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T-cell death by apoptosis in vertically human immunodeficiency virus-
infected children coincides with expansion of CD8+/interleukin-2
receptor-/HLA-DR+ T cells: sign of a possible role for herpes viruses as
cofactors?
RP Lauener, S Huttner, M Buisson, JP Hossle, M Albisetti, JM Seigneurin, RA Seger and D Nadal
Division of Immunology/Hematology, University Children's Hospital, Zurich,
Switzerland.
One mechanism proposed to play a role in T-cell depletion in human
immunodeficiency virus (HIV) infection is apoptosis (activation-induced
cell death). We assessed whether apoptosis is related to activation of T
cells in vivo and its possible triggers. DNA was extracted from peripheral
blood mononuclear cells (PBMC) taken from 16 vertically HIV- infected
children and 9 HIV-negative children born to HIV-positive mothers
(controls) and tested by agarose gel electrophoresis for the presence of
DNA fragments specific for apoptosis. Signs of apoptosis were found on in
vitro culture of PBMC from 12 of 16 HIV-infected children, but not in PBMC
from the nine controls. Eleven of the 12 HIV- infected children with
apoptosis showed an elevated (> 15%) proportion of CD3+/HLA-DR+ cells.
This was due to an increased proportion of CD8+/HLA-DR+ cells, as shown in
7 of 7 further tested patients. In none of the probands an increased (>
5%) proportion of IL-2 receptor expressing CD3+ cells was found. T cells
undergoing apoptosis were preferentially of the CD8+ phenotype. Expansion
of circulating CD8+/interleukin-2 receptor (IL-2R)-/HLA-DR+ T cells is
known to occur during active infection with herpes viruses. To investigate
the possible role of herpes viral coinfections for apoptosis in HIV
infection, we focused on Epstein-Barr virus (EBV) as an example for a
herpes virus usually acquired during childhood. In 10 of 12 patients with
apoptosis, we found increased levels of EBV genome in PBMC and/or tissues,
indicating active EBV replication. By contrast, no increased burden of EBV
was found in the four HIV-infected patients without apoptosis or in the
controls. Our data indicate that in children the occurrence of apoptosis in
HIV infection is closely related to activation of CD8+ T cells.
Furthermore, primoinfection with or reactivation of herpes viruses, such as
EBV, may substantially contribute to such T-cell activation and the ensuing
apoptosis. Additional studies are warranted to evaluate the contribution of
herpes virus-triggered apoptosis to the T-cell loss leading to the acquired
immunodeficiency syndrome.
Volume 86,
Issue 4,
pp. 1400-1407,
08/15/1995
Copyright © 1995 by The American Society of Hematology
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