ArticlePLoS pathogens2025
ADAR1 p150 prevents HSV-1 from triggering PKR/eIF2α-mediated translational arrest and is required for efficient viral replication.
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 6 papers.
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The trial behind it
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Who cites it
6 citing papers in PubMed.
- Cell death network regulation in HSV infection: immune evasion versus host defense.Apoptosis : an international journal on programmed cell death · 2026Review
- Functional amyloids as molecular switches: emerging roles in diverse signalling pathways.Biochemical Society transactions · 2026Review
- Evolution of Engineered ADAR-Based RNA Editing Systems.International journal of molecular sciences · 2026Review
- ADAR1: a central regulator of dsRNA sensing in host-virus interactions.Frontiers in immunology · 2026Review
- The Central Role of m6A as Epigenetic Regulator in Metabolic Disorders of Therapeutic Potential and Clinical Implications.Molecular neurobiology · 2025Review
- The role of ADAR1 in human pathophysiology.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Adenosine deaminase acting on dsRNA 1 (ADAR1) catalyzes the deamination of adenosines to inosines in double-stranded RNAs (dsRNA) and regulates innate immunity by preventing the hyperactivation of cytosolic dsRNA sensors such as MDA5, PKR or ZBP1. ADAR1 has been shown to exert pro- and antiviral, editing-dependent and editing-independent functions in viral infections, but little is known about its function in herpesvirus replication. We now demonstrate that herpes simplex virus 1 (HSV-1) hyperactivates PKR in the absence of ADAR1, resulting in eIF2α mediated translational arrest and reduced viral replication. Silencing of PKR or inhibition of its downstream effectors by viral (ICP34.5) or pharmacological (ISRIB) inhibitors rescues viral replication in ADAR1-deficient cells. Upon infection, ADAR1 p150 interacts with PKR and prevents its hyperactivation. Our findings demonstrate that ADAR1 is an important proviral factor that raises the activation threshold for sensors of innate immunity.
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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.