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- W2021743722 abstract "Relatively little is known about immune evasion during the productive phase of infection by the γ 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 γ 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 γ-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." @default.
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- W2021743722 date "2007-02-27" @default.
- W2021743722 modified "2023-10-11" @default.
- W2021743722 title "Host shutoff during productive Epstein–Barr virus infection is mediated by BGLF5 and may contribute to immune evasion" @default.
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- W2021743722 doi "https://doi.org/10.1073/pnas.0611128104" @default.
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