Abstract
Superantigens (SAgs) are proteins produced by pathogenic microbes to elicit potent, antigen-independent T cell responses that are believed to enhance the microbes' pathogenicity. Here we show that the human lymphotropic herpesvirus Epstein-Barr virus (EBV) transcriptionally activates the env gene of an endogenous retrovirus, HERV-K18, that possesses SAg activity. SAg activity was demonstrated by MHC class II dependent preferential activation of TCRVB13 T cells in response to murine B cells transfected with the HERV-K18 env gene. This is a unique demonstration of a pathogen inducing a host-encoded Sag and accounts for the previously described EBV associated Sag activity. The T cell activation elicited by the Sag could play a central role in EBV infection and associated diseases.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Alleles
-
Animals
-
Antibodies, Viral / immunology
-
Burkitt Lymphoma / genetics
-
Burkitt Lymphoma / immunology
-
Cell Line, Transformed
-
Cells, Cultured
-
Endogenous Retroviruses / genetics*
-
Endogenous Retroviruses / immunology*
-
Endogenous Retroviruses / metabolism
-
Epstein-Barr Virus Infections / genetics*
-
Epstein-Barr Virus Infections / immunology
-
Gene Expression Regulation, Viral
-
Gene Products, env / biosynthesis
-
Gene Products, env / genetics
-
Gene Products, env / immunology*
-
Herpesvirus 4, Human / pathogenicity*
-
Histocompatibility Antigens Class II / immunology
-
Humans
-
Lymphocyte Activation
-
Mice
-
RNA, Viral / biosynthesis
-
Receptors, Antigen, T-Cell, alpha-beta / immunology
-
Superantigens / biosynthesis
-
Superantigens / genetics*
-
Superantigens / immunology
-
T-Lymphocytes / immunology
-
Transcriptional Activation
-
Tumor Cells, Cultured
Substances
-
Antibodies, Viral
-
Gene Products, env
-
Histocompatibility Antigens Class II
-
RNA, Viral
-
Receptors, Antigen, T-Cell, alpha-beta
-
Superantigens