The SARS-CoV-2 UTR's Intrudes Host RBP's and Modulates Cellular Splicing

SARS-CoV-2 is a novel coronavirus that causes a potentially fatal respiratory disease known as coronavirus disease (COVID-19) and is responsible for the ongoing pandemic with increasing mortality. Understanding the host-virus interaction involved in SARS-CoV-2 pathophysiology will enhance our understanding of the mechanistic basis of COVID-19 infection. The characterization of post-transcriptional gene regulatory networks, particularly pre-mRNA splicing, and the identification and characterization of host proteins interacting with the 5 ' and 3 ' UTRs of SARS-CoV-2 will improve our understanding of post-transcriptional gene regulation during SARS-CoV-2 pathogenesis. Here, we demonstrate that either SARS-CoV-2 infection or exogenous overexpression of the 5 ' and 3'UTRs of the viral genomic RNAs, results in reduced mRNA levels possibly due to modulation of host cell pre-mRNA splicing. Further, we have investigated the potential RNA-binding proteins interacting with the 5 ' and 3 ' UTRs, using in-silico approaches. Our results suggest that 5 ' and 3 ' UTRs indeed interact with many RNA-binding proteins. Our results provide a primer for further investigations into the UTR-mediated regulation of splicing and related molecular mechanisms in host cells.

Automated summary

SARS-CoV-2 is a novel coronavirus responsible for the ongoing pandemic, causing COVID-19. Understanding the interaction between the virus and its host will advance our knowledge of COVID-19 infection mechanism. Research suggests that SARS-CoV-2 infection or overexpression of the viral genomic RNA's UTRs leads to reduced mRNA levels, potentially affecting host cell pre-mRNA splicing. Additionally, computational analysis indicates that the 5' and 3' UTRs interact with numerous RNA-binding proteins. These findings lay the groundwork for further investigation into UTR-mediated regulation of splicing and related molecular mechanisms in host cells.