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
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
Es would most likely not have been affected. The measures of immune activation were not assessed at enrollment into the study cohort, and we therefore cannot make temporal inferences of a causal nature nor could we control for them in the multivariable Cox models. We used prevalence rate ratios (PRRs) to estimate the associations of interest as risk was our parameter of interest. We chose PRRs as
Es would most likely not have been affected. The measures of immune activation were not assessed at enrollment into the study cohort, and we therefore cannot make temporal inferences of a causal nature nor could we control for them in the multivariable Cox models. We used prevalence rate ratios (PRRs) to estimate the associations of interest as risk was our parameter of interest. We chose PRRs as
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
Es would most likely not have been affected. The measures of immune activation were not assessed at enrollment into the study cohort, and we therefore cannot make temporal inferences of a causal nature nor could we control for them in the multivariable Cox models. We used prevalence rate ratios (PRRs) to estimate the associations of interest as risk was our parameter of interest. We chose PRRs as
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
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