Key result
DHAV-1 infection in ducklings alters 4,067 liver genes, driving immune and metabolic pathway changes.
Why the study?
Duck Hepatitis A Virus Type 1 is a major pathogen causing severe hepatomegaly and hepatic hemorrhage, but the molecular mechanisms of pathogenesis remain to be elucidated.
Absolute Event Rate: 4067% vs 0%
p-value: p=FDR < 0.01 and |log2FoldChange| > 1
DHAV-1 infection in ducklings induces significant transcriptional changes in liver tissue peaking at 24 hours post-infection, characterized by activation of immune pathways and suppression of metabolic processes.
May warrant early intervention in DHAV-1-infected ducklings; extends hepatic immune-metabolic transcriptomic mapping for antiviral development.
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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Yin et al. (2026) studied Day-old specific-pathogen-free (SPF) shelduck ducklings infected with duck hepatitis A virus type 1 (DHAV-1) isolate HA5 (n=32). Intramuscular inoculation with DHAV-1 HA5 strain vs. Mock-infected control group treated with isotonic sodium chloride was evaluated on Differential gene expression in duck liver at various time points post DHAV-1 infection correlated with viral replication kinetics (p=FDR < 0.01 and |log2FoldChange| > 1). Intramuscular DHAV-1 HA5 infection in SPF ducklings peaked viral titer at 24 hpi with 4,067 differentially expressed liver genes, predominantly immune and metabolic pathways involved.
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