Activation of an endogenous mouse type C virus by ultraviolet-irradiated herpes simplex virus types 1 and 2.

Abstract

Infection of BALB/c mouse cells with UVirradiated herpes simplex virus (HSV) types 1 and 2 resulted in activation of a xenotropic type C virus detected by infectious center formation in permissive rat cells. The levels of type C virus activated by HSV were related to the UV dose and the multiplicity of infection used. The ability of HSV to activate type C virus was eliminated by heat-inactivation and by neutralization with specific antiserum against HSV, but was not affected by purification or treatment with DNase and RNase. Maximum levels of type C virus in the cells and medium were observed within 1 day after HSV infection, and the levels returned to control cell values within 3-4 days. The possible significance of these findings with respect to the putative oncogenic potential of HSV is discussed. Cells of many, if not all, mammalian species contain repressed genomes of type C RNA viruses. Activation of these repressed genomes with resultant virus synthesis may occur spontaneously (1) or may be induced by biological (2), chemical (3-6), or physical (7) means. Evidence exists to suggest that the genomes of these vertically transmitted endogenous RNA viruses can play a role in spontaneous tumor induction (8, 9).Viruses containing DNA rather than RNA genetic material have also been implicated in the oncogenic process. Inoculation of herpesviruses into animals (10) or cells in culture (11), for example, may be followed by the appearance of tumors or cell transformants that possess malignant potential. The putative role of herpesviruses in the oncogenic process is not clearly understood, however, and one may question whether the herpesvirus genome is in itself oncogenic or whether herpesviruses serve an indirect function by affecting a cellular factor(s) which is the direct oncogen. An example consistent with an indirect role in oncogenesis would be modification of expression of endogenous type C virus information after herpesvirus infection.

Mouse Mammary Tumour Virus and Polyoma Virus Information in Mammary Tumours of Athymic Mice Inoculated with Polyoma Virus

“…This seemed possible because of the reported induction of endogenous type C retrovirus by herpesviruses (Hampar et al, 1976). An examination of the tumour cell DNA for MMTV-specific sequences showed that it contained about five to six copies of MMTV genome equivalents per cell genome.…”

“…A question, therefore, arose whether mouse mammary tumour virus (MMTV) played any part, either augumentative or essential, in the development of mammary tumours in adult athymic mice. It was possible that polyoma virus acted as a co-carcinogen in inducing endogenous MMTV, such as herpesviruses do for endogenous type C retrovirus in mouse cells (Hampar et al, 1976). Alternatively, polyoma virus could directly transform mammary gland cells resulting in neoplasia.…”

Repeated Recruitment of LTR Retrotransposons as Promoters by the Anti-apoptotic Locus NAIP During Mammalian Evolution

“…For example, activation of NAIP via an LTR promoter may provide an avenue for germ cells to escape transitory, stress-induced apoptotic signals. LTR promoters may be particularly responsive to upregulation by cellular stresses since it has been shown that activation of human and mouse ERV LTRs can occur following stresses such as viral infection [54][55][56] and UV irradiation [57,58]. Various IAPs are expressed in human [59,60], mouse [61], and rat [62,63] germ cells or their progenitors, and it has been reported that Naip expression plays a role in mouse oocyte viability [61].…”

Herpes Simplex Virus and Human Cytomegalovirus: Their Role in Morphological Transformation and Genital Cancers

“…However, it is clearly a very interesting property. It is now some time since the activation by HSV infection of an endogenous C-type virus (MuX) from a feline cell line (F81) transformed by the Moloney strain of murine sarcoma virus was reported (Hampar et al, 1976;Boyd et al, 1978). This activation is an intriguing observation and its relevance as a model system for activation of endogenous viruses in tumours has never been fully explored.…”