ArticleVirologica Sinica2022
IFN-β1b induces OAS3 to inhibit EV71 via IFN-β1b/JAK/STAT1 pathway.
Article in Virologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- RNF31 restricts EV-A71 replication through innate immune activation and VP4 degradation, and is antagonized by viral 3C proteases.PLoS pathogens · 2026Article
- DTX3L promotes ovarian cancer progression and cisplatin resistance by activating JAK1/STAT1/OAS3 pathway.Scientific reports · 2026Article
- Dysfunction of the plasmacytoid dendritic cells in enterovirus 71-induced HFMD affecting children.BMC immunology · 2026Article
- Integrated multi-omics analysis reveals shared IFN-γ-associated monocyte signatures in primary Sjögren's syndrome and Alzheimer's disease.Frontiers in immunology · 2026Article
- Antiviral Activity of Marine BacteriumInternational journal of molecular sciences · 2025Article
- A CRISPR-Cas9 knockout screening identifies IRF2 as a key driver of OAS3/RNase L-mediated RNA decay during viral infection.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- Research progress on pathogenic and therapeutic mechanisms of Enterovirus A71.Archives of virology · 2023Review
- Adaptive Evolution of the OAS Gene Family Provides New Insights into the Antiviral Ability of Laurasiatherian Mammals.Animals : an open access journal from MDPI · 2023Article
- Pterostilbene, an active constituent of blueberries, enhances innate immune activation and restricts enterovirus D68 infection.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus 71 (EV71) caused hand, foot and mouth disease (HFMD) is a serious threat to the health of young children. Although type I interferon (IFN-I) has been proven to control EV71 replication, the key downstream IFN-stimulated gene (ISG) remains to be clarified and investigated. Recently, we found that 2'-5'-oligoadenylate synthetases 3 (OAS3), as one of ISG of IFN-β1b, was antagonized by EV71 3C protein. Here, we confirm that OAS3 is the major determinant of IFN-β1b-mediated EV71 inhibition, which depends on the downstream constitutive RNase L activation. 2'-5'-oligoadenylate (2-5A) synthesis activity deficient mutations of OAS3 D816A, D818A, D888A, and K950A lost resistance to EV71 because they could not activate downstream RNase L. Further investigation proved that EV71 infection induced OAS3 but not RNase L expression by IFN pathway. Mechanically, EV71 or IFN-β1b-induced phosphorylation of STAT1, but not STAT3, initiated the transcription of OAS3 by directly binding to the OAS3 promoter. Our works elucidate the immune regulatory mechanism of the host OAS3/RNase L system against EV71 replication.
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