ArticleViruses2022
I226R Protein of African Swine Fever Virus Is a Suppressor of Innate Antiviral Responses.
Article in Viruses, 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, 50 citations in OpenAlex.
- Evaluation of An I226R and A137R deletion mutant from a genotype I/II recombinant African swine fever virus strain as a live attenuated vaccine in pigs.Veterinary research · 2026Article
- African swine fever virus-encoded protein MGF 505-3R impairs innate immunity via ubiquitin-mediated degradation of MyD88.Communications biology · 2026Article
- Host-pathogen interactions in African swine fever: From viral entry to systemic disease progression.Cell insight · 2026Review
- A chicken lncRNA is identified as a critical regulator that increases influenza virus replication by impairing innate antiviral responses.Veterinary research · 2025Article
- Article
- African swine fever virus A179L inhibits interferon induced transmembrane protein 1 activation of NF-κB pathway.Cell communication and signaling : CCS · 2025Article
- Advances in African swine fever virus molecular biology and host interactions contributing to new tools for control.Journal of virology · 2025Review
- Diversities of African swine fever virus host-virus dynamics revealed by single-cell profiling.Journal of virology · 2025Article
- Long Non-Coding RNA THRIL Promotes Influenza Virus Replication by Inhibiting the Antiviral Innate Immune Response.Viruses · 2025Article
- The regulatory roles of STAT3 protein in the pathogenesis of viral infections.Frontiers in cellular and infection microbiology · 2025Review
- How Does African Swine Fever Virus Evade the cGAS-STING Pathway?Pathogens (Basel, Switzerland) · 2024Review
- Comprehensive Characterization of the Genetic Landscape of African Swine Fever Virus: Insights into Infection Dynamics, Immunomodulation, Virulence and Genes with Unknown Function.Animals : an open access journal from MDPI · 2024Review
- African swine fever virus structural protein p17 inhibits IRF3 activation by recruiting host protein PR65A and inducing apoptotic degradation of STING.Frontiers in microbiology · 2024Article
- When ASFV Infection Meets the cGAS-STING Signaling Pathway.Transboundary and emerging diseases · 2024Review
- KAE ameliorates LPS-mediated acute lung injury by inhibiting PANoptosis through the intracellular DNA-cGAS-STING axis.Frontiers in pharmacology · 2024Article
- Host immune responses against African swine fever virus: Insights and challenges for vaccine development.Open veterinary journal · 2023Review
- The CD2v protein of African swine fever virus inhibits macrophage migration and inflammatory cytokines expression by downregulating EGR1 expression through dampening ERK1/2 activity.Veterinary research · 2023Article
- Review
- African Swine Fever Virus L83L Negatively Regulates the cGAS-STING-Mediated IFN-I Pathway by Recruiting Tollip To Promote STING Autophagic Degradation.Journal of virology · 2023Article
- Deletion of African Swine Fever Virus (ASFV) H240R Gene Attenuates the Virulence of ASFV by Enhancing NLRP3-Mediated Inflammatory Responses.Journal of virology · 2023Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
African swine fever is one of the most devastating swine diseases caused by African swine fever virus (ASFV). Although ASFV encodes more than 160 viral proteins, the implication of a majority of ASFV proteins in regulating host immunity is yet to be explored, and the mechanisms of immune evasion by ASFV proteins are largely unknown. Here, we report that the I226R protein of ASFV significantly suppressed innate immune responses. The ectopic expression of ASFV I226R in 293T cells significantly inhibited the activation of interferon-stimulated response element promoters triggered by Sendai virus (SeV), poly(I:C), or cyclic GMP-AMP synthase (cGAS)/STING. The I226R protein caused a significant decrease in the expression of interferons and interferon-stimulating genes in cells infected with SeV. Similar results were obtained from experiments using I226R-overexpressed PK15 and 3D4/21 cells stimulated with vesicular stomatitis virus. We observed that I226R inhibited the activation of both nuclear factor-kappa B (NF-κB) and interferon regulatory factor 3 (IRF3). Furthermore, it was shown that overexpression of I226R suppressed IRF3 activation and caused the degradation of NF-κB essential modulator (NEMO) protein. The I226R-induced NEMO degradation could be prevented by treatment with MG132, a proteasome inhibitor. Together, these results reveal that the ASFV I226R protein impairs antiviral responses, likely through multiple mechanisms including the suppression of NF-κB and IRF3 activation, to counteract innate immune responses during the viral infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.