Abstract
We have investigated the mechanism of cell fusion induced by Nelson Bay virus (NBV), a reovirus which possesses properties distinct from other reoviruses of avian or mammalian origin. Virions have a morphology similar to that of other members of the genus reovirus, although the diameter of the outer capsid was found to be only 62–65 nm compared to 76 nm reported for other types. Analysis of the virion RNA and polypeptide species support the classification of NBV as a member of the reovirus genus. Cell fusion was a prominent feature of viral replication in PSEK and Vero cells and was evident prior to formation of infectious progeny virus. No fusion from without was demonstrated in the presence or absence of polybrene;fusion appeared to be dependent upon viral replication and was inhibited by cycloheximide. The mechanism of fusion does not appear to involve glycosylated proteins, which could not be detected in virions or immune precipitates from infected cells. Fusion was not inhibited by tunicamycin or 2-deoxyglucose, nor by the addition following infection of antisera to purified virions or to infected cells. These results suggest that fusion might involve a newly synthesized nonglycosylated protein that is not expressed on cell surfaces.
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