EXPRESSION OF ALPHA-FETOPROTEIN AND INTERLEUKIN-2 RECEPTORS AND IMPAIRMENT OF MEMBRANE FLUIDITY IN PERIPHERAL-BLOOD MONONUCLEAR-CELLS FROM AIDS AND RELATED SYNDROMES
A. Macho et al., EXPRESSION OF ALPHA-FETOPROTEIN AND INTERLEUKIN-2 RECEPTORS AND IMPAIRMENT OF MEMBRANE FLUIDITY IN PERIPHERAL-BLOOD MONONUCLEAR-CELLS FROM AIDS AND RELATED SYNDROMES, AIDS research and human retroviruses, 10(8), 1994, pp. 995-1001
We have previously shown that the expression of a-fetoprotein (AFP) re
ceptors is impaired in mitogen-activated peripheral blood mononuclear
cells (PBMCs) from HIV+ individuals and that this novel abnormality re
flects an unusual proliferation response of PBMCs to mitogenic stimuli
. Here we comparatively analyze, in PBMCs from patients with AIDS and
related syndromes, (1) changes in membrane fluidity, measured as the c
holesterol/phospholipid ratio (CH/PL), and (2) changes in the expressi
on of AFP receptors and of the a chain of the IL-2 receptor (TAC antig
en). Relative to normal cells, the expression of AFP and IL-2 receptor
s appeared considerably reduced in AIDS-related complex (ARC) and AIDS
patients. In asymptomatic HIV+ individuals the amount of AFP receptor
s was within the normal range, whereas that of IL-2 receptors increase
d twice. CWPL ratios were significantly lower in PHA-activated than in
quiescent PBMCs from healthy donors, which implies a gain in membrane
fluidity. For seropositive groups, no statistically significant chang
es in CWPL ratios were appreciated on PHA activation, Nevertheless, in
HIV+ asymptomatic individuals, the CWPL ratio of quiescent PBMCs rese
mbled that of PHA-activated PBMCs from healthy donors, suggesting that
quiescent PBMCs are in a partially activated or ''preactivated'' stat
us. With the worsening of the disease, toward ARC and AIDS stages, how
ever, quiescent PBMCs from these groups showed a considerable loss in
membrane fluidity, evidenced by elevated values of the CH/PL ratio. Th
is radical change strongly suggest a severe alteration of the lipid me
tabolism in these cells. Thus, HIV infection impairs the fluidity of t
he cell membrane and, because the latter influences a large number of
cellular functions, it may contribute to the progress of the disease b
y altering normal sequences of lymphocyte activation and blastic trans
formation.