ArticlePLoS pathogens2022
African swine fever virus I267L acts as an important virulence factor by inhibiting RNA polymerase III-RIG-I-mediated innate immunity.
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 65 papers.
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Who cites it
65 citing papers in PubMed, 81 citations in OpenAlex.
- Review
- Involvement of the African swine fever virus protein pH108R in virion morphogenesis.Emerging microbes & infections · 2026Article
- 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
- 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
- African swine fever virus pE199L, as a mitophagy receptor, suppresses antiviral innate immunity to promote viral replication.Autophagy · 2026Article
- African swine fever virus pC147L inhibits retinoic acid-inducible gene I-like receptors pathway via targeting MAVS-TRAF6 complex.Veterinary research · 2026Article
- Article
- 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
- The B169L protein of African swine fever virus functions as a viroporin that activates the calcium-mediated inflammasome.PLoS pathogens · 2025Article
- Genetic variations of African swine fever virus MGF 505-9R/10R and I73R/I329L intergenic regions: their role in differentiation between recombinant variant and genotype I and II isolates.Archives of virology · 2025Article
- Article
- Advances in African swine fever virus molecular biology and host interactions contributing to new tools for control.Journal of virology · 2025Review
- Deletion of the African Swine Fever Virus GenViruses · 2025Article
- Article
- ASFV pS183L protein negatively regulates RLR-mediated antiviral signalling by blocking MDA5 oligomerisation.Veterinary research · 2025Article
- Diversities of African swine fever virus host-virus dynamics revealed by single-cell profiling.Journal of virology · 2025Article
- Review
- African swine fever: A highly fatal disease that is spreading globally.Open veterinary journal · 2025Review
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ASFV is a large DNA virus that is highly pathogenic in domestic pigs. How this virus is sensed by the innate immune system as well as why it is so virulent remains enigmatic. In this study, we show that the ASFV genome contains AT-rich regions that are recognized by the DNA-directed RNA polymerase III (Pol-III), leading to viral RNA sensor RIG-I-mediated innate immune responses. We further show that ASFV protein I267L inhibits RNA Pol-III-RIG-I-mediated innate antiviral responses. I267L interacts with the E3 ubiquitin ligase Riplet, disrupts Riplet-RIG-I interaction and impairs Riplet-mediated K63-polyubiquitination and activation of RIG-I. I267L-deficient ASFV induces higher levels of interferon-β, and displays compromised replication both in primary macrophages and pigs compared with wild-type ASFV. Furthermore, I267L-deficiency attenuates the virulence and pathogenesis of ASFV in pigs. These findings suggest that ASFV I267L is an important virulence factor by impairing innate immune responses mediated by the RNA Pol-III-RIG-I axis.
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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.