Persistent infections of salmonid cell lines with infectious pancreatic necrosis virus (IPNV): A model for the carrier state in trout.
Ronald P. Hedrick, J. L. Fryer
Abstract
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Ronald P. Hedrick, J. L. Fryer
Abstract
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Infectious pancreatic necrosis virus (IPNV) persistence in carrier brook trout and persistently infected cell lines was examined. Viral persistence in vivo and in vitro was characterized by a fluctuating release of infectious virus (<101.6 to 106.0 TCID50/g or ml) in the absence of external signs or cytopathic effects. Infectious center assays indicated that virus was produced by less than 1% of the cell population of persistently infected lines and carrier trout kidney tissues. Antibody was not involved in viral persistence in vitro and its role in vivo was not clear. Interferon was not detected in the two persistently infected lines or in the sera of carrier trout examined in this study. Viral replication in one of these cell lines was controlled instead by the presence of defective interfering (DI) virus which had the capability of interfering with infectious virus multiplication and viral-induced cell lysis. The similarities of viral persistence in cell lines and carrier brook trout suggested that the same virus host cell interactions occur in vitro and in vivo.
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Infectious pancreatic necrosis virus (IPNV) persistence in carrier brook trout and persistently infected cell lines was examined. Viral persistence in vivo and in vitro was characterized by a fluctuating release of infectious virus (<101.6 to 106.0 TCID50/g or ml) in the absence of external signs or cytopathic effects. Infectious center assays indicated that virus was produced by less than 1% of the cell population of persistently infected lines and carrier trout kidney tissues. Antibody was not involved in viral persistence in vitro and its role in vivo was not clear. Interferon was not detected in the two persistently infected lines or in the sera of carrier trout examined in this study. Viral replication in one of these cell lines was controlled instead by the presence of defective interfering (DI) virus which had the capability of interfering with infectious virus multiplication and viral-induced cell lysis. The similarities of viral persistence in cell lines and carrier brook trout suggested that the same virus host cell interactions occur in vitro and in vivo.
Key concepts: Infectious pancreatic necrosis virus, Biology, Virology, Virus, Viral Interference, Trout, In vivo, Viral replication