Is HDL-c plasma concentration a possible marker of HIV replication? A cross-sectional analysis in untreated HIV-infected individuals accessing HIV care in Italy

Abstract

AimsHIV infection is associated with dyslipidemia and an increased risk for cardiovascular diseases. HIV Nef protein downregulates the generation of nascent HDL. The interplay between HIV-RNA, HDL-c level and CD4/CD8 ratio in naive HIV patients remains to be elucidated. MethodsWe included untreated persons living with HIV (PLWH) of the ICONA Foundation Study cohort if they also had [&ge;]2 viral load (VL) measurements prior to ART initiation. We performed unadjusted correlation and linear regression analyses evaluating the effect of VLset on HDL-C. Vlset and CD4/CD8 ratio were fit in the log10 scale, while HDL-c, was fitted in the untransformed raw scale. ResultsWe included 3,980 untreated PLWH. Fifty-eighty (1.5%) were aviremic. We observed a negative correlation between HDL-c and VLset (Pearson R2=0.03), from fitting an unadjusted linear regression model -8.5 mg/dl (95% CI: -15,9 --0,84 p<0.03). There was a dose-response relationship between HDL-c levels and VLset, however, this association was somewhat attenuated after further controlling for gender. Despite a positive correlation between HDL-c and CD4/CD8 ratio, the HDL-c plasma concentration does not satisfy the criteria for a strong surrogate marker. ConclusionsOur data show that HDL-c plasma concentration is significantly lower per higher level of VLSet although this was in part explained by gender. Further analyses should be promoted to better understand the molecular mechanisms that underline the relationship between HIV replication, HDL-c formation, and diseases progression.