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dc.contributor.authorChoi, RY
dc.contributor.authorFarquhar, C
dc.contributor.authorJuno, J
dc.contributor.authorMbori-Ngacha, DA
dc.contributor.authorLohman-Payne, B
dc.contributor.authorVouriot, F
dc.contributor.authorWayne, S
dc.contributor.authorTuff, J
dc.contributor.authorBosire, R
dc.contributor.authorJohn-Stewart, G
dc.contributor.authorFowke, K
dc.date.accessioned2013-06-10T12:29:18Z
dc.date.available2013-06-10T12:29:18Z
dc.date.issued2010-06
dc.identifier.citationClin Exp Immunol. 2010 Jun;160(3):461-5en
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/pubmed/20132229
dc.identifier.urihttp://erepository.uonbi.ac.ke:8080/xmlui/handle/123456789/30804
dc.description.abstractThe C868T single nucleotide polymorphism (SNP) in the CD4 receptor encodes an amino acid change that could alter its structure and influence human immunodeficiency virus (HIV-1) infection risk. HIV-1-infected pregnant women in Nairobi were followed with their infants for 1 year postpartum. Among 131 infants, those with the 868T allele were more likely than wild-type infants to acquire HIV-1 overall [hazard ratio (HR) = 1.92, 95% confidence interval (CI) 1.05, 3.50, P = 0.03; adjusted HR = 2.03, 95% CI 1.03, 3.98, P = 0.04], after adjusting for maternal viral load. This SNP (an allele frequency of approximately 15% in our cohort) was associated with increased susceptibility to mother-to-child HIV-1 transmission, consistent with a previous study on this polymorphism among Nairobi sex workers.en
dc.language.isoenen
dc.publisherUniversity of Nairobi.en
dc.titleInfant CD4 C868T polymorphism is associated with increased human immunodeficiency virus (HIV-1) acquisitionen
dc.typeArticleen
local.publisherDepartment of Paediatrics and Child Health, Univeristy of Nairobi, Kenyaen


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