ArticleViruses2020
2', 5'-Oligoadenylate Synthetase 2 (OAS2) Inhibits Zika Virus Replication through Activation of Type Ι IFN Signaling Pathway.
Article in Viruses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 45 citations in OpenAlex.
- Article
- Multi-omic identification of key transcriptional regulatory programs during endurance exercise training in rats.Nature communications · 2026Article
- Zika virus and host innate immunity: mechanisms of activation and evasion.Frontiers in immunology · 2026Review
- Hypomethylation of the HumanArchives of Iranian medicine · 2026Article
- Robust antiviral innate immune response and miRNA regulatory network were identified in ZIKV-infected cells: implications in the pathogenesis of ZIKV infection.Virus genes · 2025Article
- The differential impact of HNRNPA1 isoforms on gene expression and their relevance to dsRNA-mediated innate immune response.Scientific reports · 2025Article
- Restriction of Zika Virus Replication in Human Monocyte-Derived Macrophages by Pro-Inflammatory (M1) Polarization.International journal of molecular sciences · 2025Article
- Article
- Identification immune-related hub genes in diagnosing atherosclerosis with ischemic stroke through comprehensive bioinformatics analysis and machine learning.Frontiers in neurology · 2025Article
- The placental battlefield: viral strategies and immune countermeasures.Frontiers in immunology · 2025Review
- Interleukin-27-polarized HIV-resistant M2 macrophages are a novel subtype of macrophages that express distinct antiviral gene profiles in individual cells: implication for the antiviral effect via different mechanisms in the individual cell-dependent manner.Frontiers in immunology · 2025Article
- The role of 2'-5'-oligoadenylate synthase-like protein (OASL1) in biliary and hepatotoxin-induced liver injury in mice.Scientific reports · 2024Article
- Expression of PVRL4, a molecular target for cancer treatment, is transcriptionally regulated by FOS.Oncology reports · 2024Article
- Differences in gene regulation by TLR3 and IPS-1 signaling in murine corneal epithelial cells.Scientific reports · 2023Article
- The pseudogene DUXAP10 contributes to gefitinib resistance in NSCLC by repressing OAS2 expression.Acta biochimica et biophysica Sinica · 2023Article
- Targeting Type I Interferon Induction and Signaling: How Zika Virus Escapes from Host Innate Immunity.International journal of biological sciences · 2023Review
- Values of OAS gene family in the expression signature, immune cell infiltration and prognosis of human bladder cancer.BMC cancer · 2022Article
- Betacoronavirus-specific alternate splicing.Genomics · 2022Article
- Advances in understanding of the innate immune response to human norovirus infection using organoid models.The Journal of general virology · 2022Review
- MiR-103a-3p Promotes Zika Virus Replication by Targeting OTU Deubiquitinase 4 to Activate p38 Mitogen-Activated Protein Kinase Signaling Pathway.Frontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background2', 5'-oligoadenylate synthetase 2 (OAS2) has been known as an antiviral interferon-stimulated gene (ISG). However, the role of OAS2 on Zika virus (ZIKV) replication is still unknown. In this study, we sought to explore the effect of OAS2 on ZIKV replication and its underlying mechanism.
methodsWe performed RNA-Seq in A549 cells with or without ZIKV infection. OAS2 or RIG-I was overexpressed by plasmid transfection or knocked down by siRNA in A549 cells. Expression levels of mRNA and protein of selected genes were detected by RT-qPCR and Western Blot, respectively. Interferon stimulated response element (ISRE) activity was examined by dual luciferase assay.
resultsWe found that ZIKV infection induced OAS2 expression through a RIG-I-dependent pathway. OAS2 overexpression inhibited ZIKV replication, while OAS2 knockdown increased ZIKV replication. We observed that OAS2 inhibited ZIKV replication through enhanced IFNβ expression, leading to the activation of the Jak/STAT signaling pathway.
conclusionZIKV infection induced OAS2 expression, which in turn exerted its anti-ZIKV activities through the IFN-activated Jak/STAT signaling pathway.
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