Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1175175 (SARS)
 19,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Understanding the pathophysiology of SARS-CoV-2 infection is critical for therapeutics and public health intervention strategies. Viral-host interactions can guide discovery of regulators of disease outcomes, and protein structure function analysis points to several immune pathways, including complement and coagulation, as targets of the coronavirus proteome. To determine if conditions associated with dysregulation of the complement or coagulation systems impact adverse clinical outcomes associated with SARS-CoV-2 infection, we performed a retrospective observational study of 11,116 patients suspected of SARS-CoV-2 infection. We found that history of macular degeneration (a proxy for complement activation disorders) and history of coagulation disorders (thrombocytopenia, thrombosis, and hemorrhage) are risk factors for morbidity and mortality in SARS-CoV-2 infected patients - effects that could not be explained by age or sex. In addition, using data from the UK Biobank, we implemented a candidate driven approach to evaluate linkage between severe SARS-CoV-2 disease and genetic variation associated with complement and coagulation pathways. Among our findings, our scan identified previously reported eQTLs for CD55 (a negative regulator of complement activation) and SNPs in Complement Factor H (CFH) and Complement Component 4 Binding Protein Alpha (C4BPA), which play central roles in complement activation and innate immunity and were previously linked to Age Related Macular Degeneration (AMD) in a Genome-Wide Association Study (GWAS). In addition to providing evidence that complement function modulates SARS-CoV-2 infection outcome, the data point to several putative genetic markers of susceptibility. The results highlight the value of using a multi-modal analytical approach, combining molecular information from virus protein structure-function analysis with clinical informatics and genomics to reveal determinants and predictors of immunity, susceptibility, and clinical outcome associated with infection.
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PMID:Identification of Immune complement function as a determinant of adverse SARS-CoV-2 infection outcome. 3274 30

The goal of the present investigation is to identify the differentially expressed genes (DEGs) between SARS-CoV-2 infected and normal control samples to investigate the molecular mechanisms of infection with SARS-CoV-2. The microarray data of the dataset E-MTAB-8871 were retrieved from the ArrayExpress database. Pathway and Gene Ontology (GO) enrichment study, protein-protein interaction (PPI) network, modules, target gene-miRNA regulatory network, and target gene-TF regulatory network have been performed. Subsequently, the key genes were validated using an analysis of the receiver operating characteristic (ROC) curve. In SARS-CoV-2 infection, a total of 324 DEGs (76 up- and 248 down-regulated genes) were identified and enriched in a number of associated SARS-CoV-2 infection pathways and GO terms. Hub and target genes such as TP53, HRAS, MAPK11, RELA, IKZF3, IFNAR2, SKI, TNFRSF13C, JAK1, TRAF6, KLRF2, CD1A were identified from PPI network, target gene-miRNA regulatory network, and target gene-TF regulatory network. Study of the ROC showed that ten genes (CCL5, IFNAR2, JAK2, MX1, STAT1, BID, CD55, CD80, HAL-B, and HLA-DMA) were substantially involved in SARS-CoV-2 patients. The present investigation identified key genes and pathways that deepen our understanding of the molecular mechanisms of SARS-CoV-2 infection, and could be used for SARS-CoV-2 infection as diagnostic and therapeutic biomarkers.
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PMID:Identification of potential mRNA panels for severe acute respiratory syndrome coronavirus 2 (COVID-19) diagnosis and treatment using microarray dataset and bioinformatics methods. 3325 Oct 83