dc.contributor.author | Beima-Sofie, K | |
dc.contributor.author | Wamalwa, D | |
dc.contributor.author | Maleche-Obimbo, E | |
dc.contributor.author | Lingappa, JR | |
dc.contributor.author | Mackelprang, R | |
dc.contributor.author | Gantt, S | |
dc.contributor.author | John-Stewart, G | |
dc.contributor.author | Casper, C | |
dc.contributor.author | Slyker, JA. | |
dc.date.accessioned | 2017-12-14T06:56:46Z | |
dc.date.available | 2017-12-14T06:56:46Z | |
dc.date.issued | 2017 | |
dc.identifier.citation | 10.1097/QAD.0000000000001680. [Epub ahead of print] | en_US |
dc.identifier.uri | https://www.ncbi.nlm.nih.gov/pubmed/29112074 | |
dc.identifier.uri | http://hdl.handle.net/11295/101885 | |
dc.description.abstract | Polymorphisms 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.iso | en | en_US |
dc.publisher | University of Nairobi | en_US |
dc.rights | Attribution-NonCommercial-NoDerivs 3.0 United States | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/3.0/us/ | * |
dc.title | Toll-Like Receptor (TLR) 9 polymorphism is associated with increased Epstein-Barr virus and Cytomegalovirus acquisition in HIV-exposed infants. | en_US |
dc.type | Article | en_US |