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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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

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.[1]

References

  1. HLA-A11 epitope loss isolates of Epstein-Barr virus from a highly A11+ population. de Campos-Lima, P.O., Gavioli, R., Zhang, Q.J., Wallace, L.E., Dolcetti, R., Rowe, M., Rickinson, A.B., Masucci, M.G. Science (1993) [Pubmed]
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