Naturally occurring leukemia viruses in H-2 congenic C57BL mice. II. Antibody response to viral envelope antigens.

In C57BL mice milk-borne infection with B-tropic murine leukemia virus (V+ denoting positive for milk-transmitted B-tropic virus and V- denoting negative for milk-transmitted B-tropic virus) was accompanied by an antibody response against viral envelope antigens (VEA). Milk transmission of virus led to higher virus titers and lymphoma incidence in B10.A (H-2a) mice than in B10 (H-2b) mice, and the latter strain produced higher titers of anti-VEA antibodies than did the former. H-2 control of the antivirus-antibody response was confirmed in the (B10.A V+ X B10 V+)F2 cross. B10 V+ mice produced both IgM and IgG antibodies, whereas in the sera of B10.A V+ mice only IgM antibodies were demonstrable. The production of IgG and high-titer IgM antibodies to VEA was dominant in (B10.A V+ X B10 V+)F1 animals. The failure of B10.A V+ mice to produce IgG antibodies against VEA was not due to an intrinsic defect of helper T-cell function because these mice produced IgG antivirus antibodies after sc immunization with killed viral vaccine. Furthermore, in B10.A mice without milk-transmitted virus (B10.A V- subline), expression of genetically transmitted virus upon aging was associated with the production of IgG antibodies to VEA. The combined data were compatible with the existence of an H-2-linked dominant immune-response gene regulating the antibody response to milk-transmitted murine leukemia virus.