ArticlemBio2025
Human-specific activation of the DUX4-SLC34A2 axis by herpesviruses suppresses antiviral innate immunity.
Article in mBio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- SUMOylation and ubiquitination reciprocally regulate SMCHD1 antiviral activity against herpes simplex virus 1.PLoS pathogens · 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral pathogens employ diverse strategies to antagonize host antiviral innate immune defenses. However, the human-specific nature of viral immune evasion mechanisms remains poorly understood. Here, we report that herpesvirus infection selectively activates the embryonic transcription factor DUX4 in human but not murine cells. DUX4 drives the expression of the phosphate transporter SLC34A2, which plays a critical role in suppressing antiviral innate immunity. Mechanistically, SLC34A2 increases intracellular phosphate levels, thereby suppressing the activity of multiple immune and stress-related kinases, including TBK1. Genetic disruption of DUX4 or SLC34A2 restores innate immune activation and enhances interferon responses. Our findings reveal a previously unrecognized, phosphate-mediated immunosuppressive mechanism and define a human-specific transcriptional circuit exploited by herpesviruses to antagonize innate immunity.IMPORTANCEHerpesviruses are notorious for their ability to evade host immune responses, yet the mechanisms underlying human-specific immune evasion remain poorly understood. This study identifies a previously unrecognized viral immune evasion strategy by which herpesviruses suppress antiviral immunity in human cells but not murine cells. We demonstrate that herpesvirus infection induces the expression of the embryonic transcription factor DUX4, which subsequently activates its downstream target, SLC34A2, a phosphate transporter. DUX4-SLC34A2 activation reprograms infected cells toward an embryonic-like transcriptional profile, creating an environment conducive to viral replication. Importantly, we show that SLC34A2 increases intracellular phosphate levels, thereby suppressing the activity of multiple immune and stress-related kinases, including TBK1. Our findings reveal a previously unrecognized phosphate-mediated regulation of antiviral immunity, providing insights into viral-host interactions and highlighting therapeutic targets for enhancing antiviral defense.
Indexed as
Identifiers
What Socratic holds
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.