HLA-A11 EPITOPE LOSS ISOLATES OF EPSTEIN-BARR-VIRUS FROM A HIGHLY A11+ POPULATION
HLA-A11 EPITOPE LOSS ISOLATES OF EPSTEIN-BARR-VIRUS FROM A HIGHLY A11+ POPULATION
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DOI：
10.1126/science.7682013
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发表时间：
1993-04-02
期刊：
影响因子：
56.9
通讯作者：
MASUCCI, MG
中科院分区：
文献类型：
--
作者：
DECAMPOSLIMA, PO;GAVIOLI, R;MASUCCI, MG
细胞毒性T淋巴细胞（CTL）通过识别由主要组织相容性复合体（MHC）I类分子呈递的病毒肽来控制病毒感染。人类白细胞抗原（HLA）-A11-限制性CTL识别EB病毒（EBV）核抗原-4的肽残基416至424，在A11+高加索供体中经常主导EBV诱导的应答。该表位在来自高加索人和中非人群的A型EBV株中是保守的，其中A11相对罕见。然而，来自新几内亚高A11+人群的菌株在残基424处携带赖氨酸至苏氨酸突变，该突变废除了CTL识别和肽与新生A11分子的结合。这些结果表明，一个广泛的和遗传稳定的病毒，如EB病毒的进化是由MHC限制性CTL反应的压力的影响。
Cytotoxic T lymphocytes (CTLs) control viral infections by recognizing viral peptides presented by major histocompatibility complex (MHC) class I molecules. Human leukocyte antigen (HLA)-A11-restricted CTLs that recognize peptide residues 416 to 424 of the Epstein-Barr virus (EBV) nuclear antigen-4 frequently dominate EBV-induced responses in A11+ Caucasian donors. This epitope is conserved in type A EBV strains from Caucasians and central African populations, where A11 is relatively infrequent. However, strains from highly A11+ populations in New Guinea carry a lysine-to-threonine mutation at residue 424 that abrogates CTL recognition and binding of the peptide to nascent A11 molecules. The results suggest that evolution of a widespread and genetically stable virus such as EBV is influenced by pressure from MHC-restricted CTL responses.