What happens with co-infections?

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Information Extraction Results

us | pathogenesis for | 2019-nCoV (count: 2)
Considering the sequence of 2019-nCoV is similar to the SRAS-CoV and they are reported to share the same molecular as the entry point, analyses of ACE2 expression and distribution in lung and related biological processes may help us understand the pathogenesis and design therapeutic strategies for 2019-nCoV. Recent advances in bioinformatics enable researchers to reveal the underlying mechanisms of various diseases.
These results may help us understand the pathogenesis and design therapeutic strategies for 2019-nCoV.
perturbation | contribute | pathogenesis of SARS-CoV-2 (count: 1)
These results, consistent with the previous findings found in the patients with severe illness, suggest perturbation of immune system contribute the pathogenesis of SARS-CoV-2.
We | compared | our SARS-CoV-2 interaction map (count: 1)
We compared our SARS-CoV-2 interaction map with those derived for 10 other pathogens (Fig.
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SARS-CoV-2 Orf6 | between interaction is | interferon-inducible mRNA nuclear export complex 64 (count: 1)
Orf6 of SARS-CoV has been shown to play a role in antagonizing host interferon signaling 63 ; we identified a novel, high-confidence interaction between SARS-CoV-2 Orf6 and NUP98-RAE1, an interferon-inducible mRNA nuclear export complex 64 that is hijacked or degraded by multiple viruses, including VSV, Influenza-A, KSHV, and Polio, and is a restriction factor for Influenza-A infection 58, 60, 62, 65 .
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none | disrupt | interaction with RBD of SARS-CoV-2 (count: 1)
We found that none of them is likely to disrupt the interaction with the viral RBD of SARS-CoV-2.
Homology | generate | interaction model 140 SARS-CoV-2 RBD (count: 1)
Homology based 139 protein-protein docking was conducted to generate the interaction model 140 of SARS-CoV-2 RBD with ACE2 receptor from different animal species 141 ( Figure 2C ).
interaction energy | is low for | SARS-CoV-2 143 (count: 1)
We noticed that for the civet, dog, chicken and snake forms, 142 the interaction energy is very low and very similar either for SARS-CoV-2 143 or SARS-CoV. Although the Kd are relatively low for the rat and bat forms 144 interacting with SARS-CoV RBD, those of SARS-CoV-2 are high and go 145 beyond 50 nM. On the other hand, it seems that the interaction with pig 146 ACE2 is more favorable for SARS-CoV-2 isolate since the estimated Kd is 147 3 folds lesser compared to SARS-CoV-2.
We | attribute difference to | interaction of COVID-19 (count: 1)
We attribute this difference to the unique interaction of COVID-19 at position K417 with the middle of the N-terminal ACE2 helix, thus serving as an anchor site to the receptor (Fig.
COVID-19 | creates | interaction patch (count: 1)
COVID-19 also creates a new interaction patch with the middle of the N-terminal ACE2 helix(Fig.
NCP severity | was | risk factor for AMI in COVID-19 patients (count: 1)
26 Logistic regression analysis indicated that NCP severity was a risk factor for AMI in COVID-19 patients.
presence | be | risk factor for AMI in COVID-19 patients (count: 1)
It is worth mentioning that the presence of comorbidities (OR, 4.336; 95CI% [1.11, 38.55]) may be the most critical risk factor for AMI in COVID-19 patients.
COPD | was | risk factor for COVID-19 severity (count: 1)
Despite being uncommon in our study population, COPD was by far the strongest risk factor for COVID-19 severity, followed by CVD and hypertension.
ratio | was identified as | risk factor for illness 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.
Infection | may | may risk factor for SARS-CoV-2 infection (count: 1)
Infection with M. tuberculosis (MTB), the pathogen that causes TB and latently infects ~25% of the global population, may be a risk factor for SARS-CoV-2 infection and severe COVID-19 pneumonia.
