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      Host shutoff during productive Epstein-Barr virus infection is mediated by BGLF5 and may contribute to immune evasion.

      Proceedings of the National Academy of Sciences of the United States of America

      Antigen Presentation, B-Lymphocytes, cytology, immunology, Cell Line, Tumor, Deoxyribonucleases, Epstein-Barr Virus Infections, Gene Expression Regulation, Histocompatibility Antigens Class I, biosynthesis, metabolism, Histocompatibility Antigens Class II, Humans, Microscopy, Fluorescence, Protein Biosynthesis, Viral Proteins

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          Relatively little is known about immune evasion during the productive phase of infection by the gamma(1)-herpesvirus Epstein-Barr virus (EBV). The use of a unique system to isolate cells in lytic cycle allowed us to identify a host shutoff function operating in productively EBV-infected B cells. This impairment of protein synthesis results from mRNA degradation induced upon expression of the early lytic-cycle gene product BGLF5. Recently, a gamma(2)-herpesvirus, Kaposi sarcoma herpesvirus, has also been shown to encode a host shutoff function, indicating that host shutoff appears to be a general feature of gamma-herpesviruses. One of the consequences of host shutoff is a block in the synthesis of HLA class I and II molecules, reflected by reduced levels of these antigen-presenting complexes at the surface of cells in EBV lytic cycle. This effect could lead to escape from T cell recognition and elimination of EBV-producing cells, thereby allowing generation of viral progeny in the face of memory T cell responses.

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