Transgenic mouse mammary tumor virus superantigen expression prevents viral infection.
Endogenous mouse mammary tumor virus (MMTV) proviruses have recently been shown to cosegregate genetically with the minor lymphocyte-stimulating loci, also termed self-superantigens. The antigenic activity has been localized to the open reading frame (ORF) protein encoded in the long terminal repeat of MMTV. We show here that unlike their nontransgenic littermates, transgenic mice expressing high levels of an ORF protein derived from the C3H exogenous MMTV specifically delete their V beta 14+ T cells and do not become infected with this virus when it is present in their mother's milk. Thus, it appears that MMTV utilizes cells of the immune system in its infection pathway, and mice that retain endogenous MMTVs should be immune to infection by exogenous virus. These results offer possible new approaches to anti-viral therapy or immunization.
Golovkina
T V
TV
Department of Biochemistry, University of Illinois College of Medicine, Chicago 60612.
Chervonsky
A
A
Dudley
J P
JP
Ross
S R
SR
D000818:Animals; D000956:Antigens, Viral / Q000235:genetics / Q000276:immunology*; D015870:Gene Expression; D008212:Lymphocyte Depletion; D008324:Mammary Tumor Virus, Mouse / Q000235:genetics / Q000276:immunology*; D051379:Mice; D008822:Mice, Transgenic; D012333:RNA, Messenger / Q000235:genetics; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000235:genetics; D012091:Repetitive Sequences, Nucleic Acid; D013601:T-Lymphocytes / Q000276:immunology*; D014412:Tumor Virus Infections / Q000276:immunology*
D000956:Antigens, Viral; D012333:RNA, Messenger; D016693:Receptors, Antigen, T-Cell, alpha-beta