Long-term changes in circulating CD4 T lymphocytes in virologically suppressed patients after 6 years of highly active antiretroviral therapy

K Smith, E Aga, RJ Bosch, H Valdez, E Connick… - Aids, 2004 - journals.lww.com
K Smith, E Aga, RJ Bosch, H Valdez, E Connick, A Landay, D Kuritzkes, BH Gross…
Aids, 2004journals.lww.com
In HIV-1-infected patients with long-term undetectable viraemia on highly active antiretroviral
treatment (HAART), we found that pre-HAART plasma viraemia and the baseline proviral
DNA level were significantly associated with the viraemia setpoint during scheduled
treatment interruptions. In long-term treated patients, pre-HAART viraemia may not be
available, and in these circumstances proviral DNA, measured at the time of scheduled
treatment interruption, can help to identify patients likely to reach a low viraemia setpoint …
In HIV-1-infected patients with long-term undetectable viraemia on highly active antiretroviral treatment (HAART), we found that pre-HAART plasma viraemia and the baseline proviral DNA level were significantly associated with the viraemia setpoint during scheduled treatment interruptions. In long-term treated patients, pre-HAART viraemia may not be available, and in these circumstances proviral DNA, measured at the time of scheduled treatment interruption, can help to identify patients likely to reach a low viraemia setpoint after treatment interruption.
The long-term toxicity of antiretroviral therapy [1], the emergence of HIV-1 drug-resistance [2, 3] and the cost of long-term treatment have driven new strategies of antiretroviral treatment including the delay of initiation of treatment [4], structured treatment interruptions [5–8] or simplified maintenance therapy [9–11]. In several clinical trials intermittent or simplified treatment has failed in a relatively high proportion of patients, whereas others have benefitted [5–11]. Such patients maintained stable CD4 cell counts and low viraemia off therapy. The predictors of virological failure in such studies were previous mono or bi-therapy, baseline drug resistance mutation (s) and high HIV-1-RNA levels [5–11]. The selection of patients who may benefit from treatment interruption or simplified therapy may be improved by taking into account treatment history, the detection of baseline resistance mutation (s) and an evaluation of the pool of infected cells by the quantitation of proviral DNA.
Lippincott Williams & Wilkins