8% to the model. To evaluate the effect of HCV and liver fibrosis parameters in the absence of the effects of ART, we also analysed specifically the subgroup of 110 patients who did not receive ART. The parameters predictive of higher BI6727 CD4 cell count were higher nadir CD4 cell

count (P<0.0001), which by itself explained 83.1% of the total variability in current CD4 cell count, and older age (P=0.006). The remaining parameters, including HCV- and liver fibrosis-related parameters, did not reach the P<0.05 level, although the annual fibrosis progression index was close to it (P=0.06). The variables independently associated with higher HIV-1 viral load in untreated PF-02341066 supplier patients were lower CD4 cell count (P<0.0001), younger age (P=0.008), worse CDC clinical stage (P=0.02) and current IDU (P=0.04), accounting for 36.4% of the variability in viral load. HCV and liver fibrosis parameters were not close

to reaching statistical significance. Apart from the study group with active HCV replication, we also recorded the same data for a group of 200 coinfected patients who had cleared the HCV infection, either spontaneously or as a result of anti-HCV therapy. These patients had similar CD4 cell counts and HIV-1 viral loads as patients who had active replication of HCV in the whole group (P=0.5 and P=0.8, respectively). Similar findings were also obtained in the subgroup of patients who were not receiving ART (CD4 cell count, P=0.5; HIV-1 viral load, P=0.4). Multivariate analysis did not show HCV eradication to be independently associated with CD4 cell count or HIV-1 viral load, either in the whole group (P=0.9 and P=0.3, respectively) SB-3CT or in the subgroup of patients not receiving ART (P=0.1 and P=0.3, respectively). In our study on a large population of HIV-1-infected patients with active HCV infection, we found that HCV-related variables did not significantly influence the virological and immunological outcomes of HIV-1 infection, after adjusting for other covariates. In contrast, liver fibrosis, as measured using the annual fibrosis progression

index, was independently predictive of CD4 cell count, although its influence was relatively small. A number of studies analysing the effect of HCV infection on clinical and HIV-1 viroimmunological parameters have been published, with contradictory results, mainly attributable to different designs, sample sizes, outcomes evaluated and patients’ characteristics. Regarding clinical outcomes, some studies reported that there was no significant effect of HCV on clinical progression to AIDS or death [1,7,28–33,36,37]. However, despite the absence of differences overall, some studies, not surprisingly, found that morbidity and mortality related to liver damage were more common in HIV-1/HCV-coinfected patients [1,36].