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

Authors

Anjali Singh, University of Nebraska-Lincoln
Kush Kumar Pandey, University of Nebraska-Lincoln, NCR Biotech Science ClusterFollow
Shubham Kumar Agrawal, University of Nebraska-Lincoln
Rupesh K. Srivastava, University of Nebraska-Lincoln
Sankar Bhattacharyya, NCR Biotech Science Cluster
Bhupendra Verma, University of Nebraska-Lincoln

Document Type

Article

Date of this Version

4-5-2023

Citation

Hindawi Advances in Virology Volume 2023, Article ID 2995443, 11 pages https://doi.org/10.1155/2023/2995443

Comments

Open access.

Abstract

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 posttranscriptional 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.