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

Anjali Singh1, Kush Kumar Pandey1,2, Shubham Kumar Agrawal1

  • 1Department of Biotechnology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India.

Advances in Virology
|April 17, 2023
PubMed

Insights

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection impacts host cell mRNA levels by altering pre-mRNA splicing. This study identifies host proteins interacting with viral RNA, offering insights into COVID-19 pathogenesis.

Area of Science:

  • Molecular Biology
  • Virology
  • Genetics

Background:

  • The ongoing pandemic is caused by SARS-CoV-2, a novel coronavirus responsible for COVID-19.
  • Understanding host-virus interactions is crucial for elucidating COVID-19 pathogenesis.
  • Post-transcriptional gene regulation, including pre-mRNA splicing, plays a key role in viral infections.

Purpose of the Study:

  • To investigate the impact of SARS-CoV-2 infection and viral UTRs on host cell mRNA levels.
  • To identify host proteins that interact with the 5' and 3' untranslated regions (UTRs) of SARS-CoV-2 genomic RNA.
  • To explore the role of UTR-mediated regulation of pre-mRNA splicing in SARS-CoV-2 pathogenesis.

Main Methods:

  • SARS-CoV-2 infection of host cells.
  • Exogenous overexpression of viral 5' and 3' UTRs.
  • Analysis of host cell mRNA levels.
  • In-silico identification of RNA-binding proteins interacting with viral UTRs.

Main Results:

  • SARS-CoV-2 infection or expression of viral UTRs led to reduced host cell mRNA levels.
  • These reductions were potentially mediated by the modulation of host cell pre-mRNA splicing.
  • In-silico analysis predicted interactions between viral 5' and 3' UTRs and numerous host RNA-binding proteins.

Conclusions:

  • Viral UTRs and SARS-CoV-2 infection can influence host cell mRNA levels through splicing.
  • Numerous host RNA-binding proteins are predicted to interact with SARS-CoV-2 UTRs.
  • These findings provide a foundation for further research into UTR-mediated splicing regulation during viral pathogenesis.

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