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dc.contributor.authorBeima-Sofie, K
dc.contributor.authorWamalwa, D
dc.contributor.authorMaleche-Obimbo, E
dc.contributor.authorLingappa, JR
dc.contributor.authorMackelprang, R
dc.contributor.authorGantt, S
dc.contributor.authorJohn-Stewart, G
dc.contributor.authorCasper, C
dc.contributor.authorSlyker, JA.
dc.date.accessioned2017-12-14T06:56:46Z
dc.date.available2017-12-14T06:56:46Z
dc.date.issued2017
dc.identifier.citation10.1097/QAD.0000000000001680. [Epub ahead of print]en_US
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pubmed/29112074
dc.identifier.urihttp://hdl.handle.net/11295/101885
dc.description.abstractPolymorphisms in the Toll-Like Receptor (TLR9) 1635 locus have been associated with HIV-1 acquisition and progression. Cytomegalovirus (CMV) and Epstein-Barr virus (EBV) acquisition were compared between Kenyan HIV-exposed infants by 1635 genotype. Having 1 or more copies of the 1635A allele was associated with increased CMV acquisition in HIV-infected infants (42% vs 11%, p = 0.03) and increased risk of EBV acquisition in HIV-exposed uninfected infants (HR = 4.2, p = 0.02) compared to 1635GG. Additionally, 1635A was associated with 0.4 log10 copies/ml lower median EBV levels in HIV-infected infants (p = 0.03). These data suggest a potentially important role for this locus in primary herpesvirus infection.en_US
dc.language.isoenen_US
dc.publisherUniversity of Nairobien_US
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/us/*
dc.titleToll-Like Receptor (TLR) 9 polymorphism is associated with increased Epstein-Barr virus and Cytomegalovirus acquisition in HIV-exposed infants.en_US
dc.typeArticleen_US


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