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Blood, Vol. 93 No. 12 (June 15), 1999:
pp. 4232-4241
Infection With Human Immunodeficiency Virus-1 Increases Expression
of Vascular Endothelial Cell Growth Factor in T Cells: Implications
for Acquired Immunodeficiency Syndrome-Associated Vasculopathy
G. Ascherl,
C. Hohenadl,
O. Schatz,
E. Shumay,
J. Bogner,
L. Eckhart,
E. Tschachler,
P. Monini,
B. Ensoli, and
M. Stürzl
From the Department of Virology, Max Planck Institute for
Biochemistry, Martinsried, Germany; the Institute of Molecular
Virology, GSF-National Research Center for Environment and Health,
Neuherberg, Germany; the Policlinic of the Ludwig Maximilians
University, Munich, Germany; the Department of Dermatology, University
of Vienna, Medical School, Vienna, Austria; the Laboratory of Virology,
Istituto Superiore di Sanità, Rome, Italy; and the Bavarian
Nordic Research Institute/AS, Martinsried, Germany.
Alterations in the vascular system and the onset of
angioproliferative lesions such as Kaposi's sarcoma (KS) are common
traits of human immunodeficiency virus-1 (HIV-1)-infected patients. To investigate possible factors involved in acquired immunodeficiency syndrome (AIDS)-associated vasculopathy and vascular malfunction, expression of vascular endothelial cell growth factor-A (VEGF-A) was
analyzed in HUT 78 T lymphocytes upon infection with HIV-1. VEGF-A was found to be increased in supernatants from infected cells as
compared with uninfected cells. In addition, VEGF-A mRNA expression and
protein secretion were significantly increased in HUT 78 cells
incubated with conditioned medium (CM) derived from HIV-1 chronically
infected HUT 78 cells (HIV-TCM) as compared with CM from uninfected
cells (TCM). Increase of VEGF-A production in T cells was promoted by
inflammatory cytokines (IC) present in HIV-TCM, including tumor
necrosis factor  (TNF), interferon  (IFN), interleukin-1
(IL-1), and IL-6. These IC that have been shown to be increased in
sera of HIV-1-infected patients and to be increased by HIV-1 infection
or cell activation in these individuals as well as HIV-TCM also
increased VEGF-A expression in primary T lymphocytes. Consistent with
this, VEGF-A concentrations were found to be higher in sera of
HIV-1-infected patients with (mean, 357.1 ± 197.9 pg/mL) and without
KS (mean, 256.7 ± 137.5 pg/mL) as compared with uninfected
individuals (mean, 188.6 ± 91.7 pg/mL). These data suggest that
increased secretion of VEGF-A by T lymphocytes of
HIV-1-infected individuals may induce vascular leakage and stimulate
proliferation of vascular endothelial cells, which are hallmarks of
AIDS-associated vasculopathy and especially of KS development.
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