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Single-stranded RNA viruses activate and hijack host apical DNA damage response kinases for efficient viral

Pengcheng Li1,2, Chenchen Xu1, Xiaoyan Zhang2

  • 1The First Affiliated Hospital of USTC, MOE Key Laboratory for Membraneless Organelles and Cellular Dynamics, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001 Anhui China.

Genome Instability & Disease
|March 7, 2022
PubMed

Insights

Single-stranded RNA viruses hijack host DNA damage response kinases, ataxia-telangiectasia mutated (ATM) and ATM-Rad3-related (ATR), to boost viral replication. Inhibiting ATM/ATR blocks virus proliferation, revealing a new role for these kinases.

Area of Science:

  • Virology
  • Molecular Biology
  • Cellular Biology

Background:

  • The DNA damage response (DDR) network, involving kinases like ATM and ATR, is crucial for maintaining genomic stability.
  • The role of the host DDR machinery in RNA virus replication remains largely unexplored.

Purpose of the Study:

  • To investigate whether single-stranded RNA viruses manipulate the host DDR pathway to facilitate their replication.
  • To elucidate the specific roles of ATM and ATR kinases in the context of viral infection.

Main Methods:

  • Analysis of host ATM and ATR pathway activation during single-stranded RNA virus infection.
  • Localization studies of activated ATM and ATR in virus replication factories.
  • Assessment of viral proliferation and protein expression in the presence of ATM and ATR inhibitors.

Main Results:

  • Single-stranded RNA virus replication specifically activates and upregulates host ATM and ATR kinases.
  • Activated ATM and ATR are recruited to cytoplasmic viral replication sites, promoting viral gene expression and replication.
  • Pharmacological inhibition of ATM and ATR significantly impairs viral proliferation and protein synthesis.

Conclusions:

  • Host ATM and ATR kinases play a conserved, noncanonical role in promoting single-stranded RNA virus replication outside of their canonical DNA damage response functions.
  • This interaction represents a novel mechanism in host-pathogen interactions, offering potential therapeutic targets.
Keywords:
ATMATRDNA damage responseRNA virus replication

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