ArticleFrontiers in microbiology2022
African swine fever virus ubiquitin-conjugating enzyme pI215L inhibits IFN-I signaling pathway through STAT2 degradation.
Article in Frontiers in microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 32 citations in OpenAlex.
- Multiple directed mutagenesis reduces enzymatic activity and antibody recognition of the African Swine Fever Virus E2 ubiquitin-conjugating protein (ASFV-pI215L).Emerging microbes & infections · 2026Article
- Autophagy and ubiquitination in important swine viral infections: Host defense and viral antagonism.Virulence · 2026Review
- Comparative genomic analysis of pigs differing in survival following African swine fever virus infection.Veterinary research communications · 2026Article
- Transcriptome analysis of African swine fever virus I9R-mediated modulation of host antiviral immunity.Virus research · 2026Article
- Exploiting Ubiquitination: African Swine Fever Virus-Mediated Recruitment of Host E3 Ligases During Viral Infection and Immune Regulation.Pathogens (Basel, Switzerland) · 2026Review
- Review
- Host-pathogen interactions in African swine fever: From viral entry to systemic disease progression.Cell insight · 2026Review
- Immunoevasion strategies for African swine fever virus: Modulation of antigen presentation pathways.Virulence · 2025Review
- Dynamic Gene Network Alterations and Identification of Key Genes in the Spleen During African Swine Fever Virus (ASFV) Infection.Life (Basel, Switzerland) · 2025Article
- Temporal Dynamics of Cytokine, Leukocyte, and Whole Blood Transcriptome Profiles of Pigs Infected with African Swine Fever Virus.Pathogens (Basel, Switzerland) · 2025Article
- Article
- African swine fever virus MGF505-4R facilitates cGAS degradation through TOLLIP-mediated selective autophagy and inhibits the formation of ISGF3 to evade innate immunity.Veterinary research · 2025Article
- The African swine fever virus p22 inhibits the JAK-STAT signaling pathway by promoting the TAX1BP1-mediated degradation of the type I interferon receptor.PLoS pathogens · 2025Article
- Advances in African swine fever virus molecular biology and host interactions contributing to new tools for control.Journal of virology · 2025Review
- Review
- The African swine fever virus MGF300-4L protein is associated with viral pathogenicity by promoting the autophagic degradation of IKKEmerging microbes & infections · 2024Article
- 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
- Article
- Interactome between ASFV and host immune pathway proteins.mSystems · 2023Article
- Novel Epitope Mapping of African Swine Fever Virus pI215L Protein Using Monoclonal Antibodies.Viruses · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
African swine fever virus (ASFV) is the causative agent of one of the most lethal diseases affecting domestic pig and wild boar, which is endangering the swine industry due to its rapid expansion. ASFV has developed different mechanisms to evade the host immune response, including inhibition of type I IFN (IFN-I) production and signaling, since IFN-I is a key element in the cellular antiviral response. Here, we report a novel mechanism of evasion of the IFN-I signaling pathway carried out by the ASFV ubiquitin-conjugating enzyme pI215L. Our data showed that pI215L inhibited IFN-stimulated response element (ISRE) activity and the consecutive mRNA induction of the IFN-stimulated genes ISG15 and IFIT1 through the ubiquitination and proteasomal degradation of STAT2. Additionally, by immunofluorescence, co-immunoprecipitation and nucleus-cytoplasm fractionation approaches, we have confirmed the interaction and colocalization of STAT2 and pI215L, in ectopic experiments and during ASFV infection. Moreover, expression of the catalytic mutant (I215L-C85A) did not inhibit the induction of ISG15 and IFIT1, nor the activity of ISRE. Furthermore, we confirmed that STAT2 degradation by pI215L is dependent on its catalytic activity, since expression of the pI215L-C85A mutant did not affect STAT2 levels, compared to the wild-type protein. Yet, our data reveal that the interaction of pI215L with STAT2 does not require the integrity of its catalytic domain since the pI215L-C85A mutant co-immunoprecipitates with STAT2. All these findings reveal, for the first time, the involvement of E2-ubiquitin-conjugating enzyme activity of pI215L in the immune response modulation.
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