ArticleEmerging microbes & infections2025
Mpox virus poxin-schlafen fusion protein suppresses innate antiviral response by sequestering STAT2.
Article in Emerging microbes & infections, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Convergent evolution of viral nucleases targeting cyclic dinucleotides.PLoS pathogens · 2026Review
- Molecular mechanism of 2',3'-cGAMP degradation by monkeypox virus poxin-schlafen protein.The Journal of biological chemistry · 2026Article
- Review
- Recent advances in Mpox across innate immunity, evasion, and clinical outcomes.Communications biology · 2026Review
- Monkeypox virus protein OPG188 antagonizes cGAS-STING antiviral signaling pathway to mediate immune evasion.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- SAMHD1 depletion restricts SARS-CoV-2 infection by suppressing HNF1-dependent ACE2 expression in lung epithelial cells.PLoS pathogens · 2026Article
- Article
- Foot-and-mouth disease virus 3D polymerase antagonizes the interferon signaling pathway by blocking STAT2 nuclear translocation.Virus research · 2026Article
- The Impact of Monkeypox Virus Infection on Pregnancy Outcome: Clinical Features and Potential Pathogenic Mechanisms.Journal of immunology research · 2026Review
- SAMHD1 promotes SARS-CoV-2 infection by enhancing HNF1-dependent ACE2 expression in lung epithelial cells.bioRxiv : the preprint server for biology · 2025Article
- Review
- The evolving mpox threat (2022-2024): clade dynamics, immune evasion, and escalating global health challenges.Frontiers in cellular and infection microbiology · 2025Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mpox virus (MPXV) has to establish efficient interferon (IFN) antagonism for effective replication. MPXV-encoded IFN antagonists have not been fully elucidated. In this study, the IFN antagonism of poxin-schlafen (PoxS) fusion gene of MPXV was characterized. MPXV PoxS was capable of decreasing cGAS-produced 2'3'-cGAMP, like its ortholog poxin of vaccinia virus, which is the first known cytosolic nuclease that hydrolyses the 3'-5' bond of 2'3'-cyclic GMP-AMP (cGAMP). However, MPXV PoxS did not suppress cGAS-STING-mediated type I IFN production. Instead, MPXV PoxS antagonized basal and type I IFN-induced expression of IFN-stimulated genes such as OAS1, SAMD9, SAMD9L, ISG15, ISG56 and IFIT3. Consistently, MPXV PoxS inhibited both basal and type I IFN-stimulated activity of interferon-stimulated response elements, but did not affect activation of IFN-γ-activated sites. Mechanistically, MPXV PoxS interacted with STAT2 and sequestered it in the cytoplasm. Both the viral schlafen fusion and the active site of 2'3'-cGAMP nuclease were required for STAT2 sequestration and consequent suppression of IFN-stimulated gene expression. MPXV PoxS conferred resistance to the suppression of MPXV replication by type I IFN. Taken together, our findings suggested that MPXV PoxS counteracts host antiviral response by sequestering STAT2 to circumvent basal and type I IFN-induced expression of antiviral genes.
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