Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2010
Determinants of HIV type 1 shedding from genital ulcers among men in South Africa.
СтатьяПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод в очереди
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Paz-Bailey Gabriela, Sternberg Maya, Puren Adrian J, Steele Lisa, Lewis David A
Аннотация
BACKGROUND: Our study evaluated correlates of human immunodeficiency virus (HIV)-1 lesional shedding among men with genital ulcer disease (GUD).
METHODS: Participants were recruited at primary health care clinics as part of a randomized trial of episodic acyclovir among men with GUD. This analysis was done among HIV-positive men identified at baseline. Participants were serologically screened for HIV infection, syphilis, and herpes simplex virus type 2 infection and for urethritis and ulcer etiology by polymerase chain reaction. Plasma and genital ulcer HIV-1 loads and CD4 cell counts were quantified. We evaluated variables associated with the presence and quantity of HIV-1 in ulcers.
RESULTS: Among 387 HIV-positive men, the median plasma HIV-1 load and CD4 cell count were 87,200 copies/mL and 282 cells/mm(3). Overall, 173 (45.6%) had detectable HIV-1 RNA in ulcers. Men with Trichomonas vaginalis infection had higher ulcer viral loads on average than did those who were not infected (mean difference, 0.62; 95% confidence interval [CI], 0.07-1.2; P=.027). After multivariable analysis, higher plasma HIV-1 load (odds ratio [OR], 2.5; 95% CI, 1.7-3.5; P< .001), larger lesions (OR, 2.5; 95% CI, 1.5-4.1; P < .001), purulent ulcers (OR, 2.2; 95% CI, 1.1-4.2; P <.02), multiple ulcers (>5; OR, 3.6; 95% CI, 1.6-8.4; P=.002), and herpes seropositivity (OR, 3.4; 95% CI, 1.7-7.0; P < .001) remained associated with increased odds of HIV-1 lesional shedding. Ulcers associated with herpes simplex virus type 2 infection were less likely to shed (OR, 0.6; 95% CI, 0.3-1.0; P =.05), compared with ulcers with unknown etiology.
CONCLUSIONS: HIV-positive men should be screened and treated for GUD to minimize HIV shedding and transmission to uninfected sexual partners.
METHODS: Participants were recruited at primary health care clinics as part of a randomized trial of episodic acyclovir among men with GUD. This analysis was done among HIV-positive men identified at baseline. Participants were serologically screened for HIV infection, syphilis, and herpes simplex virus type 2 infection and for urethritis and ulcer etiology by polymerase chain reaction. Plasma and genital ulcer HIV-1 loads and CD4 cell counts were quantified. We evaluated variables associated with the presence and quantity of HIV-1 in ulcers.
RESULTS: Among 387 HIV-positive men, the median plasma HIV-1 load and CD4 cell count were 87,200 copies/mL and 282 cells/mm(3). Overall, 173 (45.6%) had detectable HIV-1 RNA in ulcers. Men with Trichomonas vaginalis infection had higher ulcer viral loads on average than did those who were not infected (mean difference, 0.62; 95% confidence interval [CI], 0.07-1.2; P=.027). After multivariable analysis, higher plasma HIV-1 load (odds ratio [OR], 2.5; 95% CI, 1.7-3.5; P< .001), larger lesions (OR, 2.5; 95% CI, 1.5-4.1; P < .001), purulent ulcers (OR, 2.2; 95% CI, 1.1-4.2; P <.02), multiple ulcers (>5; OR, 3.6; 95% CI, 1.6-8.4; P=.002), and herpes seropositivity (OR, 3.4; 95% CI, 1.7-7.0; P < .001) remained associated with increased odds of HIV-1 lesional shedding. Ulcers associated with herpes simplex virus type 2 infection were less likely to shed (OR, 0.6; 95% CI, 0.3-1.0; P =.05), compared with ulcers with unknown etiology.
CONCLUSIONS: HIV-positive men should be screened and treated for GUD to minimize HIV shedding and transmission to uninfected sexual partners.