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O predict the probability of having detectable drug and the probability that the level of tenofovir diphosphate (TFV-DP) in PBMCs was .16 fmol per million viable cells, the concentration associated with an estimated 90 reduction in HIV acquisition. [15] Drug levels were multiply imputed [16] for visits at which drug level testing was not conducted but the participant was still taking study drug,

Infection in vitro, this protein was tested for clinical efficacy in HIV-1-infected individuals; however, no effect on plasma viral loads was observed [13]. Further examination revealed that doses of sCD4 that were significantly higher than those achieved in the clinical trial were required to neutralize primary clinical isolates of HIV-1, in contrast to the relatively sensitive, laboratory-adapte

Infection in vitro, this protein was tested for clinical efficacy in HIV-1-infected individuals; however, no effect on plasma viral loads was observed [13]. Further examination revealed that doses of sCD4 that were significantly higher than those achieved in the clinical trial were required to neutralize primary clinical isolates of HIV-1, in contrast to the relatively sensitive, laboratory-adapte

Lications, even after controlling for CD4+ Tcell level, sex, and older age. Chronic inflammation is thought to be associated with CD4+ T-cell depletion and higher levels of immune activation.[21,26] Similarly, HCV coinfection remained significantly associated with a higher prevalence of complications when individual immune activation markers were controlled for. This study found that HCV coinfecte

N of cRAI in the past three months being reported more frequently in the placebo arm (P = 0.01). Of the 1,383 participants who tested seronegative for HSV-2 at baseline, 36 (2.6 ) did not contribute person-time to incidence analyses because they were retrospectively found to be HIVinfected at baseline, tested seropositive for HSV-2 at the enrollment visit subsequent to screening, or were lost to f

N of cRAI in the past three months being reported more frequently in the placebo arm (P = 0.01). Of the 1,383 participants who tested seronegative for HSV-2 at baseline, 36 (2.6 ) did not contribute person-time to incidence analyses because they were retrospectively found to be HIVinfected at baseline, tested seropositive for HSV-2 at the enrollment visit subsequent to screening, or were lost to f

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