ArticleThe Journal of experimental medicine2024
A viral E3 ubiquitin ligase produced by herpes simplex virus 1 inhibits the NLRP1 inflammasome.
Article in The Journal of experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- IFN-κ directs antiviral immunity in human skin.bioRxiv : the preprint server for biology · 2026Article
- Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026Review
- Cell-autonomous immunity as an integrated immune network against bacterial and viral pathogens.Nature microbiology · 2026Review
- Duck plague virus US2 promotes p62-mediated autophagic degradation of RIG-I to suppress antiviral signaling.Poultry science · 2026Article
- NLR Inflammasomes in Viral Infections: From Molecular Mechanisms to Therapeutic Interventions.Viruses · 2026Review
- Ubiquitination and autophagy in host-pathogen interactions: from immune surveillance to therapeutic targeting.Nature reviews. Immunology · 2026Review
- Antiviral Inflammasomes and How to Find Them.Viruses · 2026Review
- NINJ1 blocks HSV-1 entry into macrophages to impact viral replication and immunity.EMBO reports · 2026Article
- Mammalian innate antiviral defenses: beyond interferon.Journal of virology · 2025Review
- Ubiquitination Regulates Reorganization of the Membrane System During Cytomegalovirus Infection.Life (Basel, Switzerland) · 2025Article
- Next-generation replication-defective HSV vectors for delivery of large DNA payloads.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- The precise function of alphaherpesvirus tegument proteins and their interactions during the viral life cycle.Frontiers in microbiology · 2024Review
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Authors and funding
5 authors.
Funding
Abstract
Guard proteins initiate defense mechanisms upon sensing pathogen-encoded virulence factors. Successful viral pathogens likely inhibit guard protein activity, but these interactions have been largely undefined. Here, we demonstrate that the human pathogen herpes simplex virus 1 (HSV-1) stimulates and inhibits an antiviral pathway initiated by NLRP1, a guard protein that induces inflammasome formation and pyroptotic cell death when activated. Notably, HSV-1 infection of human keratinocytes promotes posttranslational modifications to NLRP1, consistent with MAPK-dependent NLRP1 activation, but does not result in downstream inflammasome formation. We identify infected cell protein 0 (ICP0) as the critical HSV-1 protein that is necessary and sufficient for inhibition of the NLRP1 pathway. Mechanistically, ICP0's cytoplasmic localization and function as an E3 ubiquitin ligase prevents proteasomal degradation of the auto-inhibitory NT-NLRP1 fragment, thereby preventing inflammasome formation. Further, we demonstrate that inhibiting this inflammasome is important for promoting HSV-1 replication. Thus, we have established a mechanism by which HSV-1 overcomes a guard-mediated antiviral defense strategy in humans.
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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.