Source:http://linkedlifedata.com/resource/pubmed/id/21187897
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
2010-12-28
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pubmed:abstractText |
The V3 loop of the HIV-1 Env protein is the primary determinant of viral coreceptor usage, whereas the V1V2 loop region is thought to influence coreceptor binding and participate in shielding of neutralization-sensitive regions of the Env glycoprotein gp120 from antibody responses. The functional properties and antigenicity of V1V2 are influenced by changes in amino acid sequence, sequence length and patterns of N-linked glycosylation. However, how these polymorphisms relate to HIV pathogenesis is not fully understood. We examined 5185 HIV-1 gp120 nucleotide sequence fragments and clinical data from 154 individuals (152 were infected with HIV-1 Subtype B). Sequences were aligned, translated, manually edited and separated into V1V2, C2, V3, C3, V4, C4 and V5 subregions. V1-V5 and subregion lengths were calculated, and potential N-linked glycosylation sites (PNLGS) counted. Loop lengths and PNLGS were examined as a function of time since infection, CD4 count, viral load, and calendar year in cross-sectional and longitudinal analyses. V1V2 length and PNLGS increased significantly through chronic infection before declining in late-stage infection. In cross-sectional analyses, V1V2 length also increased by calendar year between 1984 and 2004 in subjects with early and mid-stage illness. Our observations suggest that there is little selection for loop length at the time of transmission; following infection, HIV-1 adapts to host immune responses through increased V1V2 length and/or addition of carbohydrate moieties at N-linked glycosylation sites. V1V2 shortening during early and late-stage infection may reflect ineffective host immunity. Transmission from donors with chronic illness may have caused the modest increase in V1V2 length observed during the course of the pandemic.
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pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/AI047734,
http://linkedlifedata.com/resource/pubmed/grant/AI058894,
http://linkedlifedata.com/resource/pubmed/grant/AI27757,
http://linkedlifedata.com/resource/pubmed/grant/AI45402,
http://linkedlifedata.com/resource/pubmed/grant/AI49109,
http://linkedlifedata.com/resource/pubmed/grant/AI52791,
http://linkedlifedata.com/resource/pubmed/grant/AI55336,
http://linkedlifedata.com/resource/pubmed/grant/AI57005,
http://linkedlifedata.com/resource/pubmed/grant/R37 AI047734-12
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
1553-7374
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
e1001228
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pubmed:meshHeading |
pubmed-meshheading:21187897-Cross-Sectional Studies,
pubmed-meshheading:21187897-Disease Progression,
pubmed-meshheading:21187897-HIV Envelope Protein gp120,
pubmed-meshheading:21187897-HIV Infections,
pubmed-meshheading:21187897-HIV-1,
pubmed-meshheading:21187897-Host-Pathogen Interactions,
pubmed-meshheading:21187897-Humans,
pubmed-meshheading:21187897-Immune Evasion,
pubmed-meshheading:21187897-Pandemics
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pubmed:year |
2010
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pubmed:articleTitle |
HIV-1 envelope subregion length variation during disease progression.
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pubmed:affiliation |
Department of Medicine, University of Washington School of Medicine, Seattle, Washington, United States of America. cemarcel@u.washington.edu
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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