Source:http://linkedlifedata.com/resource/pubmed/id/21670313
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2011-7-7
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pubmed:abstractText |
Polymorphism in the HLA region of a chromosome is the major source of host genetic variability in HIV-1 outcome, but there is limited understanding of the mechanisms underlying the beneficial effect of protective class I alleles such as HLA-B57, -B27, and -B51. Taking advantage of a unique cohort infected with clade B' HIV-1 through contaminated blood, in which many variables such as the length of infection, the infecting viral strain, and host genetic background are controlled, we performed a comprehensive study to understand HLA-B51-associated HIV-1 control. We focused on the T cell responses against three dominant HLA-B51-restricted epitopes: Gag327-345(NI9) NANPDCKTI, Pol743-751(LI9) LPPVVAKEI, and Pol283-289(TI8) TAFTIPSI. Mutations in all three dominant epitopes were significantly associated with HLA-B51 in the cohort. A clear hierarchy in selection of epitope mutations was observed through epitope sequencing. L743I in position 1 of epitope LI9 was seen in most B51(+) individuals, followed by V289X in position 8 of the TI8, and then, A328S, in position 2 of the NI9 epitope, was also seen in some B51(+) individuals. Good control of viral load and higher CD4(+) counts were significantly associated with at least one detectable T cell response to unmutated epitopes, whereas lower CD4(+) counts and higher viral loads were observed in patients who had developed escape mutations in all three epitopes or who lacked T cell responses specific to these epitope(s). We propose that patients with HLA-B51 benefit from having multiple layers of effective defense against the development of immune escape mutations.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes, T-Lymphocyte,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-B Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-B51 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Immunodominant Epitopes,
http://linkedlifedata.com/resource/pubmed/chemical/gag Gene Products, Human...,
http://linkedlifedata.com/resource/pubmed/chemical/pol Gene Products, Human...
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1550-6606
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pubmed:author |
pubmed-author:ChenXinYueX,
pubmed-author:DongTaoT,
pubmed-author:EnoNN,
pubmed-author:JohnMinaM,
pubmed-author:KuseNozomiN,
pubmed-author:LeligdowiczAleksandraA,
pubmed-author:LiNingN,
pubmed-author:LiWeiHuaW,
pubmed-author:McMichaelAndrewA,
pubmed-author:PengYanChunY,
pubmed-author:PowellTimT,
pubmed-author:RanasingheSrinikaS,
pubmed-author:Rowland-JonesSarahS,
pubmed-author:SaitoMasumichiM,
pubmed-author:TakiguchiMasafumiM,
pubmed-author:XiaFengF,
pubmed-author:XuKeyiK,
pubmed-author:XuXiaoNingX,
pubmed-author:YanHuiPingH,
pubmed-author:ZhangXinX,
pubmed-author:ZhangYongHongY,
pubmed-author:ZhaoYanY
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pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
187
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
684-91
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:21670313-Clone Cells,
pubmed-meshheading:21670313-Cohort Studies,
pubmed-meshheading:21670313-Cytotoxicity, Immunologic,
pubmed-meshheading:21670313-Epitopes, T-Lymphocyte,
pubmed-meshheading:21670313-HEK293 Cells,
pubmed-meshheading:21670313-HIV-1,
pubmed-meshheading:21670313-HLA-B Antigens,
pubmed-meshheading:21670313-HLA-B51 Antigen,
pubmed-meshheading:21670313-Humans,
pubmed-meshheading:21670313-Immunodominant Epitopes,
pubmed-meshheading:21670313-Mutation,
pubmed-meshheading:21670313-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:21670313-gag Gene Products, Human Immunodeficiency Virus,
pubmed-meshheading:21670313-pol Gene Products, Human Immunodeficiency Virus
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pubmed:year |
2011
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pubmed:articleTitle |
Multilayered defense in HLA-B51-associated HIV viral control.
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pubmed:affiliation |
Beijing You An Hospital, Capital Medical University, Beijing 100069, People's Republic of China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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