Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1994-5-5
pubmed:abstractText
Epstein-Barr virus (EBV) is a B lymphotropic herpesvirus of humans that elicits strong HLA class I-restricted cytotoxic T lymphocyte (CTL) responses. An influence of such responses on virus evolution was first suggested by our finding that EBV isolates from the highly HLA A11-positive Papua New Guinea (PNG) population carried a lys-thr mutation at residue 424 of the nuclear antigen EBV-encoded nuclear antigen (EBNA4) that destroyed the immunodominant target epitope for A11-restricted CTL recognition. Here we turn to a much larger population, Southern Chinese, where the A11 allele is again present in over 50% of the individuals. Each of 23 EBV isolates analyzed from this population were also mutated in the EBNA4 416-424 epitope, the mutations selectively involving one of the two anchor residues in positions 2 (417 val-leu) or 9 (424 lys-asp, -arg or -thr) that are critical for A11-peptide interaction. The majority of the Chinese isolates and all 10 PNG isolates also carried mutations affecting positions 1 and 2 of the next most immunodominant A11-restricted epitope, EBNA4 residues 399-408. These changes clearly affected antigenicity since A11-positive lymphoblastoid cell lines (LCLs) carrying these mutant EBV strains were not recognized by A11-restricted CTLs raised against the prototype B95.8 virus. Furthermore, Chinese donors naturally infected with these mutant viruses did not mount detectable A11-restricted CTL responses on in vitro stimulation with autologous LCL cells carrying either the B95.8 or their endogenous EBV strain. In two different highly A11-positive populations, therefore, immune pressure appears to have selected for resident EBV strains lacking immunodominant A11-restricted CTL epitopes.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-1169135, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-1319456, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-1321426, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-1377222, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-1688611, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-1695259, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-1696684, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-1700303, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-1721107, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-1734720, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-2420472, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-2426185, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-3016710, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-3023050, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-3029268, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-306072, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-3217935, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-4346033, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-6319303, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-649177, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-6975300, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-7679748, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-7688791, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-7693972, http://linkedlifedata.com/resource/pubmed/commentcorrection/7511684-8384718
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1007
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
179
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1297-305
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
T cell responses and virus evolution: loss of HLA A11-restricted CTL epitopes in Epstein-Barr virus isolates from highly A11-positive populations by selective mutation of anchor residues.
pubmed:affiliation
Microbiology and Tumor Biology Center, Karolinska Institute, Stockholm, Sweden.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't