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Background: It is uncertain whether episodic acyclovir will enhance ulcer healing if delivered at primary health care settings, because there is often a delay in treatment initiation., Methods: A double-blind, randomized, placebo-controlled trial of 5-day acyclovir (400 mg 3 times daily) was conducted among men with genital ulcers in South Africa. Participants received syndromic management; were tested for ulcer etiology, human immunodeficiency virus (HIV), syphilis, and herpes simplex virus type 2 (HSV-2); and were seen over the course of a month to evaluate ulcer healing and HIV-1 RNA shedding. Outcomes were ulcer duration and HIV-1 RNA shedding, assessed on day 7 among HIV-1-seropositive participants with a herpetic ulcer., Results: A total of 309 men received acyclovir, and 306 received placebo; 63% were HIV-1 positive. There were 295 HIV-1-positive participants with a herpetic ulcer. Acyclovir improved ulcer healing--61% of those receiving acyclovir healed by day 7, compared with 42% of those receiving placebo (adjusted relative risk, 1.4 [95% confidence interval, 1.1-1.8]; P= .003). Acyclovir also improved healing by a median of 3 days (P= .002) and reduced HIV-1 ulcer shedding on day 7 (24% for acyclovir vs 37% for placebo; P= .05)., Conclusions: Addition of acyclovir to syndromic management will improve healing of genital ulcers and may potentially reduce HIV transmission in combination with other interventions.

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/mm3. 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. [ABSTRACT FROM AUTHOR]