ReviewViruses2025
The Dual Role of A20 (TNFAIP3) in Viral Infection: A Context-Dependent Regulator of Immunity and Pathogenesis.
Review in Viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Integrative Transcriptomic Analysis Reveals Distinct and Shared Host Responses in Dengue and Chikungunya Infections.International journal of molecular sciences · 2026Article
- Subtype-Independent Activation of NF-κB Signaling in Breast Cancer.International journal of molecular sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A20 (TNFAIP3) is a ubiquitin-editing enzyme that plays a central role in the regulation of inflammation and cell death, primarily through modulation of NF-κB signaling. In the context of viral infection, A20 exhibits a dual nature: it can both suppress antiviral immune responses to facilitate viral replication and act as a host-protective factor to prevent immunopathology. This review synthesizes current findings on the context-dependent roles of A20, focusing on its capacity to switch between antiviral and proviral functions. We examine how specific determinants-including viral genetic makeup, the infected cell type, and the temporal stage of infection-dictate whether A20 protects the host or facilitates viral persistence. We propose a systematic framework for understanding A20 as a dynamic regulator that orchestrates the balance between pathogen clearance and tissue protection.
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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 Socratic graph.