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Selective Polyprotein Processing Determines Norovirus Sensitivity to Trim7.

Meagan E Sullender1, Linley R Pierce2, Mridula Annaswamy Srinivas2

  • 1Division of Infectious Diseases, Department of Medicine, Edison Family Center for Genome Sciences & Systems Biology, Washington University School of Medicine, St. Louis, Missouri, USA.

Journal of Virology
|August 16, 2022
PubMed
Summary
This summary is machine-generated.

Murine norovirus (MNV) evades host restriction by the antiviral protein Trim7 through selective polyprotein processing. This evasion strategy comes at a significant evolutionary cost, attenuating viral replication and pathogenesis.

Keywords:
antiviralnoroviruspolyprotein

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Noroviruses cause widespread gastroenteritis, but host restriction mechanisms remain unclear.
  • Understanding host-pathogen interactions is crucial for combating viral infections.

Purpose of the Study:

  • Identify host genes restricting murine norovirus (MNV) replication using CRISPR activation.
  • Investigate the role of Trim7 in inhibiting MNV infection and viral evasion strategies.

Main Methods:

  • CRISPR activation screen to identify host restriction factors.
  • In vitro evolution to generate and study viral escape mutants.
  • Biochemical assays to analyze protein-protein interactions and polyprotein processing.

Main Results:

  • Trim7 potently inhibits early MNV replication.
  • MNV mutants escaping Trim7 restriction alter NS6-7 polyprotein cleavage.
  • Trim7 binds viral protein NS6, but not the NS6-7 precursor.
  • Altered polyprotein processing for Trim7 evasion significantly attenuates viral fitness.

Conclusions:

  • Selective polyprotein processing is a novel viral immune evasion mechanism.
  • Viral resistance to host restriction factors involves evolutionary trade-offs.
  • Findings offer insights into norovirus-host interactions and viral evolution.