ArticlePLoS pathogens2024
Natural variation in infection specificity of Caenorhabditis briggsae isolates by two RNA viruses.
Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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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
7 citing papers in PubMed.
- A gap-free, telomere-to-telomere genome assembly for the Caenorhabditis briggsae reference strain AF16.G3 (Bethesda, Md.) · 2026Article
- 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
- Article
- A gap-free, telomere-to-telomere genome assembly for thebioRxiv : the preprint server for biology · 2026Article
- Repeated mutation of a GT92 glycosyltransferase gene confers antiviral resistance in twobioRxiv : the preprint server for biology · 2026Article
- Dynamic control of Argonautes by a rapidly evolving immunological switch.Current biology : CB · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Antagonistic relationships such as host-virus interactions potentially lead to rapid evolution and specificity in interactions. The Orsay virus is so far the only horizontal virus naturally infecting the nematode C. elegans. In contrast, several related RNA viruses infect its congener C. briggsae, including Santeuil (SANTV) and Le Blanc (LEBV) viruses. Here we focus on the host's intraspecific variation in sensitivity to these two intestinal viruses. Many temperate-origin C. briggsae strains, including JU1264 and JU1498, are sensitive to both, while many tropical strains, such as AF16, are resistant to both. Interestingly, some C. briggsae strains exhibit a specific resistance, such as the HK104 strain, specifically resistant to LEBV. The viral sensitivity pattern matches the strains' geographic and genomic relationships. The heavily infected strains mount a seemingly normal small RNA response that is insufficient to suppress viral infection, while the resistant strains show no small RNA response, suggesting an early block in viral entry or replication. We use a genetic approach from the host side to map genomic regions participating in viral resistance polymorphisms. Using Advanced Intercrossed Recombinant Inbred Lines (RILs) between virus-resistant AF16 and SANTV-sensitive HK104, we detect Quantitative Trait Loci (QTLs) on chromosomes IV and III. Building RILs between virus-sensitive JU1498 and LEBV-resistant HK104 followed by bulk segregant analysis, we identify a chromosome II QTL. In both cases, further introgressions of the regions confirmed the QTLs. This diversity provides an avenue for studying virus entry, replication, and exit mechanisms, as well as host-virus specificity and the host response to a specific virus infection.
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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.