# Transcriptional analysis of duck liver infected with duck hepatitis A virus type 1 isolate HA5

## TL;DR

This study explores how duck liver gene expression changes when infected with a specific strain of duck hepatitis A virus, revealing key immune and metabolic pathways involved in the disease.

## Contribution

The study provides novel insights into the molecular mechanisms of DHAV-1 pathogenesis through comprehensive transcriptomic analysis.

## Key findings

- Viral titers peaked at 24 hpi and declined by 48 hpi, correlating with transcriptional changes.
- The most pronounced transcriptional response occurred at 24 hpi, with 4,067 differentially expressed genes detected.
- DEGs were predominantly associated with immune and metabolic pathways like Jak–STAT, oxidative phosphorylation, and Toll-like receptor signaling.

## 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.