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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

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Ination findings. Given the inhibition of HSV-2 replication observed after administration of tenofovir, it is biologically plausible that FTC/ TDF reduced the frequency or severity of ulcers. Unlike acyclovir, tenofovir does not require the presence of the herpes virus for drug activation, suggesting that it may suppress ulcers before phosphorylation occurs. However, topical dosing may be required

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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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Ine for drug testing. Plasma was stored at a central repository for resistance testing. We monitored adherence with electronic pill bottle monitors (MEMS 6 TrackCap, AARDEX Group, Ltd., Sion, Switzerland) for the first 2 months after subjects started antiretroviral therapy (ART). We selected a single medication for monitoring according to the following hierarchy: dosed most frequently, combination