Mammary tumor viruses (MMTVs) as well as their endogenous counterparts
encode superantigens which react with T cells expressing particular T
cell receptor Vp chains, Several lines of evidence indicated that MHC
class II is required for the functional presentation of these superan
tigens, Here we provide direct proof that the function of superantigen
s is abrogated in the absence of MHC class II expression. No deletion
of MIs-1-reactive T cells was observed in MHC class II-deficient mice,
and splenocytes from these animals did not stimulate MIs-1-reactive T
cell hybrids in vitro. Furthermore, the viral spread in MHC class II-
deficient mice, maternally infected with MMTV(C3H), was severely reduc
ed. While initial infection in the gut-associated lymphocytes was comp
arable between MHC class II-deficient and normal mice, the level of in
fection in the spleen and the mammary tissue was much lower in the def
icient animals. Quantitation of proviral DNA in spleen revealed a dire
ct correlation between the magnitude of superantigen stimulation and d
egree of infection. These experiments document the direct effect of su
perantigen stimulation on viral amplification. (C) 1996 Academic Press
, Inc.