TB | is | risk factor for SARS-CoV-2 infection (count: 1)
First, the medical and wider community should be informed that latent/active TB is a risk factor for SARS-CoV-2 infection, and those at risk should be encouraged to pay special attention to preventive measures.
C. Distinct interaction patterns | is in | SARS-CoV-2 RBD-ACE2 interfaces (count: 1)
C. Distinct interaction patterns in the SARS-CoV-2 and SARS-CoV RBD-ACE2 interfaces.
K933 | forms interaction in | SARS-CoV-2 (count: 1)
https://doi.org/10.1101/2020.03.09.983247 doi: bioRxiv preprint S929 in SARS-CoV2 HR1, a new, strong hydrogen bond was formed with a distance 390 of 2.4 Å. K933 forms a new interaction with N1192 in SARS-CoV-2 with a distance 391 of 2.7 Å, whereas the corresponding position in SARS-CoV has no such interaction.
COVID-19 epitope | interaction of are | online (count: 1)
The RMSD and contact distance plots for all the trajectories versus time, the structure of virus antibody complex and the residues at the contact region, native contacts in antigen-antibody complex, the interaction of COVID-19 epitope with 2GHW antibody, tables for all neutralizing point mutations, co-mutations and their neutralization potentials, the structures of stable antibodies in PDB format, and IC50 data interpretation are available online.
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crucial role | is in | pathogenesis of 1 4 0 SARS-CoV-2 (count: 1)
results of our study suggested a crucial role of IP-10 in the pathogenesis of 1 4 0 SARS-CoV-2, which has also been shown to be associated with disease severity of In summary, we compared the differences of cytokines profiles between severe and 1 4 7 moderate COVID-19 cases, and found that IP-10, MCP-3 and IL-1ra were antibodies against theses cytokines, especially IP-10.
Our findings | provide | model of SARS-CoV-2 infection for pathogenesis study 85 (count: 1)
Our 84 findings also provide a useful model of SARS-CoV-2 infection for pathogenesis study 85 and novel drug discovery.
current published data | showed | interaction between protein of SARS-CoV-2 (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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we | measure | interaction between SARS-CoV-2 Spike S1 protein receptor binding domain (count: 1)
Here we use surface plasmon resonance and circular dichroism to measure the interaction between the SARS-CoV-2 Spike S1 protein receptor binding domain (SARS-CoV-2 S1 RBD) and heparin.
smoking | be | risk factor for 2019-nCoV (count: 1)
Besides, based on the expression of ACE2 in smoking individuals, we inferred that long-term smoking might be a risk factor for 2019-nCoV. Analyzing the ACE2 in SARS-CoV infected cells suggested that ACE2 was more than just a receptor but also participated in post-infection regulation, including immune response, cytokine secretion, and viral genome replication.
researchers | pathogenesis for | 2019-nCoV (count: 1)
Our findings may explain the clinical symptoms so far and help clinicians and researchers understand the pathogenesis and design therapeutic strategies for 2019-nCoV. : medRxiv preprint GO biological process annotation gmt file was downloaded from MSigDB (https://www.gsea-msigdb.org/gsea/msigdb/).
it | has become in | pathogenesis of COVID-19 6 (count: 1)
There are ACE2 receptors in type II alveolar epithelial cells of human lung, so it has become the main target of SARS-CoV-2 in the pathogenesis of COVID-19 6 .
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abnormalities | contributed to | pathogenesis of COVID-19 (count: 1)
At the same time, the level of total protein, albumin and HDL-C significantly decreased with the process of the disease, suggesting that metabolic abnormalities contributed to the pathogenesis of COVID-19.
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hepatic injury | is in | pathogenesis of COVID-19 (count: 1)
Pathological findings were also in favor of more attention to the hepatic injury in the pathogenesis of COVID-19.
