ArticleThe Journal of biological chemistry2017
Enterovirus 71 suppresses interferon responses by blocking Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling through inducing karyopherin-α1 degradation.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 66 citations in OpenAlex.
- Foot-and-mouth disease virus 3C protease as virulence determinant plays multiple roles in cleaving viral polyprotein and host factors.Virulence · 2026Review
- The JAK/STAT pathway: a pivotal therapeutic target in disease and advances in natural product modulation.Molecular diversity · 2026Review
- Foot-and-mouth disease virus VP4 interferes with host interferon response by targeting the nuclear translocation of interferon regulatory factor 3 (IRF3).Veterinary research · 2026Article
- Human bocavirus NP1 antagonizes host type I interferon response through repressing the nuclear transport of STAT1.Virulence · 2025Article
- Identifying a novel region in the Tembusu virus NS5 protein antagonizing type I interferon signaling.Journal of virology · 2025Article
- Article
- The strategies and mechanisms of enteroviruses to evade innate immunity and the vaccine progress of enteroviruses.Frontiers in cellular and infection microbiology · 2025Review
- The nuclear localization signal of monkeypox virus protein P2 orthologue is critical for inhibition of IRF3-mediated innate immunity.Emerging microbes & infections · 2024Article
- Impaired interferon response in senecavirus A infection and identification of 3CJournal of virology · 2024Article
- Recent Progress in Innate Immune Responses to Enterovirus A71 and Viral Evasion Strategies.International journal of molecular sciences · 2024Review
- Review
- Review
- Current status of hand-foot-and-mouth disease.Journal of biomedical science · 2023Review
- DHAV 3CD targets IRF7 and RIG-I proteins to block the type I interferon upstream signaling pathway.Veterinary research · 2023Article
- Phosphorylation of enteroviral 2AJournal of medical virology · 2023Article
- Review
- Potential therapeutic effects of Ivermectin in COVID-19.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Porcine Epidemic Diarrhea Virus nsp7 Inhibits Interferon-Induced JAK-STAT Signaling through Sequestering the Interaction between KPNA1 and STAT1.Journal of virology · 2022Article
- Intrinsic features of Zika Virus non-structural proteins NS2A and NS4A in the regulation of viral replication.PLoS neglected tropical diseases · 2022Article
- Repositioning Ivermectin for Covid-19 treatment: Molecular mechanisms of action against SARS-CoV-2 replication.Biochimica et biophysica acta. Molecular basis of disease · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus 71 (EV71) has emerged as one of the most important enteroviruses since the eradication of poliovirus, and it causes severe neurological symptoms for which no effective antiviral drugs are available. Type I interferons (IFN) α/β have been used clinically as antiviral therapy as the first line of defense against virus infections successfully for decades. However, treatment with type I interferons has not been effective in patients with EV71 infection. In this study, we found that in cells pretreated with IFN-β, EV71 infection could still lead to a cytopathic effect, and the viral replication was not affected. The mechanism by which EV71 antagonizes interferon signaling, however, has been controversial. Our study indicated that EV71 infection did not inhibit phosphorylation of STAT1/2 induced by IFN-β stimulation, but p-STAT1/2 transport into the nucleus was significantly blocked. We showed that EV71 infection reduced the formation of STAT/karyopherin-α1 (KPNA1) complex upon interferon stimulation and that the virus down-regulated the expression of KPNA1, a nuclear localization signal receptor for p-STAT1. Using specific caspase inhibitors and siRNA for caspase-3, we demonstrated that EV71 infection induced degradation of cellular KPNA1 in a caspase-3-dependent manner, which led to decreased induction of interferon-inducible genes and IFN response. Viral 2A and 3C proteases did not degrade KPNA1, inhibit the activity of ISRE or suppress the transcription of interferon-inducible genes induced by IFN-β. Our study demonstrates a novel mechanism by which antiviral signaling is suppressed through degradation of KPNA1 by activated caspase-3 induced in an enteroviral infection.
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