Source:http://linkedlifedata.com/resource/pubmed/id/11181160
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
|
| pubmed:dateCreated |
2001-2-22
|
| pubmed:abstractText |
The effect of CC-chemokine receptor 5 (CCR5) promoter polymorphisms on the natural history of human immunodeficiency virus (HIV) disease was studied in 73 HIV-1-infected children. The CCR5(59338-59537) promoter haplotype, CCR5-59029A/G polymorphism, and CCR5Delta32 and CCR2-64I alterations were investigated. After exclusion of carriers of CCR5Delta32 or CCR2-64I, Kaplan-Meier analysis disclosed that children with the P1/P1(59353C,59356C,59402A) genotype progressed faster to disease than did children with other haplotypes (P=.016). When CCR2-64I carriers were included, this effect had borderline significance (P=.065) and was lost when CCR5Delta32 carriers were also considered (P=.387). The P1/P1 effect was strongest early after infection, when progression to disease was mainly associated with CCR5 coreceptor-using viruses. These results indicate that the P1/P1 genotype is predictive of rapid progression in HIV-1-infected children lacking CCR5Delta32 or CCR5-64I alleles. The observation of a linkage disequilibrium between P1 and 59029A might explain the previously reported association between 59029A homozygosity and rapid disease progression.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0022-1899
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
183
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
814-8
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:11181160-Adolescent,
pubmed-meshheading:11181160-Adult,
pubmed-meshheading:11181160-Age Factors,
pubmed-meshheading:11181160-Alleles,
pubmed-meshheading:11181160-Child,
pubmed-meshheading:11181160-Child, Preschool,
pubmed-meshheading:11181160-Disease Progression,
pubmed-meshheading:11181160-Female,
pubmed-meshheading:11181160-HIV Infections,
pubmed-meshheading:11181160-HIV-1,
pubmed-meshheading:11181160-Haplotypes,
pubmed-meshheading:11181160-Humans,
pubmed-meshheading:11181160-Infant,
pubmed-meshheading:11181160-Infant, Newborn,
pubmed-meshheading:11181160-Infectious Disease Transmission, Vertical,
pubmed-meshheading:11181160-Linkage Disequilibrium,
pubmed-meshheading:11181160-Male,
pubmed-meshheading:11181160-Perinatal Care,
pubmed-meshheading:11181160-Point Mutation,
pubmed-meshheading:11181160-Polymorphism, Genetic,
pubmed-meshheading:11181160-Promoter Regions, Genetic,
pubmed-meshheading:11181160-Receptors, CCR5
|
| pubmed:year |
2001
|
| pubmed:articleTitle |
Polymorphisms in the CCR5 promoter region influence disease progression in perinatally human immunodeficiency virus type 1-infected children.
|
| pubmed:affiliation |
Department of Oncology and Surgical Sciences, Oncology Section, AIDS Reference Center, Via Gattamelata 64, 35128 Padova, Italy.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|