期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 104, 期 9, 页码 3366-3371出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0611128104
关键词
herpesvirus; HLA; immune escape; RNA degradation
资金
- Wellcome Trust [GR072425] Funding Source: Medline
- Medical Research Council [G9818340B] Funding Source: researchfish
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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