Transcriptomic analysis reveals the mechanism of viral modulation of host immunity facilitating calicivirus replication in Pelteobagrus fulvidraco.

Yellow catfish (Pelteobagrus fulvidraco), an economically significant aquaculture species in East Asia, faces substantial threats from pathogens, with yellow catfish calicivirus (YcCV) being the primary causative agent of spring outbreaks leading to massive mortality and economic losses. Although the YcCV genome has been fully characterized, the immune response mechanisms of P. fulvidraco during infection remain poorly understood. Here, we conducted histopathological and transcriptomic analyses of head kidney from YcCV-infected fish at 1 and 5 days post-infection (dpi). Histopathological analysis revealed severe tissue damage, including liver coagulative necrosis, splenic hemorrhage, and widespread inflammatory infiltration in the kidney and heart. Compared to controls, 142 and 3402 differentially expressed genes (DEGs) were identified at 1 dpi and 5 dpi, respectively. GO and KEGG enrichment analyses revealed these DEGs were predominantly involved in signal transduction, cellular growth, apoptosis, immune responses, and metabolic processes. Notably, significant upregulation of IL4i1 suggested its potential role in modulating host immunity to control viral replication. siRNA-mediated knockdown of IL4i1 in yellow catfish brain cells suppressed YcCV replication, as evidenced by reduced viral load and mRNA levels, indicating a proviral regulatory function of IL4i1. Collectively, these findings provide novel insights into virus-host interactions, advancing our understanding of YcCV pathogenesis and informing future antiviral strategies.