ArticlePLoS pathogens2024
African swine fever virus pB318L, a trans-geranylgeranyl-diphosphate synthase, negatively regulates cGAS-STING and IFNAR-JAK-STAT signaling pathways.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 25 citations in OpenAlex.
- African swine fever virus pI73R hijacks host mRNA to suppress interferon beta and reveals a druggable target for antiviral intervention.Emerging microbes & infections · 2026Article
- African swine fever virus pM448R protein promotes STUB1-mediated ubiquitin-proteasome degradation of IRF1 to attenuate type III interferon induction.Journal of virology · 2026Article
- African swine fever virus pE199L, as a mitophagy receptor, suppresses antiviral innate immunity to promote viral replication.Autophagy · 2026Article
- TANK potentiates antiviral innate immunity by recruiting deubiquitinase USP46 to activate IKKε.PLoS pathogens · 2026Article
- A decoy receptor antagonizes interferon mediated antiviral responses in teleost fish.BMC biology · 2026Article
- Review
- Article
- STING-STAT1-ZBP1 axis orchestrates PANoptotic signaling in ischemia-reperfusion induced acute kidney injury.Cell communication and signaling : CCS · 2026Article
- 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
- Host-pathogen interactions in African swine fever: From viral entry to systemic disease progression.Cell insight · 2026Review
- Bridging innate immunity and iron-dependent death: the interplay between cyclic GMP-AMP synthase-stimulator of interferon genes nexus and ferroptosis in cancer and inflammation.Frontiers in cell and developmental biology · 2026Review
- In Silico Prediction of Potential pTLR7/pSTING Dual-Targeting Ligands via Virtual Screening and Molecular Dynamics Simulation.International journal of molecular sciences · 2025Article
- Immunoevasion strategies for African swine fever virus: Modulation of antigen presentation pathways.Virulence · 2025Review
- African swine fever virus pB318L suppresses inflammatory response by inhibiting NF-κB activation and NLRP3 inflammasome formation.PLoS pathogens · 2025Article
- Temporal Dynamics of Cytokine, Leukocyte, and Whole Blood Transcriptome Profiles of Pigs Infected with African Swine Fever Virus.Pathogens (Basel, Switzerland) · 2025Article
- African swine fever virus MGF505-3R facilitates ferroptosis to restrict TBK1-IRF3 pathway.Microbiology spectrum · 2025Article
- African swine fever virus infection enhances CD14-dependent phagocytosis of porcine alveolar macrophages to promote bacterial uptake and apoptotic body-mediated viral transmission.Journal of virology · 2025Article
- Advances in African swine fever virus molecular biology and host interactions contributing to new tools for control.Journal of virology · 2025Review
- The African swine fever virus B125R protein antagonizes JAK-STAT signalling by promoting the degradation of IFNAR2.Veterinary research · 2025Article
- Structure-function insights into the dual role of African swine fever virus pB318L: A typical geranylgeranyl-diphosphate synthase and a nuclear import protein.Virologica Sinica · 2025Article
Corrections and comments
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
African swine fever (ASF) is an acute, hemorrhagic, and severe infectious disease caused by the ASF virus (ASFV). ASFV has evolved multiple strategies to escape host antiviral immune responses. Here, we reported that ASFV pB318L, a trans-geranylgeranyl-diphosphate synthase, reduced the expression of type I interferon (IFN-I) and IFN-stimulated genes (ISGs). Mechanically, pB318L not only interacted with STING to reduce the translocation of STING from the endoplasmic reticulum to the Golgi apparatus but also interacted with IFN receptors to reduce the interaction of IFNAR1/TYK2 and IFNAR2/JAK1. Of note, ASFV with interruption of B318L gene (ASFV-intB318L) infected PAMs produces more IFN-I and ISGs than that in PAMs infected with its parental ASFV HLJ/18 at the late stage of infection. Consistently, the pathogenicity of ASFV-intB318L is attenuated in piglets compared with its parental virus. Taken together, our data reveal that B318L gene may partially affect ASFV pathogenicity by reducing the production of IFN-I and ISGs. This study provides a clue to design antiviral agents or live attenuated vaccines to prevent and control ASF.
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