Implications of the virus-encoded miRNA and host miRNA in the pathogenicity of SARS-CoV-2

TL;DR

This study uses computational methods to analyze how virus and host miRNAs influence SARS-CoV-2 pathogenicity, revealing key regulatory processes and potential targets affecting infection severity.

Contribution

It identifies specific virus and host miRNAs involved in SARS-CoV-2 infection and predicts their roles in immune response and viral enhancement mechanisms.

Findings

hsa-miR-4661-3p targets the S gene of SARS-CoV-2

Virus-encoded miRNA MR147-3p may increase TMPRSS2 expression

Infection modulates miRNAs affecting immune response and cytoskeleton

Abstract

The outbreak of COVID-19 caused by SARS-CoV-2 has rapidly spread worldwide and has caused over 1,400,000 infections and 80,000 deaths. There are currently no drugs or vaccines with proven efficacy for its prevention and little knowledge was known about the pathogenicity mechanism of SARS-CoV-2 infection. Previous studies showed both virus and host-derived MicroRNAs (miRNAs) played crucial roles in the pathology of virus infection. In this study, we use computational approaches to scan the SARS-CoV-2 genome for putative miRNAs and predict the virus miRNA targets on virus and human genome as well as the host miRNAs targets on virus genome. Furthermore, we explore miRNAs involved dysregulation caused by the virus infection. Our results implicated that the immune response and cytoskeleton organization are two of the most notable biological processes regulated by the infection-modulated miRNAs. Impressively, we found hsa-miR-4661-3p was predicted to target the S gene of SARS-CoV-2, and a virus-encoded miRNA MR147-3p could enhance the expression of TMPRSS2 with the function of strengthening SARS-CoV-2 infection in the gut. The study may provide important clues for the mechisms of pathogenesis of SARS-CoV-2.