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SARS-CoV-2 hijacks host cell genome instability pathways

Joshua Victor1, Tristan Jordan2, Erica Lamkin1

  • 1University of Vermont.

Research Square
|April 20, 2022
PubMed

Insights

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection causes genome instability and genetic alterations in host cells. A novel inhibitor, JH-RE-06, suppresses viral proliferation and DNA damage, offering therapeutic potential.

Area of Science:

  • Molecular Biology
  • Genetics
  • Virology

Background:

  • The molecular mechanisms underlying COVID-19's adverse health outcomes, including long-COVID, remain unclear.
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection's impact on host cell genome integrity is poorly understood.

Approach:

  • Investigated SARS-CoV-2's effect on host cell DNA repair and translesion synthesis pathways.
  • Analyzed genetic alterations such as mutagenesis, telomere dysregulation, and microsatellite instability (MSI) in infected cells.
  • Examined the impact of a REV1 inhibitor (JH-RE-06) on viral proliferation and genome instability.

Key Points:

  • SARS-CoV-2 infection induces host cell genome instability by altering DNA repair and translesion synthesis.
  • Infection leads to increased mutagenesis, telomere dysregulation, and MSI, linked to reduced DNA repair proteins (MLH1, MSH6, MSH2).
  • JH-RE-06, a translesion DNA synthesis inhibitor, suppressed SARS-CoV-2 proliferation and genome instability, potentially via autophagy induction.

Conclusions:

  • SARS-CoV-2 infection compromises host cell genome stability, contributing to COVID-19's pathology.
  • Targeting translesion DNA synthesis with inhibitors like JH-RE-06 may offer a therapeutic strategy against SARS-CoV-2 and its associated genomic consequences.
Keywords:
REV1SARS-CoV-2autophagymicrosatellite-instabilitymutagenesistelomeres

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