Increased immunogenicity of rat tumors after superinfection with endogenous murine C-type virus

Four chemical carcinogen-induced and two polyoma virus-induced rat tumors were repeatedly passaged through nude mice. A 3-methyl-cholanthrene (MC)-induced tumor in BDIX rats (MBDB) and a polyoma virus-induced tumor in Wistar/Fu rats (PW41) became infected with endogenous mouse virus (EMV), as judged by the expression of murine C-type virus-associated gp71, p30, and p12 antigens on their cell surface. Two ethylnitrosourea-induced tumors in BDIX rats (290T and GE3A) were exposed in vitro to the supernatant of EMV-infected PW41. Subsequently, 290T but not GE3A converted to murine gp71, p30, and p12 positivity. All these successfully infected rat tumors (EMV-MBDB, EMV-PW41, and EMV-290T) became less transplantable to, and more rejectable in otherwise susceptible syngeneic rats. To compare the immunogenicity of the virus-infected and noninfected tumors, syngeneic rats were immunized 3 times with irradiated cells, and challenged with the noninfected tumor. Wistar/Fu rats immunized with irradiated EMV-PW41 showed no improvement of PW41 rejection, compared to rats immunized with irradiated noninfected cells. On the other hand, BDIX rats immunized with EMV-MBDB or EMV-290T rejected MBDB or 290T, respectively, with no cross immunity, while the rats immunized with irradiated but noninfected tumors showed no significant rejection. These results indicate that EMV infection increased the immunogenicity of non-, or only low immunogenic rat tumors.