ReviewFrontiers in cellular and infection microbiology2025
Human endogenous retroviruses in schizophrenia: clinical evidence, molecular mechanisms, and implications.
Review in Frontiers in cellular and infection microbiology, 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.
- Toward a Unified Neuroimmune Framework for Infection-Associated Psychiatric Disorders.Diseases (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human endogenous retroviruses (HERVs), comprising 8% of the human genome, are implicated in schizophrenia, a complex psychiatric disorder driven by genetic, epigenetic, and environmental factors. This review examines the role of HERVs in schizophrenia pathogenesis. We synthesized clinical evidence, molecular mechanisms, and gene-environment interactions from studies on HERVs expression in schizophrenia, focusing on HERV-W and HERV-K in peripheral blood, cerebrospinal fluid, and brain tissues. Elevated HERV-W and HERV-K env and gag transcripts are consistently observed in individuals with schizophrenia, indicating potential diagnostic biomarkers. HERVs contribute to neuroinflammation, neurotoxicity, and epigenetic dysregulation of risk genes. The HERV-W env activates the Toll-like receptor 4 (TLR4)/MyD88 pathway, disrupting glutamatergic and dopaminergic signaling, leading to synaptic dysfunction and neuronal apoptosis. Environmental triggers, such as viral infections and early-life stress, activate HERVs, linking genetic and environmental risks. Variability in HERV expression across disease stages highlights the need for standardized assays and longitudinal studies. Emerging technologies and preclinical models targeting HERV-W env offer promise for developing novel diagnostics and therapies. HERVs serve as pivotal mediators of schizophrenia's etiology, advancing precision psychiatry through biomarker and therapeutic innovation.
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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.