In human immunodeficiency virus (HIV)-1 infection, decrease of telomere len
gth is mainly found in CD8(+) T cells and not in CD4(+) T cells. Telomerase
, a ribonucleoprotein enzyme that can synthesize telomeric sequence onto ch
romosomal 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-2 infection. Telomerase activity was higher in CD8(+)
than in CD4(+) T cells from HIV-infected patients, but still in the same r
ange as in healthy controls, and upregulation after stimulation was compara
ble 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 ma
rrow 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 n
ot lead to accelerated toss of telomere length in vivo. Thus, differential
telomere loss in CD4(+) and CD8(+) T cells in HIV-1 infection cannot be exp
lained by telomerase activity. (C) 1999 by The American Society of Hematolo
gy.