R. Zangerle et al., DECREASED PLASMA-CONCENTRATIONS OF HDL CHOLESTEROL IN HIV-INFECTED INDIVIDUALS ARE ASSOCIATED WITH IMMUNE ACTIVATION, Journal of acquired immune deficiency syndromes, 7(11), 1994, pp. 1149-1156
We investigated 63 individuals with HIV infection, 34 of whom were asy
mptomatic (nine had oral candidiasis, four had constitutional signs an
d symptoms, and 16 had AIDS), for plasma lipids, soluble tumor necrosi
s factor receptor 75 (sTNF-R75) and other immune activation markers, n
amely urinary neopterin, beta 2-microglobulin, and the CD4(+) T cell c
ount. The median CD4(+) T cell count was 318 x 10(6)/L. All individual
s were allowed to have light breakfast in the morning; the venipunctur
e for the plasma lipids was done between 11 a.m. and 3 p.m.. Decreased
plasma concentrations were found for total cholesterol, and HDL and L
DL cholesterol in 3.2%, 46%, and 56% of the subjects, respectively. Pl
asma triglyceride levels were increased in 31.7% of the study populati
on. The frequency and the extent of the decrease of HDL and LDL choles
terol and the increase in triglyceride levels were greater in those wi
th a CD4(+) T cell count below the median (p = 0.003, p = 0.05, and p
= 0.01); when comparing individuals with CD4(+) T cell counts above an
d below 500 x 10(6)/L (19 individuals), a difference was only found fo
r HDL cholesterol (p = 0.01). Plasma levels of triglycerides correlate
d significantly however weakly with serum concentrations of sTNF-R75 (
r(s) = 0.32, p = 0.01) but not at all with urinary neopterin or serum
beta 2-microglobulin. HDL cholesterol correlated inversely with sTNF-R
75 (r(s) = -0.53, p < 0.0001) and to a lesser extent with urinary neop
terin(r(s) = -0.46, p = 0.0003) and beta(2)-microglobulin (r(s) = -0.3
4, p = 0.008). When only the individuals with a CD4(+) T cell count ab
ove the median or 500 x 10(6)/L were analyzed, HDL cholesterol correla
ted with sTNF-R75 (r(s) = -0.45, p = 0.01 or r(s) = -0.38, p > 0.05),
but no longer with urinary neopterin and beta 2-microglobulin. Immune
activation in HIV infection is associated with disturbances in lipid m
etabolism, which may influence biological properties of HIV. HDL chole
sterol may also be a useful marker of disease progression.