ArticleNature communications2025
Latent infection of Caenorhabditis elegans by Orsay virus induces age-dependent immunity and cross-protection.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed.
- Species-specific barriers restrict virus spillover potential across the Caenorhabditis genus.PLoS biology · 2026Article
- Repeated mutation of a GT92 glycosyltransferase gene confers antiviral resistance in two Caenorhabditis species.Molecular biology and evolution · 2026Article
- Repeated mutation of a GT92 glycosyltransferase gene confers antiviral resistance in twobioRxiv : the preprint server for biology · 2026Article
- Reduced gravity and muon flux absence affectMicrobiology spectrum · 2026Article
- Cosmic silence and viral noise: transcriptomic crosstalk inFrontiers in microbiology · 2026Article
- The interplay betweeniScience · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
The C. elegans-Orsay virus pathosystem provides a powerful model for investigating the mechanisms that govern viral infection and immunity. Here, we focus on two key aspects of this interaction: the impact of lifelong latent infections and the dynamics of superinfection. By tracking the course of a lifelong infection, we demonstrate that the infection remains latent, with animals maintaining control over viral replication for most of their lifespan. Furthermore, we show that animals previously exposed to the virus can suppress viral replication following a second inoculation, indicative of an acquired immune response. Primary infections led to changes in transcriptomic and small RNA profiles, which varied depending on the developmental stage of the host and the timing of analysis. In contrast, superinfection disrupted multiple sRNA classes. Over time, the ability to control repeated viral reactivations declined, whereas resistance to superinfection was stable, ultimately favoring the primary infecting virus. This phenomenon was dependent on a functional RNA interference pathway.
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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.