D if the HSV-2 diagnosis occurred at or after HIV seroconversion, and ulcers were excluded if they occurred at or after HIV seroconversion. We estimated the proportion of participants with 1 ulcer AE classified as Gradeor above (i.e., moderate, severe, or potentially life-threatening), 1 STI examination during which a perianal ulcer was detected, and 1 STI examination during which a groin ulcer

Used acyclovir or valacyclovir during study follow-up.HSV-2 prevalenceOf the 2,499 participants, 1383 (55.3 ) tested negative for HSV-2 at baseline, 892 (35.7 ) tested positive, 223 (8.9 ) had indeterminate tests, and one test was not done. Of the 223 with indeterminate tests at baseline, 114 (51.1 ) tested positive for HSV-2 infection at some point during follow-up. Factors associated with testin

Istically significant period effect was found (P values i0.52). The primary statistical analysis gave an estimate of the reduction in saquinavir exposure when coadministered with rifabutin, as measured by AUC(0,8 h) and Cmax(0,8 h) of 47 (95 CI 30, 60 ) and 39 (95 CI 11, 59 ), respectively. Figure 1 illustrates the plasma concentrationtime profiles for saquinavir when administered alone (Treat

Nt populations [6,7]. Opioid treatment programs (OTPs) provide a potential framework for DAART because patients visit multiple times each week to receive opioid agonist medication. Moreover, maintenance treatment at OTPs permits prolonged DAART, which is difficult in models based on outreach workers. Based on promisingDirectly Administered Therapy for HIVFigure 1. Study screening, enrollment, and

Ing administration of rifabutin 300 mg once daily (Treatment A, #) or rifabutin 300 mg once daily plus SQV-SGC 1200 mg three times daily (Treatment C, ).treatment was greater (33 ) compared to when coadministered with saquinavir (21 ). The within patient variability was approximately 29 .Effects of rifabutin on saquinavirpharmacokineticsThe mean ( CV) AUC(0,8 h), Cmax and C8 for saquinavir when a

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A and adjusting for differences based on sex, we no longer see this correlation. In addition, in this study, HCV coinfection is not associated with loss of elite controller status. Taken together, this suggests that HCV coinfection does not directly affect HIV replication dynamics or natural history, but that it may act synergistically with HIV to produce a greater number of associated complicatio

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