ArticleGenome instability & disease2022
Single-stranded RNA viruses activate and hijack host apical DNA damage response kinases for efficient viral replication.
Article in Genome instability & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- USP39 promotes antiviral defense through post-transcriptional control of RIG-I and stabilization of STING.PLoS biology · 2026Article
- Analysis of the Porcine Reproductive and Respiratory Syndrome Virus Nucleocapsid Interactome.Journal of proteome research · 2025Article
- Contribution of critical amino acid residues in the RNA-dependent RNA polymerase to the replication fidelity and viral ribavirin sensitivity of porcine reproductive and respiratory syndrome virus.Veterinary research · 2025Article
- Article
- miR-155 facilitates the synergistic replication between avian leukosis virus subgroup J and reticuloendotheliosis virus by targeting a dual pathway.Journal of virology · 2023Article
- Article
- Pharmacokinetic Study and Metabolite Identification of CAM106 in Rats by Validated UHPLC-MS/MS.Pharmaceuticals (Basel, Switzerland) · 2023Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ataxia-telangiectasia mutated (ATM) and ATM-Rad3-related (ATR) are apical kinases that orchestrate the multifaceted DNA damage response (DDR) to a variety of genotoxic insults and regulate genomic stability. Whether RNA virus also manipulates the host's DDR machine to facilitate replication is largely unknown. In this study, we revealed that single-stranded RNA virus replication specifically elicits host ATM- and ATR-mediated pathway activation and boosts their expression. The activated ATM and ATR are hijacked to the virus replication factory in the cytoplasm and facilitate viral gene expression and replication. Specific inhibitors targeting ATM and ATR strikingly block the viral proliferation and replication and inhibit expression of virus proteins. Our results reveal a novel, or otherwise noncanonical, conserved function of ATM/ATR outside DDR in promoting the replication of single-stranded RNA virus and provide an important mechanism of host-pathogen interactions. Supplementary Information: The online version contains supplementary material available at 10.1007/s42764-022-00064-3.
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