516, P=0.03), CD4 lymphocyte count<50 cells/μL (r=0.626, P<0.001), CD4 lymphocyte count between 50 and 200 cells/μL (r=0.617, P<0.001) and BMI (r=0.701, P=0.0002). No correlations were observed among TC (r=0.051; P=0.143), LDLC (r=−0.020; P=0.710) and CD4 count<200 cells/μL. There was also no association between lipid

parameters and CD4 count>200 cells/μL in HIV-infected patients (groups 3 and 4). TC:HDLC and LDLC:HDLC ratios were highly positively correlated (r=0.641; P=0.005 and r=0.512; P=0.003 respectively) with low CD4 count (groups 1 and 2) and with the occurrence RAD001 order of OIs (r=0.602; P=0.0003 and r=0.520; P=0.002, respectively). Our study confirms previous reports of a higher prevalence of HIV infection in women

than in men [25], and in the 31–49-year age group [24]. Most HIV-positive subjects were in categories B and C of CDC/Organisation Mondiale de la Santé (OMS) [25]. This may be because the HIV-infected patients were not on treatment; most them (74.41%) had CD4 counts<200 cells/μL. The variations found in lipid parameters in HIV-positive subjects in this study are comparable to those of Grunfeld et al. [26], Henry et al. [27], Ducobu and Payen [28], Lando et al. [5] and Oumarou et al. [7]. In the study of Grunfeld et al. [26], TC was lower in HIV-positive patients than in controls, but the difference was not significant. It has been found that HIV infection induces a progressive increase in TG and progressive Selleck SAHA HDAC reductions in TC, HDLC and LDLC as reported by Ducobu and Payen [28]. The observed alteration of cholesterol metabolism in HIV-infected patients may be explained by lipid peroxidation, as suggested by Constans et al. [29]. The cytokine tumour necrosis factor

(TNF)-α has been found to play a role in plasma lipoprotein peroxidation in HIV-infected patients by stimulating the production of reactive oxygen species [30]. These modifications may have major effects (-)-p-Bromotetramisole Oxalate on the immune system. Apo A1 can interfere with HIV-induced syncitium formation (a late event in HIV disease), and a decrease in Apo A1 might accelerate the course of HIV infection [31]. Malnutrition can also induce disturbances in lipids, in association with increases in some cytokines (e.g. TNF and interleukin 1) [32]. In addition, it seems that the increase in TG is linked to decreases in the activities of lipoprotein lipases and hepatic lipases [26,32], because the half-life of particles rich in TG in AIDS patients is three-times higher than in HIV-negative individuals [28]. Further, it has been shown that during viral infections the cholesterol level drops whereas the TG level rises [12,15]. However, the mechanisms responsible for these alterations have not generally been established. The relationships we found here between the lipid parameters and CD4 cell count are consistent with those found by Constans et al.