Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2004-7-21
pubmed:abstractText
According to a number of previous reports, control of HIV replication in humans appears to be linked to the presence of anti-HIV-1 Gag-specific CD8 responses. During the chronic phase of HIV-1 infection, up to 75% of the HIV-infected individuals who express the histocompatibility leukocyte Ag (HLA)-A*0201 recognize the Gag p17 SLYNTVATL (aa residues 77-85) epitope (SL9). However, the role of the anti-SL9 CD8 CTL in controlling HIV-1 infection remains controversial. In this study we determined whether the pattern of SL9 immunodominance in uninfected, HLA-A*0201 HIV vaccine recipients is similar to that seen in chronically HIV-infected subjects. The presence of anti-SL9 responses was determined using a panel of highly sensitive cellular immunoassays, including peptide:MHC tetramer binding, IFN-gamma ELISPOT, and cytokine flow cytometry. Thirteen HLA-A*0201 vaccinees with documented anti-Gag CD8 CTL reactivities were tested, and none had a detectable anti-SL9 response. These findings strongly suggest that the pattern of SL9 epitope immunodominance previously reported among chronically infected, HLA-A*0201-positive patients is not recapitulated in noninfected recipients of Gag-containing canarypox-based candidate vaccines and may be influenced by the relative immunogenicity of these constructs.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/AIDS Vaccines, http://linkedlifedata.com/resource/pubmed/chemical/Epitopes, T-Lymphocyte, http://linkedlifedata.com/resource/pubmed/chemical/Gene Products, gag, http://linkedlifedata.com/resource/pubmed/chemical/HIV Antigens, http://linkedlifedata.com/resource/pubmed/chemical/HLA-A*02:01 antigen, http://linkedlifedata.com/resource/pubmed/chemical/HLA-A Antigens, http://linkedlifedata.com/resource/pubmed/chemical/HLA-A2 Antigen, http://linkedlifedata.com/resource/pubmed/chemical/Immunodominant Epitopes, http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments, http://linkedlifedata.com/resource/pubmed/chemical/Vaccines, DNA, http://linkedlifedata.com/resource/pubmed/chemical/Vaccines, Synthetic, http://linkedlifedata.com/resource/pubmed/chemical/env Gene Products, Human..., http://linkedlifedata.com/resource/pubmed/chemical/p17 gag peptide, human...
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
173
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2126-33
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:15265949-AIDS Vaccines, pubmed-meshheading:15265949-Alleles, pubmed-meshheading:15265949-Canarypox virus, pubmed-meshheading:15265949-Epitopes, T-Lymphocyte, pubmed-meshheading:15265949-Gene Products, gag, pubmed-meshheading:15265949-HIV Antigens, pubmed-meshheading:15265949-HIV Infections, pubmed-meshheading:15265949-HIV Seronegativity, pubmed-meshheading:15265949-HIV-1, pubmed-meshheading:15265949-HLA-A Antigens, pubmed-meshheading:15265949-HLA-A2 Antigen, pubmed-meshheading:15265949-Humans, pubmed-meshheading:15265949-Immunization, Secondary, pubmed-meshheading:15265949-Immunodominant Epitopes, pubmed-meshheading:15265949-Peptide Fragments, pubmed-meshheading:15265949-T-Cell Antigen Receptor Specificity, pubmed-meshheading:15265949-T-Lymphocytes, Cytotoxic, pubmed-meshheading:15265949-Vaccination, pubmed-meshheading:15265949-Vaccines, DNA, pubmed-meshheading:15265949-Vaccines, Synthetic, pubmed-meshheading:15265949-env Gene Products, Human Immunodeficiency Virus
pubmed:year
2004
pubmed:articleTitle
Absence of immunodominant anti-Gag p17 (SL9) responses among Gag CTL-positive, HIV-uninfected vaccine recipients expressing the HLA-A*0201 allele.
pubmed:affiliation
Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA. gflmp@duke.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.