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Blood, Vol. 93 No. 3 (February 1), 1999:
pp. 1011-1019
Normal T-Cell Telomerase Activity and Upregulation in Human
Immunodeficiency Virus-1 Infection
Katja C. Wolthers,
Sigrid A. Otto,
G. Bea A. Wisman,
Sylvain Fleury,
Peter Reiss,
Reinier W. ten Kate,
Ate G.J. van der Zee, and
Frank Miedema
From the Department of Clinical Viro-Immunology, CLB, Sanquin Blood
Supply Foundation, Amsterdam; the Laboratory for
Experimental and Clinical Immunology and the Department of Human
Retrovirology, Academic Medical Centre, University of Amsterdam,
Amsterdam; the Department of Gynaecology and Obstetrics, Academic
Hospital Groningen, University of Groningen, Groningen; the National
AIDS Therapy Evaluation Centre, Academic Medical Centre, University of
Amsterdam, Amsterdam; the Department of Internal Medicine, Kennemer
Gasthuis, Haarlem, The Netherlands; and the Laboratorie
d'Immunopathologie du SIDA, Division des maladies infectieuses,
Department de medecine interne, Hopital de Beaumont, Lausanne,
Switzerland.
In human immunodeficiency virus (HIV)-1 infection, decrease of
telomere length is mainly found in CD8+ T cells and not
in CD4+ T cells. Telomerase, a ribonucleoprotein enzyme
that can synthesize telomeric sequence onto chromosomal ends, can
compensate for telomere loss. Here, we investigated if telomerase
activity could explain differential telomere loss of CD4+
and CD8+ T cells in HIV-1 infection. Telomerase activity
was higher in CD8+ than in CD4+ T cells
from HIV-infected patients, but still in the same range as in healthy
controls, and upregulation after stimulation was comparable to normal.
Telomerase activity in lymph node CD4+ and
CD8+ T cells from HIV-infected patients was in the same
range as that in CD4+ and CD8+ T cells from
peripheral blood (PB) and was normal in unseparated bone marrow cells.
Thus, our study did not provide evidence for compartmentalized
elongation of telomeres in HIV infection. In patients treated with
reverse transcriptase inhibitors, telomerase activity was
inhibited, but this did not lead to accelerated loss of telomere length
in vivo. Thus, differential telomere loss in CD4+ and
CD8+ T cells in HIV-1 infection cannot be explained by
telomerase activity.
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