Version 1
: Received: 15 July 2020 / Approved: 20 July 2020 / Online: 20 July 2020 (02:50:36 CEST)
How to cite:
Pulai, S.; Basu, M.; Saha, C.; Bhattacharyya, N.P.; Ray Chaudhury, A.; Ghosh, S. Molecular Basis of Kidney Defects in COVID-19 Patients. Preprints2020, 2020070452. https://doi.org/10.20944/preprints202007.0452.v1
Pulai, S.; Basu, M.; Saha, C.; Bhattacharyya, N.P.; Ray Chaudhury, A.; Ghosh, S. Molecular Basis of Kidney Defects in COVID-19 Patients. Preprints 2020, 2020070452. https://doi.org/10.20944/preprints202007.0452.v1
Pulai, S.; Basu, M.; Saha, C.; Bhattacharyya, N.P.; Ray Chaudhury, A.; Ghosh, S. Molecular Basis of Kidney Defects in COVID-19 Patients. Preprints2020, 2020070452. https://doi.org/10.20944/preprints202007.0452.v1
APA Style
Pulai, S., Basu, M., Saha, C., Bhattacharyya, N.P., Ray Chaudhury, A., & Ghosh, S. (2020). <strong>Molecular Basis of Kidney Defects in COVID-19 Patients</strong>. Preprints. https://doi.org/10.20944/preprints202007.0452.v1
Chicago/Turabian Style
Pulai, S., Arpita Ray Chaudhury and Sujoy Ghosh. 2020 "<strong>Molecular Basis of Kidney Defects in COVID-19 Patients</strong>" Preprints. https://doi.org/10.20944/preprints202007.0452.v1
Abstract
Background: Kidney damage is considered to be one of the risk factors for severity and mortality among COVID-19 patients. However, molecular nature of such observations remains unknown. Hypothesis: Altered gene expressions due to infection and in chronic kidney disease could explain severity in COVID-19 with kidney defects. Methods: We collected gene expression data from publicly available resources Gene Expression Omnibus CKD, Enrichr for deregulated genes in SARS-CoV infected cells in vitro, DisGeNET and others and carried out enrichment analysis using Enrichr. Result: Number of common genes altered in chronic kidney disease (CKD) and SARS-CoV infected cells was 2834. Enrichment analysis revealed that biological processes related viral life cycle and growth, cytokines, immunity, interferon, inflammation, apoptosis, autophagy, oxidative stress and others were significantly enriched with common deregulated genes. Similarly, significantly enriched pathways related to viral and bacterial infections, immunity and inflammation, cell cycle, ubiquitin mediated proteolysis, signaling pathways like Relaxin signaling pathway, mTOR signaling pathway, IL-17 signaling pathway, NF-kappa B signaling pathway were enriched with the common deregulated genes. These processes and pathways are known to be related to kidney damage. DisGeNET terms enriched include and related to Dengue fever, chronic Hepatitis, measles, retroviridae infections, respiratory syncytial virus Infections and many others. Kidney dysfunction related terms ischemia of kidney, renal fibrosis and diabetic nephropathy. Conclusion: Common deregulated genes in SARS-CoV infected cells and chronic kidney disease, as well as their enrichment with molecular processes and pathways relevant for viral pathogenesis and renal dysfunctions, could explain the severity of COVID-19 with kidney disease. This observation not only provides molecular relation of severity in COVID-19 with renal dysfunctions but might also help in the management and treatment targets for these cases.
Keywords
COVID-19; kidney disease; comorbidity; enrichment analysis; biological processes and pathways
Subject
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
