HLA-A11 epitope loss isolates of Epstein-Barr virus from a highly A11+ population

Pedro Otavio De Campos-Lima, Riccardo Gavioli, Qian Jin Zhang, Lesley E. Wallace, Riccardo Dolcetti, Martin Rowe, Alan B. Rickinson, Maria G. Masucci

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)98-100
Number of pages3
JournalScience
Volume260
Issue number5104
Publication statusPublished - 1993

ASJC Scopus subject areas

  • General

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