1)
COVID-19 is proving to be more infectious than severe acute respiratory syndrome, leading to 10 times as many cases in one-quarter of the time.
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severe disease | women with | COVID-19 (count: 1)
Based on these limited reports, and the available data from other 316 respiratory pathogens such as SARS and influenza, it is unknown whether pregnant women with 317 COVID-19 will experience more severe disease.
-- Coronavirus Disease 2019 (COVID-19) and Pregnancy: What obstetricians need to know. American Journal of Obstetrics and Gynecology. 2020-02-24.