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
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
Espite successful HCV eradication. Other complications such as development of carcinoma may be more readily amenable to more rapid risk reduction with antiviral therapy. Further studies with long periods of follow-up will be needed to address these questions. Our study has several limitations. Not all patients had measures of immune activation documented in their study records and were therefore e