Abstract

GENETIC sequences coding for type-C RNA viruses exist within the DNA of mouse cells1,2. In some inbred mouse strains endogenous viruses infectious for mouse cells are spontaneously activated and replicate in the animal: there is an associated incidence of lymphoreticular neoplasia correlated with the age of onset and level of virus expression3,4. Isolates from these naturally occurring lymphoreticular neoplasms as well as isolates activated from cells in vitro can directly induce lymphoreticular tumours in the same or an appropriately susceptible host strain3,5–8. These findings have led to the question of whether, after experimental immunisation, the host might be able to control or prevent tumours associated with these endogenous viruses. Irradiation induced thymomas of C57BL/6 mice are of probable endogenous type-C virus aetiology9,10 and an antiviral immunity can be induced in these mice by active or passive means which results in a significant reduction in endogenous type-C virus expression and tumour incidence11. Similar results have been obtained by Huebner and co-workers by induction of antiviral immunity in AKR mice12,13. We have examined induction of immunity to endogenous type-C viruses in three inbred mouse strains, BALB/c, NIH Swiss and C57BL, known to differ in their immunological responsiveness14 as well as their expression of endogenous type-C virus. Inactivated murine ecotropic type-C virus was found to be effective in preventing the natural expression of endogenous ecotropic as well as the immunologically related xenotropic viruses. These findings have important implications in the potential for prevention of naturally occurring neoplasms by antiviral immunity.

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