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dc.contributor.authorLavreys, L
dc.contributor.authorBaeten, JM
dc.contributor.authorKreiss, JK
dc.contributor.authorRichardson, BA
dc.contributor.authorChohan, BH
dc.contributor.authorHassan, W
dc.contributor.authorPanteleeff, DD
dc.contributor.authorMandaliya, K
dc.contributor.authorNdinya-Achola Jeckoniah O
dc.contributor.authorOverbaugh, J
dc.date.accessioned2013-04-25T07:21:08Z
dc.date.available2013-04-25T07:21:08Z
dc.date.issued2004
dc.identifier.citationJ Infect Dis. 2004 Jan 15;189(2):303-11en
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/pubmed/14722896
dc.identifier.urihttp://erepository.uonbi.ac.ke:8080/xmlui/handle/123456789/16683
dc.description.abstractWe examined the association between host factors present near the time of human immunodeficiency virus type 1 (HIV-1) acquisition and subsequent virus loads, in a prospective cohort study of women in Mombasa, Kenya. Women were prospectively followed monthly before HIV-1 infection. One hundred sixty-one commercial sex workers who became infected with HIV-1 were followed for a median of 34 months, and 991 plasma samples collected > or =4 months after infection were tested for HIV-1 RNA. The median virus set point at 4 months after infection was 4.46 log10 copies/mL, and the average virus load increase during subsequent follow-up was 0.0094 log10 copies/mL/month. In a multivariate analysis that controlled for sexual behavior, the use of the injectable contraceptive depot medroxyprogesterone acetate (DMPA) at the time of HIV-1 infection was associated with a higher virus set point, and the presence of genital ulcer disease (GUD) during the early phase of HIV-1 infection was associated with greater change in virus load during follow-up. These findings suggest that, in women, the use of DMPA and the presence of GUD during the early phase of HIV-1 infection may influence the natural course of infection.en
dc.language.isoenen
dc.titleInjectable contraceptive use and genital ulcer disease during the early phase of HIV-1 infection increase plasma virus load in women.en
dc.typeArticleen
local.publisherDepartment of Epidemiology, Medicine, and Biostatistics, University of Washington, Seattle, Washington 98104-2499, USAen
local.publisherDepartment of Medical Microbiology, University of Nairobien


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