ReviewViruses2026
RETRACTED: Endogenous Retroviruses as Regulators of Innate Immune Signaling and Inflammation
Review in Viruses, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. 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.
Corrections and comments
- Retracted
Authors and funding
6 authors.
Funding
Abstract
Endogenous retroviruses (ERVs) are remnants of ancient retroviral infections that were integrated into the human genome millions of years ago. They constitute approximately 8% of the human genome. Once considered "Junk DNA" it is now clear that ERVs are dynamic elements engaged in a continuous dialogue with the host innate immune system. This review further advances our current understanding of how ERV expression interfaces with innate immune signalling by providing insights into the dual nature of this interaction: (i) how the accidental detection of ERV-derived nucleic acids and proteins by pattern recognition receptors (PRRs), such as cGAS, RIG-I, and TLRs, can trigger protective interferon responses and inflammation, and (ii) the key innate immune regulatory mechanisms that suppress or control ERV activity, maintaining genomic stability. Furthermore, the study also sheds light on this balance for maintaining cellular homeostasis, providing the idea of how the disruption of this balance leads to the pathogenesis of autoimmune diseases, cancer, and neurological disorders, consequently unlocking therapeutic innovations.
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.