Studies on the mechanism of temperature sensitivity of infectious pancreatic necrosis virus replication.

Yields of infectious pancreatic necrosis virus from fathead minnow cell cultures were maximal at 20 degrees C. The virus failed to replicate at 28 degrees C and neither virus-specific mRNA nor virus-specific polypeptides could be detected when infected cells were maintained at this temperature. Intrinsic thermolability of virus infectivity or inability to adsorb to cells at 28 degrees C could not account for the temperature-dependent block in virus morphogenesis. Analysis of infectious virus production and virus-specific polypeptide and RNA synthesis following shifts from the permissive (20 degrees C) to the non-permissive temperature (28 degrees C) at various times after infection indicated that multiple temperature-sensitive (ts) steps were involved in the inhibition of virus replication.