ArticlePLoS pathogens2022
PIAS1-mediated SUMOylation of influenza A virus PB2 restricts viral replication and virulence.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Ubiquitin-Dependent Regulation of Influenza A Virus Polymerase and vRNP Function: Mechanisms and Therapeutic Opportunities.Microorganisms · 2026Review
- Cellular hnRNP D promotes influenza A virus replication by inhibiting TBK1-IRF3-mediated innate immune response.Journal of virology · 2026Article
- Enolase 1 suppresses influenza A virus replication by blocking the nuclear import of the viral ribonucleoprotein complex.Cellular and molecular life sciences : CMLS · 2026Article
- Opening the black box: insights into ubiquitin-mediated control of innate antiviral immunity and AI-enhanced therapeutics.Frontiers in immunology · 2026Review
- CBX4 facilitates EV71 replication by SUMOylation and stabilizing 3D polymerase.Frontiers in microbiology · 2026Article
- The roles of post-translational modifications in the pathogenesis of RNA viruses: allies or adversaries?Frontiers in microbiology · 2026Review
- SUMOylation-dependent degradation of nucleocapsid is responsible forJournal of virology · 2025Article
- Chicken PIAS2 enhances H6N2 avian influenza virus replication by promoting SUMOylation of viral NP.Veterinary research · 2025Article
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- Endothelial TRIM35-Regulated MMP10 Release Exacerbates Calcification of Vascular Grafts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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- Proteomic Analysis of Differentially Expressed Proteins in A549 Cells Infected with H9N2 Avian Influenza Virus.International journal of molecular sciences · 2025Article
- Pathogen-induced hijacking of host SUMOylation: from molecular mechanisms and prospects for therapeutic modulation.Frontiers in immunology · 2025Review
- Human ANP32A/B are SUMOylated and utilized by avian influenza virus NS2 protein to overcome species-specific restriction.Nature communications · 2024Article
- Host proteins interact with viral elements and affect the life cycle of highly pathogenic avian influenza A virus H7N9.Heliyon · 2024Article
- BAG6 inhibits influenza A virus replication by inducing viral polymerase subunit PB2 degradation and perturbing RdRp complex assembly.PLoS pathogens · 2024Article
- Influenza Virus Host Restriction Factors: The ISGs and Non-ISGs.Pathogens (Basel, Switzerland) · 2024Review
- ABTB1 facilitates the replication of influenza A virus by counteracting TRIM4-mediated degradation of viral NP protein.Emerging microbes & infections · 2023Article
- Article
- Rapid detection of avian influenza virus based on CRISPR-Cas12a.Virology journal · 2023Article
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Authors and funding
17 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Host defense systems employ posttranslational modifications to protect against invading pathogens. Here, we found that protein inhibitor of activated STAT 1 (PIAS1) interacts with the nucleoprotein (NP), polymerase basic protein 1 (PB1), and polymerase basic protein 2 (PB2) of influenza A virus (IAV). Lentiviral-mediated stable overexpression of PIAS1 dramatically suppressed the replication of IAV, whereas siRNA knockdown or CRISPR/Cas9 knockout of PIAS1 expression significantly increased virus growth. The expression of PIAS1 was significantly induced upon IAV infection in both cell culture and mice, and PIAS1 was involved in the overall increase in cellular SUMOylation induced by IAV infection. We found that PIAS1 inhibited the activity of the viral RNP complex, whereas the C351S or W372A mutant of PIAS1, which lacks the SUMO E3 ligase activity, lost the ability to suppress the activity of the viral RNP complex. Notably, the SUMO E3 ligase activity of PIAS1 catalyzed robust SUMOylation of PB2, but had no role in PB1 SUMOylation and a minimal role in NP SUMOylation. Moreover, PIAS1-mediated SUMOylation remarkably reduced the stability of IAV PB2. When tested in vivo, we found that the downregulation of Pias1 expression in mice enhanced the growth and virulence of IAV. Together, our findings define PIAS1 as a restriction factor for the replication and pathogenesis of IAV.
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