期刊
JOURNAL OF VIROLOGY
卷 86, 期 1, 页码 572-577出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.05151-11
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资金
- Dutch Cancer Foundation [RUL 2005-3259]
- Netherlands Scientific Organization [NWO Vidi 917.76.330]
- National Health and Medical Research Council of Australia
- UK Medical Research Council
- MRC [G0801822] Funding Source: UKRI
- Medical Research Council [G0801822] Funding Source: researchfish
The Epstein-Barr virus (EBV)-encoded immune evasion protein BNLF2a inhibits the transporter associated with antigen processing (TAP), thereby downregulating HLA class I expression at the cell surface. As a consequence, recognition of EBV-infected cells by cytotoxic T cells is impaired. Here, we show that sequence polymorphism of the BNLF2a protein is observed with natural EBV isolates, with evidence for positive selection. Despite these mutations, the BNLF2a variants efficiently reduce cell surface HLA class I levels. This conservation of BNLF2a function during evolution of EBV implies an important role for the viral TAP inhibitor in preventing T cell recognition during viral infection.
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