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co-infections | is with | SARS-CoV-2 (count: 1)
Third, suspected SARS-CoV-2 patients sometimes have a different respiratory viral infection or have co-infections with SARS-CoV-2 and other respiratory viruses [7] .
we | believe According to | literature on pathogenesis of COVID-19 (count: 1)
According to previous literature [21] on the pathogenesis and morphology of COVID-19, we believe that there may be a statistical rule in the pathogenesis (see Feature Analysis section in Methods).
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understanding | immunopathogenesis during | SARS-CoV-2 infection (count: 1)
This work may help to achieve a better understanding of immune function disorder as well as immunopathogenesis during SARS-CoV-2 infection.
virus entry | disruption of | SARS-CoV-2-RBD-host ACE2 interaction with peptide-based binders (count: 1)
We hypothesize that disruption of the viral SARS-CoV-2-RBD-host ACE2 interaction with 72 peptide-based binders will prevent virus entry into human cells, offering a novel opportunity for 73 therapeutic intervention.
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age | is | risk factor for death in patients infected with COVID-19 (count: 1)
It is clear that age is a significant risk factor for death in patients infected with COVID-19.
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SARS-CoV-2 | infect cells through | interaction on cells (count: 1)
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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Gender | is | risk factor for severity in patients with COVID-19 (count: 1)
Therefore, Gender is a risk factor for higher severity and mortality in patients with both COVID-19 and SARS independent of age and susceptibility.
interaction alpha/beta signaling genes | is in | COVID-19 patients (count: 1)
S6 Differential expression patterns of interaction alpha/beta signaling genes in COVID-19 patients vs other diseases A. SARS-COV-2 vs influenza A B. SARS-COV-2 vs acute pharyngitis C. SARS-COV-2 vs cerebral infarction Fig.
we | identify For | 2019-nCoV protein in protein-protein interaction complex (count: 1)
For each 2019-nCoV protein in a protein-protein interaction complex, we identify .
Future researches | should | should focused in pathogenesis of COVID-19 (count: 1)
Future researches should be focused on involvements of CRP in the pathogenesis of COVID-19.There are some limitations in our study.
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finding | was consistent with | pathogenesis of SARS-CoV-2 (count: 1)
This finding that increased urine K + was the primary cause of hypokalemia was consistent with the pathogenesis of SARS-CoV-2.
Our work | understanding | pathogenesis of COVID-19 (count: 1)
Our work has thus provided a basis for further analysis of protective immunity to SARS-CoV-2, and understanding the pathogenesis of COVID-19, especially in the severe cases.
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co-infection | is common in | children with COVID-19 (count: 1)
28, 29 It can be seen that co-infection is common in children with COVID-19, indicating SARS-CoV-2 screening is necessary to identify COVID-19 cases, especially during the peak season for colds, influenza and other respiratory ailments.
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Red color | highlights | interaction positions of SARS-CoV-2 (count: 1)
Red color highlights interaction positions of SARS-CoV-2 and pangolin CoVs with different amino acids residues.
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HIV inhibitors | produce | interaction with site of SARS-CoV-2 protease (count: 1)
Our results showed that several HIV inhibitors such as lopinavir, ritonavir, and saquinavir produce strong interaction with the active site of SARS-CoV-2 main protease.
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hypertension | is | host risk factor for 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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modification | could improve interaction in | SARS-CoV-2 (count: 1)
However, in SARS-CoV-2, slight modification of some residues could improve the interaction with the human cellular receptor: L455, F486, Q493, and N501.
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SARS-CoV-2 | may lead to | misunderstanding of pathogenesis of coronavirus (count: 1)
Based on genotyping, SARS-CoV-2 is unlikely to be significantly linked to SARS-CoV. Rather, SARS-CoV-2 may lead to the misunderstanding of the pathogenesis of the new coronavirus, which is less pathogenic compared with SARS-CoV.
spike protein priming | is | essential for entry of SARS-CoV-2 through interaction with ACE2 receptor (count: 1)
25] recently demonstrated that initial spike protein priming by transmembrane protease serine 2 (TMPRSS2) is essential for entry and viral spread of SARS-CoV-2 through interaction with the ACE2 receptor [26, 27] .
