Exploring the role of differential splicing of Pekin ducks resistant to DHAV-3 based on full-length transcriptome.

Duck Hepatitis A Virus type 3 (DHAV-3) causes high mortality in Pekin ducks, and the role of post-transcriptional regulation in disease resistance remains unclear. Here, we performed Oxford Nanopore full-length transcriptome sequencing on liver samples from resistant and susceptible ducks at 0 h and 24 h after DHAV-3 infection. Only one differentially expressed gene (DEG) and four differentially expressed transcripts (DETs) were identified pre-infection (0 h), whereas post-infection (24 h) we detected 2,539 DEGs and 2,909 DETs, indicating strong group-specific expression divergence. Functional enrichment revealed immune-related and metabolic pathway dysregulation in susceptible ducks, while resistant ducks maintained homeostasis. BulkSignalR identified an ECM-Integrin-JAK/Src module unique to the resistant group. Alternative splicing (AS) events increased from 16 pre-infection to 310 post-infection, enriched in immune and signaling pathways. Key immune genes showed isoform switching; in susceptible ducks, SELENOP transcripts lacked multiple selenocysteine sites, and a truncated PRPF8 isoform was highly expressed, while high DHX58 expression may suppress RIG-I activation. These findings highlight the critical role of post-transcriptional regulation in antiviral immunity and provide potential targets for improvement of disease resistance.