ABSTRACT
The coronavirus disease (COVID-19) caused by SARS-COV-2, a highly infectious pathogen, genetically similar to SARS-COV is an unprecedented worldwide health crisis. Rapidly accumulating clinical research revealed that COVID-19 is manifested by various neurological symptoms and also affects the brain in many ways including direct infection to systemic inflammation. Which indicates it may substantially increase the incidence of developing neurodegenerative diseases (NDGDs). To discourse this issue we studied the computable frameworks to address the gene expression association of COVID-19 and NDGDs to identify the link among them. We analyzed GEO microarray datasets from COVID-19 and NDGDs including Epilepsy, Stroke, Multiple Sclerosis, Alzheimer's disease, and Parkinson's disease. We constructed disease-gene relationship networks and identified dysregulated pathways, ontological pathways, protein-protein interaction (PPI) network, and protein-drug interaction (PDI) network. We observed that COVID-19 associated genes share 19, 26, 20, 19, 22 differentially expressed genes with Epilepsy, Stroke, Multiple Sclerosis, Alzheimer's disease, and Parkinson's disease respectively. Gene expression dysregulation, PPI and PDI relationship networks, different pathways suggest that COVID-19 may have a significant link to the development of these NDGDs. This analysis may help to develop therapeutic strategies and raise awareness about the influence of COVID-19 on the progression of NDGDs. © 2021 IEEE.
ABSTRACT
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is cause of a global pandemic which is demolishing global health and economy. SARS-CoV-2 infected patients are hospitalized with pneumonia where almost 20-30% of patients are led to kidney failure. The entry of SARS-CoV-2 into the systemic circulation leads to acute kidney injury (AKI) which may develop chronic kidney disease (CKD). In addition, patients who are diagnosed with AKI or CKD are at major risk of SARS-CoV-2 infection. Although a significant number of compounds have been proposed and the existing drugs have also been tested for repurposing, no specific therapy has been approved yet. SARS-CoV-2 invades human cells binding to the receptor of angiotensin-converting enzyme 2 (ACE2) via the receptor-binding domain. Cells that express ACE2 are susceptible to SARS-CoV-2 infection and the proportion of ACE2-positive cells in kidney proximal tubule is approximately 4%, indicating that SARS-CoV-2 might damage the kidney tubules leading to fatal kidney injury. Therefore, a better understanding of the potential mechanisms involved in SARS-CoV-2 infection-mediated kidney disease may unveil a novel therapeutic strategy against kidney diseases during COVID-19. © 2020, Bangladesh Society for Microbiology, Immunology and Advanced Biotechnology. All rights reserved.