Increased immunogenicity of low-antigenic rat tumors after superinfection with endogenous murine C-type virus in nude mice.

Four chemical carcinogen-induced and two polyoma-virus-induced rat tumors were repeatedly passaged through nude mice. A methylcholanthrene-induced tumor in BDIX rats (MBDB) and a polyomavirus-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 non-infected tumors, syngeneic rats were immunized three times with irradiated cells, and challenged with the non-infected tumor. Wistar/Fu rats immunized with irradiated EMV-PW41 showed no improvement in PW41 rejection, compared to rats immunized with irradiated, non-infected 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 non-infected tumors showed no significant rejection. These results indicate that EMV infection augmented the immunogenicity of non-immunogenic or only low-immunogenic rat tumors.