ArticleNucleic acids research2018
miR-122 does not impact recognition of the HCV genome by innate sensors of RNA but rather protects the 5' end from the cellular pyrophosphatases, DOM3Z and DUSP11.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Discovery of 5' NAD capped viral RNAs reveals evolutionary divergent 5' metabolite capping across hepaciviruses.Nature communications · 2026Article
- Evolutionary refinement of the ZIKV 5' UTR dictates a trade-off between RNA stability and promoter accessibility.NAR molecular medicine · 2026Article
- Structural insights into polymerase-catalyzed FAD capping of hepatitis C virus RNA.Nature communications · 2025Article
- Viral piracy of host RNA phosphatase DUSP11 by avipoxviruses.PLoS pathogens · 2025Article
- The immune sensitivity caused by DUSP11, an RNA 5'-end maturation phosphatase, is adjusted by a human non-coding RNA, nc886.Cellular and molecular life sciences : CMLS · 2025Article
- Article
- Article
- Unraveling the dynamics of hepatitis C virus adaptive mutations and their impact on antiviral responses in primary human hepatocytes.Journal of virology · 2024Article
- Binding of microRNA-122 to the hepatitis C virus 5' untranslated region modifies interactions with poly(C) binding protein 2 and the NS5B viral polymerase.Nucleic acids research · 2023Article
- Enhanced Virus Translation Enables miR-122-Independent Hepatitis C Virus Propagation.Journal of virology · 2023Article
- The ribosome quality control factor Asc1 determines the fate of HSP70 mRNA on and off the ribosome.Nucleic acids research · 2023Article
- Article
- Elucidating the distinct contributions of miR-122 in the HCV life cycle reveals insights into virion assembly.Nucleic acids research · 2023Article
- The 11th Canadian Symposium on Hepatitis C Virus: 'Getting back on track towards hepatitis C elimination'.Canadian liver journal · 2023Article
- Transcriptional Inhibition of MicroRNA miR-122 by Small Molecules Reduces Hepatitis C Virus Replication in Liver Cells.Journal of medicinal chemistry · 2022Article
- Mechanistic Insights into the Protection Effect of Argonaute-RNA Complex on the HCV Genome.Biomolecules · 2022Article
- MicroRNA-122 Regulation of HCV Infections: Insights from Studies of miR-122-Independent Replication.Pathogens (Basel, Switzerland) · 2022Review
- Review
- Next RNA Therapeutics: The Mine of Non-Coding.International journal of molecular sciences · 2022Review
- Effectiveness of germicidal ultraviolet light to inactivate coronaviruses on personal protective equipment to reduce nosocomial transmission.Infection control and hospital epidemiology · 2022Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Hepatitis C virus (HCV) recruits two molecules of the liver-specific microRNA-122 (miR-122) to the 5' end of its genome. This interaction promotes viral RNA accumulation, but the precise mechanism(s) remain incompletely understood. Previous studies suggest that miR-122 is able to protect the HCV genome from 5' exonucleases (Xrn1/2), but this protection is not sufficient to account for the effect of miR-122 on HCV RNA accumulation. Thus, we investigated whether miR-122 was also able to protect the viral genome from innate sensors of RNA or cellular pyrophosphatases. We found that miR-122 does not play a protective role against recognition by PKR, RIG-I-like receptors, or IFITs 1 and 5. However, we found that knockdown of both the cellular pyrophosphatases, DOM3Z and DUSP11, was able to rescue viral RNA accumulation of subgenomic replicons in the absence of miR-122. Nevertheless, pyrophosphatase knockdown increased but did not restore viral RNA accumulation of full-length HCV RNA in miR-122 knockout cells, suggesting that miR-122 likely plays an additional role(s) in the HCV life cycle, beyond 5' end protection. Overall, our results support a model in which miR-122 stabilizes the HCV genome by shielding its 5' terminus from cellular pyrophosphatase activity and subsequent turnover by exonucleases (Xrn1/2).
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