Immunophenotype of HIV+ patients during CD4 cell-monitored treatment interruption: role of the IL-7/IL-7 receptor system.
Nemes, Elisa a; Lugli, Enrico a; Nasi, Milena a; Ferraresi, Roberta a; Pinti, Marcello a; Bugarini, Roberto a; Borghi, Vanni b; Prati, Francesca b; Esposito, Roberto b; Cossarizza, Andrea a; Mussini, Cristina b
20(16):2021-2032, October 24, 2006.
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Objective: To investigate immunological changes during CD4-guided therapy interruption in HIV patients who suspended HAART.
Patients: Seventeen patients aged > 18 years, who had received HAART for at least 12 months, and had a pre-interruption CD4 cell count > 500 cells/[mu]l, interrupted treatment. Median nadir CD4 cell count was 288 cells/[mu]l. HIV plasma viral load at discontinuation was < 50 or > 50 copies/ml. Criteria for restarting treatment were: a CD4 T-lymphocyte count < 350 cells/[mu]l on two separate occasions, a clinical manifestation of AIDS, and the patient's desire to resume HAART. Eleven patients were still off therapy after 12 months (group A); according to the first criterion, six patients restarted therapy within 12 months (group B).
Methods: Haematological, viro-immunological, cytofluorimetic and molecular assays were performed at baseline and every 2 months following standard methods. Statistical analysis was performed under Stata 7.0.
Results: In the first 2 months of treatment interruption, a significant increase in viral load and CD8 lymphocyte activation occurred. Then such parameters decreased and remained stable. In all patients, a decrease in CD4 lymphocytes took place as well, that affected in a similar manner naive, central memory, effector memory and terminally differentiated cells. Group B always presented lower amounts of CD4 effector memory lymphocytes. The expression of CD127 was always higher in group A.
Conclusions: The loss of CD4 lymphocytes upon viral rebound is equal among naive and memory subsets. Patients with higher expression of CD127, who are likely to exert a better capacity to utilize endogenous interleukin-7 by T cells, could remain off therapy for longer periods.
(C) 2006 Lippincott Williams & Wilkins, Inc.