tetano
Editor, Senior Moderator
Adv Virol
. 2023 Apr 5;2023:2995443.
doi: 10.1155/2023/2995443. eCollection 2023.
The SARS-CoV-2 UTR's Intrudes Host RBP's and Modulates Cellular Splicing
Anjali Singh[SUP] 1 [/SUP], Kush Kumar Pandey[SUP] 1 2 [/SUP], Shubham Kumar Agrawal[SUP] 1 [/SUP], Rupesh K Srivastava[SUP] 1 [/SUP], Sankar Bhattacharyya[SUP] 3 [/SUP], Bhupendra Verma[SUP] 1 [/SUP]
Affiliations
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 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.
. 2023 Apr 5;2023:2995443.
doi: 10.1155/2023/2995443. eCollection 2023.
The SARS-CoV-2 UTR's Intrudes Host RBP's and Modulates Cellular Splicing
Anjali Singh[SUP] 1 [/SUP], Kush Kumar Pandey[SUP] 1 2 [/SUP], Shubham Kumar Agrawal[SUP] 1 [/SUP], Rupesh K Srivastava[SUP] 1 [/SUP], Sankar Bhattacharyya[SUP] 3 [/SUP], Bhupendra Verma[SUP] 1 [/SUP]
Affiliations
- PMID: 37065904
- PMCID: PMC10098413
- DOI: 10.1155/2023/2995443
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 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.