19
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

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

      Immunity
      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

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          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.

          Related collections

          Author and article information

          Comments

          Comment on this article