Temperature-sensitive viral infection:: Inhibition of hemagglutinating virus of Japan (Sendai virus) infection at 41°

While investigating myoblast fusion using enveloped viruses, we unexpectedly found that the production of hemagglutinating virus of Japan (HVJ; Sendai virus) was suppressed temperature dependently in quail myoblasts transformed with a temperature-sensitive Rous sarcoma virus, which proliferate at 35.5degrees but differentiate at 41; viral production was normal at 35.5degrees but suppressed at 41 irrespective of the species of host cells. The production of some viruses, i.e. measles virus, influenza virus, herpes simplex virus type 1 and poliovirus, was also markedly suppressed at 41, suggesting that a temperature of 41 affects viral infection generally. To clarify the mechanism of the suppression, the infectious pattern of HVJ was examined both at 37 and at 41 in LLC-MK2 cells. The synthesis of HVJ-specific proteins was inhibited at the transcriptional level at 41, although viral penetration by envelope fusion was not affected. The transcriptional inhibition was also seen in quail fibroblasts, which do not express a 70-kD heat shock protein (HSP70), suggesting that HSP70 is dispensable for the inhibition of viral gene transcription at 41. Further, when the infected cells were incubated at 41 after the viral proteins had been synthesized at 37, viral production was also inhibited. Immunofluorescent staining of the cells exposed to 41 showed that HVJ envelope proteins formed large aggregates on the cell surface, into which both M and NP proteins-were assembled. Under-the electron microscope, HVJ virions appeared normal even at 41, but were detected in clusters on the cell surface, unlike at 37degrees. These observations suggested that the release of HVJ virions from the cell surface was inhibited for some reason at 41. Consequently, it was indicated that two steps, viral gene transcription and the release of virions, were inhibited at 41. Copyright (C) 2002 S. Karger AG, Basel.