COVID-19 infection | pathogenesis of was | 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] .
it | pathogenesis of | COVID-19 (count: 1)
This dearth of pathology description made it difficult to understand the pathogenesis of COVID-19.
-- Editorial: Coronaviruses: Facts, Myths and Hypotheses.. Journal of Thoracic Oncology. 2020-03-07.
us | pathogenesis of | COVID-19 (count: 1)
This important work helps us understand the pathogenesis of COVID-19 and to be better prepared to identify potentially infected patients.
-- Editorial: Coronaviruses: Facts, Myths and Hypotheses.. Journal of Thoracic Oncology. 2020-03-07.
we | understand | contribution of receptor interaction to infectivity of SARS-CoV-2 (count: 1)
To understand the contribution of receptor interaction to the infectivity of SARS-CoV-2, we characterized engagement of hACE2 by SARS-CoV-2 S B and SARS-CoV S B side-by-side.
we | make | pathogenesis of SARS-CoV-2 (count: 1)
To make explicit the pathogenesis and pathophysiology of SARS-CoV-2, we retrospectively analyzed a cohort of patients who were diagnosed with "2019 novel coronavirus disease (COVID-19)" in the Zhongnan Hospital of Wuhan University, describing the clinical features of laboratoryconfirmed cases of SARS-CoV-2 infection. (
cell activity | be activated in | pathogenesis of COVID-19 patients (count: 1)
As the rise of IL-1β is a downstream indicator of cell pyroptosis, this may suggest that cell pyroptotic activity is likely to be activated and involved in the pathogenesis of COVID-19 patients.
diabetes | was seen as | risk factor for Data about COVID-19 (count: 1)
Indeed, diabetes was seen as an important risk factor for Data about COVID-19 in patients with diabetes is limited at present.
-- Clinical considerations for patients with diabetes in times of COVID-19 epidemic. Diabetes & Metabolic Syndrome: Clinical Research & Reviews. 2020-06-30.
Our findings | will facilitate | understanding of pathogenesis of COVID-19 (count: 1)
Our findings will facilitate understanding of the pathogenesis of COVID-19 and improve clinical strategies against the disease.
co-infection | is with | SARS-CoV-2 (count: 1)
For patients with chronic hepatitis B in immunotolerant phases or with viral suppression under long-term treatment with nucleos(t)ide analogues, evidence of persistent liver injury and active viral replication after co-infection with SARS-CoV-2 need to be further investigated.
-- Liver injury in COVID-19: management and challenges. The Lancet Gastroenterology & Hepatology. 2020-03-04.
hamster ACE2 | potential interaction between | SARS-CoV-2 (count: 1)
Interaction interface of SARSr-CoV RBD and cat/dog/pangolin/Chinese hamster ACE2 confirmed the potential interaction between SARS-CoV-2 and cat/dog/pangolin/ Chinese hamster ACE2, indicating that these ACE2 could support SARS-CoV-2 entry.
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diagnosis | pathogenesis of | COVID-19 (count: 1)
The review tries to explain the molecular immune pathogenesis and diagnosis of COVID-19 and provide a reference for the prevention and drug development of SARS-CoV-2 infection, based on the recent research progress of SARS-CoV-2 and the knowledge from researches on SARS-CoV and MERS-CoV.
-- Molecular immune pathogenesis and diagnosis of COVID-19. Journal of Pharmaceutical Analysis. 2020-03-05.
diseases | may | may linked to pathogenesis of COVID-19 (count: 1)
cardiovascular diseases, and their susceptibility conditions, may be linked to the pathogenesis of COVID-19.
age | were | two risk factor for SARS-CoV-2 infection (count: 1)
Binary logistic regression analysis showed that gender and age were two risk factor for SARS-CoV-2 infection (Table 4 ).