Characterization of cell lines persistently infected with infectious pancreatic necrosis virus.

Infectious pancreatic necrosis virus (IPNV) is a major pathogen of salmonids that is capable of establishing persistent infections, yet the cellular mechanisms underlying viral persistence remain poorly understood. In this study, we characterized two Chinook salmon embryo-derived cell lines - a wild-type and a Protein Kinase R (PKR)-deficient cell line - which were found to be persistently infected with IPNV. Both cell lines displayed hallmark features of viral persistence, including sustained cell growth without cytopathic effect, continuous production of infectious virus over successive passages and resistance to superinfection by homologous IPNV strains and susceptibility to heterologous viruses. Longitudinal analyses over 40 weekly passages revealed pronounced oscillations in extracellular infectious titres, which partially correlated with fluctuations in intracellular viral RNA levels. Despite these variations in viral replication, persistent infection did not trigger a robust type I interferon response, and basal expression of key interferon-stimulated genes was dampened. Notably, the absence of PKR did not alter viral persistence dynamics, indicating that PKR is not a regulator of this process. Taken together, these findings suggest that persistent IPNV employs immune evasion strategies to suppress host innate immune signalling while maintaining low-level replication.