During the course of progressive Friend virus-induced leukemia in Rfv-3(r/s) mice, antiviral antibody caused a marked reduction in the frequency of leukemic spleen cells releasing infectious virus. We investigated the mechanism of this antibody-induced alteration of leukemia cell phenotype in a series of passive transfer experiments using monoclonal antiviral antibodies. Our results indicated that two IgG2a anti-gp70 cytotoxic antibodies could reduce the frequency of virus-producing cells within the leukemic spleen as well as maintain the virus-nonproducing phenotype once it was established. IgG2a and IgG2b monoclonal anti-p15 antibodies, IgM, and IgA anti-gp70 antibodies, and an IgG3 anti-p15(E) antibody were not effective. The mechanism of this phenotypic alteration appeared to involve an antibody-mediated cytostasis of virus-producing leukemia cells with the subsequent overgrowth of virus-nonproducing cells. The maintenance of the virus-nonproducing phenotypes was dependent on the presence of anti-gp70 antibodies capable of neutralizing and clearing infectious F-MuLV in vivo. The presence of these neutralizing antibodies appeared to prevent reinfection of virus-nonproducing cells and therefore interfered with reversion to the virus-producing phenotype.
