The in vivo effects of combination antiretroviral drug therapy on peripheral blood CD34(+) cell colony forming units from HIV type 1 infected patients

Citation
Gb. Adams et al., The in vivo effects of combination antiretroviral drug therapy on peripheral blood CD34(+) cell colony forming units from HIV type 1 infected patients, AIDS RES H, 15(6), 1999, pp. 551-559
Citations number
27
Categorie Soggetti
Immunology
Journal title
AIDS RESEARCH AND HUMAN RETROVIRUSES
ISSN journal
08892229 → ACNP
Volume
15
Issue
6
Year of publication
1999
Pages
551 - 559
Database
ISI
SICI code
0889-2229(19990410)15:6<551:TIVEOC>2.0.ZU;2-P
Abstract
This study investigated the effects of a combination antiretroviral drug re gimen (indinavir and two nucleoside analogs or ritonavir and saquinavir) on the levels of CD34(+) colony-forming units (CFU-Cs) in the peripheral bloo d of HIV-1(+) patients, Ten patients who were receiving combination antiret roviral drug therapy were studied and their peripheral blood CD34+ CFU-Cs w ere measured prior to, 1 month after, and 4 to 6 months after the commencem ent of therapy, The levels of CD4(+) T cells increased significantly in the se patients (paired t test, p = 0.0027) and plasma viral load became undete ctable in all but one patient studied. Measurements of the CFU-Cs showed th at their levels tended to increase on the commencement of therapy, nd these levels became significantly higher than baseline by 4-6 months (paired t t est, p = 0.0293), Analysis of the different colony phenotype demonstrated t hat the main contributor to this increase consisted of burst-forming unit e rythroid (BFU-E) cells, These data also demonstrated that there was an inve rse correlation between the rise in CFU-Cs at 4-6 months compared with CD4( +) cell, CD8(+) cell, and neutrophil counts, and hemoglobin concentration, at baseline. The demonstrated increase in the levels of CD34(+) CFU-Cs sugg ests that HIV-1 may have an inhibitory effect on these cells in vivo, and t hat this inhibition may be abrogated by suppression of viral replication.