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Blood, Vol. 95 No. 10 (May 15), 2000:
pp. 3191-3198
Alteration of tumor necrosis factor- T-cell homeostasis
following potent antiretroviral therapy: contribution to the
development of human immunodeficiency virus-associated lipodystrophy
syndrome
Eric Ledru,
Névéna Christeff,
Olivier Patey,
Pierre de
Truchis,
Jean-Claude Melchior, and
Marie-Lise Gougeon
From the Unité d'Oncologie Virale, URA CNRS 1930, Département SIDA et Rétrovirus, Institut Pasteur, Paris,
France; the Service des Maladies Infectieuses et Tropicales, Centre
Hospitalier Intercommunal, Villeneuve Saint Georges, France; and the
Service des Maladies Infectieuses et Tropicales, Hôpital Raymond
Poincaré, Garches, France.
Highly-active antiretroviral therapy (HAART) has lead to a dramatic
decrease in the morbidity of patients infected with the human
immunodeficiency virus (HIV). However, metabolic side effects, including lipodystrophy-associated (LD-associated) dyslipidemia, have
been reported in patients treated with antiretroviral therapy. This
study was designed to determine whether successful HAART was
responsible for a dysregulation in the homeostasis of tumor necrosis
factor- (TNF-), a cytokine involved in lipid metabolism. Cytokine
production was assessed at the single cell level by flow cytometry
after a short-term stimulation of peripheral blood T cells from
HIV-infected (HIV+) patients who were followed during 18 months of HAART. A dramatic polarization to TNF- synthesis of both
CD4 and CD8 T cells was observed in all patients. Because it was
previously shown that TNF- synthesis by T cells was highly
controlled by apoptosis, concomitant synthesis of TNF- and priming
for apoptosis were also analyzed. The accumulation of T cells primed
for TNF- synthesis is related to their escape from
activation-induced apoptosis, partly due to the cosynthesis of
interleukin-2 (IL-2) and TNF-. Interestingly, we observed that LD is
associated with a more dramatic TNF- dysregulation, and positive
correlations were found between the absolute number of TNF- CD8
T-cell precursors and lipid parameters usually altered in LD including
cholesterol, triglycerides, and the atherogenic ratio apolipoprotein B
(apoB)/apoA1. Observations from the study indicate that HAART
dysregulates homeostasis of TNF- synthesis and suggest that this
proinflammatory response induced by efficient antiretroviral therapy is
a risk factor of LD development in HIV+ patients.
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