Induction of murine p30 by superinfecting herpesviruses

Abstract

The interaction of endogenous type C viruses with superinfecting herpes simplex virus type 2 (HSV-2) [which may be necessary for the induction of neoplastic disease] was investigated in 2 murine cell lines. Replication of HSV-2 was suboptimal in random-bred Swiss/3T3A cells and, in initial experiments, infection with a low virus-to-cell ratio resulted in carrier cultures with enhanced murine leukemia virus (MuLV) [structural polypeptide] p30 expression. Immunofluorescence tests with [mouse embryo fibroblast] Swiss/3T3A cells productively infested with HSV-2 also showed HSV-associated cytoplasmic antigens and enhanced MuLV p30 expression when compared with uninfected controls. Inactivation of HSV-2 with UV light did not abolish this reaction, although the number of cells expressing p30 was reduced. HSV-2 replicated more efficiently in a line of NIH Swiss cells (N cl A cl 10). These cells are not readily inducible for type C expression by conventional methods; but untreated and UV-inactivated HSV-2 induced HSV-2-associated antigens and MuLV p30 in these cells. Although the Birch strain of human cytomegalovirus induced MuLV p30, neither mouse cytomegalovirus nor vesticular stomatitis virus induced MuLV p30 in either cell line.