ArticlePLoS neglected tropical diseases2025
Crimean-Congo hemorrhagic fever virus NSm protein inhibits the type I interferon signaling by binding to STAT2.
Article in PLoS neglected tropical diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Pathogenicity and virulence of Crimean-Congo hemorrhagic fever virus: From enzootic maintenance to severe human disease.Virulence · 2026Review
- Extracellular Vesicles from Probiotic and BeneficialPharmaceutics · 2026Article
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Authors and funding
5 authors.
Funding
Abstract
The type I interferon (IFN-I) response, which includes IFN-I induction and signaling, plays an important role in a host's defence against viral infections. Many pathogenic viruses target it to evade the host immunity. Crimean-Congo hemorrhagic fever virus (CCHFV), the causative agent of Crimean-Congo hemorrhagic fever, which features high mortality in humans, has been reported in southeastern Europe, Africa, the Middle East, and Asia. Although a previous study reported that CCHFV antagonizes IFN-I signaling in human cell lines, it is unclear how it inhibits IFN-I signaling. Here we demonstrated that the non-structural protein of CCHFV, NSm, suppresses IFN-I signaling in human cell lines. Furthermore, we discovered that NSm binds to STAT2, an important host protein in IFN-I signaling, and induces its degradation within cells. Taken together, our results imply that NSm suppresses IFN-I signaling by targeting human STAT2.
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