ArticleMolecular medicine reports2015
Hepatitis C virus represses the cellular antiviral response by upregulating the expression of signal transducer and activator of transcription 3 through sponging microRNA‑122.
Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The development and controversy of competitive endogenous RNA hypothesis in non-coding genes.Molecular and cellular biochemistry · 2021Review
- RNA regulatory processes in RNA virus biology.Wiley interdisciplinary reviews. RNA · 2019Review
- MicroRNA-122 supports robust innate immunity in hepatocytes by targeting the RTKs/STAT3 signaling pathway.eLife · 2019Article
- STAT3 roles in viral infection: antiviral or proviral?Future virology · 2018Review
- Transcriptomic Characterization of a Chicken Embryo Model Infected With Duck Hepatitis A Virus Type 1.Frontiers in immunology · 2018Article
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Authors and funding
7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) are small, non‑coding RNAs that inhibit the expression of target protein coding genes at the post‑transcriptional level. miR‑122 is a liver specific miRNA. Notably, miR‑122 is used by the hepatitis C virus (HCV) for triggering viral replication by interacting with the 5' untranslated region of the HCV RNA. The present study demonstrated that miR‑122 inhibited the expression of signal transducer and activator of transcription 3 (STAT3), an antivirus response repressor. The HCV RNA acted as an 'miRNA sponge', which upregulated the expression of STAT3 by sealing miR‑122. Subsequently, it was confirmed that this miR‑122 sponge function of HCV RNA repressed the expression of polyinosinic‑polycytidylic acid‑stimulated type I interferons. The present study provided a deeper understanding of the complex role of miR‑122 in the progression of HCV infection and supported the miR‑122 inhibition strategy in anti‑HCV infection treatment.
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