ArticleViruses2021
The A179L Gene of African Swine Fever Virus Suppresses Virus-Induced Apoptosis but Enhances Necroptosis.
Article in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 23 citations in OpenAlex.
- HSV-1 metabolic hijacking: Mechanisms to precision therapeutics.Virulence · 2026Review
- Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026Review
- Exploiting Ubiquitination: African Swine Fever Virus-Mediated Recruitment of Host E3 Ligases During Viral Infection and Immune Regulation.Pathogens (Basel, Switzerland) · 2026Review
- Host-pathogen interactions in African swine fever: From viral entry to systemic disease progression.Cell insight · 2026Review
- Identification of Regulators for Antigen-Specific CD8Veterinary sciences · 2025Article
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- Identification of T-Cell Epitopes and Vaccine Development for African Swine Fever Virus.Vaccines · 2025Review
- Review
- African Swine Fever Virus Immunosuppression and Virulence-Related Gene.Current issues in molecular biology · 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
- Nonstructural Protein A238L of the African Swine Fever Virus (ASFV) Enhances Antiviral Immune Responses by Activating the TBK1-IRF3 Pathway.Veterinary sciences · 2024Article
- Review
- Molecular and functional characterization of porcine poly C binding protein 1 (PCBP1).BMC veterinary research · 2024Article
- Immune cell early activation, apoptotic kinetic, and T-cell functional impairment in domestic pigs after ASFV CADC_HN09 strain infection.Frontiers in microbiology · 2024Article
- ASFV infection induces macrophage necroptosis and releases proinflammatory cytokine by ZBP1-RIPK3-MLKL necrosome activation.Frontiers in microbiology · 2024Article
- Host immune responses against African swine fever virus: Insights and challenges for vaccine development.Open veterinary journal · 2023Review
- Riding apoptotic bodies for cell-cell transmission by African swine fever virus.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Functional Landscape of African Swine Fever Virus-Host and Virus-Virus Protein Interactions.Viruses · 2023Review
- Review
- African Swine Fever Virus Host-Pathogen Interactions.Sub-cellular biochemistry · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A179L, a non-structural protein of African swine fever virus (ASFV), is capable of suppressing apoptosis by binding the BH3 domain of the pro-apoptotic Bcl-2 family proteins via a conserved ligand binding groove. Our present study aims to determine if A179L affects necroptosis, the second form of programmed cell death induced by DNA and RNA viruses. Here we report that A179L enhanced TNF-α or TSZ (TNF-α, Smac, and Z-Vad)-induced receptor-interacting protein kinase (RIPK1), RIPK3, and mixed lineage kinase domain like peudokinase (MLKL) phosphorylation in L929 cells, a murine fibrosarcoma cell line. Sytox green staining revealed that A179L significantly increased the number of necroptotic cells in TSZ-treated L929 cells. Using human herpes simplex virus 1 (HSV-1) to model DNA virus-induced cell death, we found that A179L blocked the HSV-1-induced cleavage of poly (ADP-ribose) polymerase (PARP), caspase 8, and caspase 3 and decreased the number of apoptotic cells in HSV-1-infected IPEC-DQ cells, a porcine intestinal epithelial cell line. In contrast, A179L transfection of IPEC-DQ cells enhanced HSV-1-induced RIPK1, RIPK3, and MLKL phosphorylation and increased the number of necroptotic cells. Consistently, A179L also suppressed apoptosis but enhanced the necroptosis induced by two RNA viruses, Sendai virus (SeV) and influenza virus (IAV). Our study uncovers a previously unrecognized role of A179L in regulating cell death and suggests that A179L re-directs its anti-apoptotic activity to necroptosis.
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