Induction of murine p30 by superinfecting herpesviruses

Abstract

The interaction of endogenous type C viruses with superinfecting herpes simplex virus type 2 (HSV-2) was investigated in two 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) p30 expression. Immunofluorescence tests with Swiss/3T3A cells productively infected 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; however, untreated and UV-inactivated HSV-2 induced both HSV-2associated antigens and MuLV p30 in these cells. Although the Birch strain of human cytomegalovirus induced MuLV p30, neither mouse cytomegalovirus nor vesicular stomatitis virus induced MuLV p30 in either cell line.

Herpes simplex virus‐induced amplification of SV40 sequences in transformed Chinese hamster embryo cells

“…In recent years additional evidence has accumulated pointing to specific interactions of HSV infections with host-cell DNA: stimulation of host-cell DNA synthesis has been reported (Kucera and Gusdon, 1976) and data have been presented revealing the induction of host-cell DNA repair (Lorentz et al, 1977;Nishiyama and Rapp, 1981), possibly as a consequence of the induced chromosomal damage. Infection with partially inactivated HSV leads to activation of endogenous retroviral genes (Hampar et al, 1976;Reed and Rapp, 1976) and efficient transformation of rodent cells by photo-or UV-inactivated HSV (Duff and Rapp, 1971) has been reported by various laboratories.…”

Evidence for type‐C retrovirus production by Burkitt's lymphoma‐derived cell line

“…Several lines of investigation on animal systems seem to point to a possible interaction between a DNA herpesvirus and an RNA tumor virus as responsible for oncogenesis. Thus, it was demonstrated that UV-irradiated herpes simplex virus types 1 and 2 activated the production of an endogenous type-C virus of mouse (Hampar et al, 1976;Reed and Rapp, 1976;Hampar et al, 1977a, b ) , and that oncornavirus-like particles were present in a simian lymphoid cell line derived from a lymphoma induced by herpesvirus saimiri (Yang et al, 1974); furthermore, the presence of both an oncornavirus and a herpesvirus was necessary for the manifestation of neoplastic disease in guinea-pigs (Hsiung et al, 1973), while the association of the Marek's disease herpesvirus with an avian leukosis type-C virus caused enhanced tumor responses and mortality (Peters et al, 1973;Frankel et al, 1974;Smith et al, 1975;Campbell et al, 1978).…”

Concanavalin A‐Mediated Agglutination of 3T3 Cells After Exposure to UV‐Irradiated Herpes Simplex Virus

“…It has been reported previously that UV-irradiated HSV can activate an endogenous type C virus (9,17). However, neither type C virus nor its antigen could be detected in cells transformed by UV-irradiated HSV (8).…”