ArticleMolecular ecology2016
The genetic architecture of resistance to virus infection in Drosophila.
Article in Molecular ecology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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
32 citing papers in PubMed.
- Genomic Structure Predicts Granulovirus Resistance Without a Detectable Life-History Trade-Off in Plodia interpunctella.Molecular ecology · 2026Article
- Article
- Cumulative effects of mutation and selection on susceptibility to bacterial pathogens in Caenorhabditis elegans.Evolution; international journal of organic evolution · 2025Article
- Persistent viral infections impact key biological traits in Drosophila melanogaster.PLoS biology · 2025Article
- Wolbachia Offers Protection Against Two Common Natural Viruses of Drosophila.Microbial ecology · 2025Article
- Bdelloid rotifers deploy horizontally acquired biosynthetic genes against a fungal pathogen.Nature communications · 2024Article
- The genetic basis of variation in immune defense against Lysinibacillus fusiformis infection in Drosophila melanogaster.PLoS pathogens · 2023Article
- Investigating the outcomes of virus coinfection within and across host species.PLoS pathogens · 2023Article
- Molecular mechanisms of adaptive evolution in wild animals and plants.Science China. Life sciences · 2023Review
- Galbut Virus Infection Minimally InfluencesViruses · 2023Article
- Discovery of malathion resistance QTL in Drosophila melanogaster using a bulked phenotyping approach.G3 (Bethesda, Md.) · 2022Article
- Genetic slippage after sex maintains diversity for parasite resistance in a natural host population.Science advances · 2022Article
- Powerful, efficient QTL mapping in Drosophila melanogaster using bulked phenotyping and pooled sequencing.Genetics · 2022Article
- Coevolutionary theory of hosts and parasites.Journal of evolutionary biology · 2022Review
- Genetic dissection of innate immune memory inFrontiers in immunology · 2022Article
- Between virus correlations in the outcome of infection across host species: Evidence of virus by host species interactions.Evolution letters · 2021Article
- A Two-Locus System with Strong Epistasis Underlies Rapid Parasite-Mediated Evolution of Host Resistance.Molecular biology and evolution · 2021Article
- Genomic Signatures of Coevolution between Nonmodel Mammals and Parasitic Roundworms.Molecular biology and evolution · 2021Article
- Genomic Responses to Climate Change: Making the Most of theFrontiers in genetics · 2021Article
- A natural variant of the essential host geneeLife · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Variation in susceptibility to infection has a substantial genetic component in natural populations, and it has been argued that selection by pathogens may result in it having a simpler genetic architecture than many other quantitative traits. This is important as models of host-pathogen co-evolution typically assume resistance is controlled by a small number of genes. Using the Drosophila melanogaster multiparent advanced intercross, we investigated the genetic architecture of resistance to two naturally occurring viruses, the sigma virus and DCV (Drosophila C virus). We found extensive genetic variation in resistance to both viruses. For DCV resistance, this variation is largely caused by two major-effect loci. Sigma virus resistance involves more genes - we mapped five loci, and together these explained less than half the genetic variance. Nonetheless, several of these had a large effect on resistance. Models of co-evolution typically assume strong epistatic interactions between polymorphisms controlling resistance, but we were only able to detect one locus that altered the effect of the main effect loci we had mapped. Most of the loci we mapped were probably at an intermediate frequency in natural populations. Overall, our results are consistent with major-effect genes commonly affecting susceptibility to infectious diseases, with DCV resistance being a near-Mendelian trait.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.