ArticleMicrobiology spectrum2026
DNA methylation-mediated suppression of endocytosis confers resistance to duck hepatitis A virus type 3.
Article in Microbiology spectrum, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Host DNA methylation plays a crucial role in antiviral defense, yet its impact on viral susceptibility remains unclear. Using ducklings resistant (R) or susceptible (S) to duck hepatitis A virus type 3 (DHAV-3), we integrated whole-genome bisulfite and oxidative bisulfite sequencing with transcriptomics. We observed a distinct intragenic 5-methylcytosine (5mC) signature between the two lines, with endocytic pathway genes being hypomethylated in susceptible, while hypermethylated in resistant ducklings. Critically, the genebody 5mC level displayed a dominant negative correlation with gene expression, and functionally determined viral entry efficiency. Following infection, the methylation program further coordinated post-entry host responses, including immune, fatty acid metabolism, and autophagy pathways. This genebody methylation signature defines a regulatory framework governing DHAV-3 susceptibility, offering insights for antiviral strategies and disease-resistance breeding.IMPORTANCEDuck hepatitis A virus type 3 (DHAV-3) causes severe mortality in ducklings, leading to substantial economic losses in poultry production. Understanding why some ducks resist infection while others succumb is critical for developing sustainable control strategies. Here, we discovered that a chemical "tag" on DNA-called methylation-acts as a natural switch that determines susceptibility. Resistant ducks carry higher methylation on genes controlling viral entry, effectively closing the door to the virus. Susceptible ducks lack this protective methylation, allowing viral access. Experimentally manipulating this switch directly altered infection efficiency, proving methylation is a functional controller of disease outcome. Our findings reveal that epigenetic variation, independent of genetic sequence, shapes host vulnerability. This opens new possibilities for breeding virus-resistant poultry through epigenetic markers, reducing reliance on vaccines and antiviral drugs. The work also provides a framework for understanding how animals defend against viral pathogens at the molecular level.
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.