ArticleFrontiers in veterinary science2026
Transcriptional analysis of duck liver infected with duck hepatitis A virus type 1 isolate HA5.
Article in Frontiers in veterinary science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
- Therapeutic, preventive, and pathogenetic advances in viral hepatitis.Frontiers in cellular and infection microbiology · 2026Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duck Hepatitis A Virus Type 1 (DHAV-1) is a major pathogen in ducklings, characterized by severe hepatomegaly and punctate hepatic hemorrhage. In this study, we investigated host gene expression dynamics in specific-pathogen-free (SPF) ducklings infected with the DHAV-1 isolate HA5 using high-throughput RNA sequencing (RNA-seq). We performed comprehensive transcriptomic analyses, integrating Clusters of Orthologous Groups (COG) classification, Gene Ontology (GO) annotation, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment. By combining these data with viral replication kinetics, we aimed to elucidate the molecular mechanisms of DHAV-1 pathogenesis. Differentially expressed genes (DEGs) were identified at 6, 12, 24, and 48 h post-infection (hpi). Viral titers peaked at 24 hpi and declined by 48 hpi, correlating with the observed transcriptional changes. The most pronounced transcriptional response occurred at 24 hpi, with 4,067 DEGs detected. Functional enrichment analyses revealed that these DEGs were predominantly associated with immune and metabolic pathways, including the Jak-STAT signaling pathway, oxidative phosphorylation, and Toll-like receptor signaling pathway. Collectively, these findings highlight the complex interplay between host immune responses and metabolic reprogramming. This study provides novel insights into the molecular basis of DHAV-1-induced liver pathology.
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