ArticlePLoS pathogens2025
The African swine fever virus p22 inhibits the JAK-STAT signaling pathway by promoting the TAX1BP1-mediated degradation of the type I interferon receptor.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Deletion of the D345L gene attenuates ASFV and induces protection against homologous and heterologous challenge by enhancing host innate immunity.Emerging microbes & infections · 2026Article
- Development and Evaluation of Three Indirect ELISA Methods Based on Novel Recombinant ASFV Antigens for Serological Detection of African Swine Fever.Pathogens (Basel, Switzerland) · 2026Article
- Transcriptome analysis of African swine fever virus I9R-mediated modulation of host antiviral immunity.Virus research · 2026Article
- Review
- Host-pathogen interactions in African swine fever: From viral entry to systemic disease progression.Cell insight · 2026Review
- African swine fever virus pEP364R acts as an important inflammatory-inducing factor to activate NLRP3 inflammasome-mediated pyroptosis by regulating DDX3X.PLoS pathogens · 2026Article
- Lumpy skin disease virus protein LSDV122 impairs IFN-I receptor complex formation to evade host innate immunity.PLoS pathogens · 2026Article
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Authors and funding
15 authors.
Funding
Abstract
African swine fever virus (ASFV) is the causative agent of African swine fever (ASF), a devastating disease epidemic in Asia and Europe. Large knowledge gaps regarding the biological characteristics of viral structural proteins have severely hindered the development of vaccines against ASF. The p22 protein, an internal envelope membrane protein of ASFV, is one such protein that is yet to be deciphered despite its significance. Here, our results indicated that p22 is not essential for the morphogenesis and replication of ASFV in porcine alveolar macrophages. The ASFV p22 negatively regulates the IFN-β-triggered activation of the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway. Mechanistically, the ASFV p22 promotes the association of the Tax1-binding protein 1 (TAX1BP1) with the type I IFN receptor 1 (IFNAR1) via its transmembrane region, thereby facilitating the autophagic degradation of IFNAR1 and impairing the host antiviral responses at the initial step of JAK-STAT signaling pathway. These findings clarify the biological functions of p22 in ASFV replication and uncover a novel autophagy degradation mechanism for IFNAR1, which provide a novel theoretical basis for understanding the biological characteristics of ASFV and may contribute to the development of vaccines and antiviral therapies against ASF.
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