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      Epstein-Barr virus transactivates the human endogenous retrovirus HERV-K18 that encodes a superantigen.

      Alleles, Animals, Antibodies, Viral, immunology, Burkitt Lymphoma, genetics, Cell Line, Transformed, Cells, Cultured, Endogenous Retroviruses, metabolism, Epstein-Barr Virus Infections, Gene Expression Regulation, Viral, Gene Products, env, biosynthesis, Herpesvirus 4, Human, pathogenicity, Histocompatibility Antigens Class II, Humans, Lymphocyte Activation, Mice, RNA, Viral, Receptors, Antigen, T-Cell, alpha-beta, Superantigens, T-Lymphocytes, Transcriptional Activation, Tumor Cells, Cultured

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          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.

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