Persistent Infection of Three Salmonid Cell Lines with Infectious Pancreatic Necrosis Virus (IPNV)

抄録

Persistent infections were established with infectious pancreatic necrosis virus (IPNV) in chinook salmon (CHSE-214), steelhead trout (STE-137) and in rainbow trout (RTG-2) cell lines. Viral persistence was characterized by the release of infectious virus, positive immunofluorescence, resistance to superinfection with homologous virus and susceptibility to challenges with heterologous viruses.
The morphology and growth characteristics of persistently infected (PI) and uninfected cell lines was indistinguishable. PI CHSE-214 and STE-137 cell lines produce little or no interferon. Activity suggesting interferon was detected in culture fluids from PI RTG-2 cells.
Temperature-sensitive virus was not detected in the culture fluids of PI CHSE-214 or STE-137 cell lines and the RTG-2 line has not been tested. Virus in the culture fluids of both PI STE-137 and RTG-2 cell lines demonstrated autointerference when inoculated onto uninfected control cells. The autointerfering component from PI STE-137 cells was removed from the culture fluid by ultracentrifugation and had a bouyant density of 1.29 g/cc in a cesium chloride gradient. Infectious virus also produced by PI STE-137 cells had a density of 1.33 g/cc. The production of defective interfering (DI) virus during viral persistence was further supported by electron microscopic examination of PI STE-137 cells. The production of DI virus by PI STE-137 cells as well as interferon in the PI RTG-2 cells were proposed as two mechanisms by which the cytocidal course of infection in these cell lines is prevented.