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Immunological markers after long-term treatment interruption in chronically HIV-1 infected patients with CD4 cell count above 400 × 106 cells/l

Thiébaut, Rodolphea,b; Pellegrin, Isabelled; Chêne, Genevièveb; Viallard, Jean Françoise; Fleury, Hervéd; Moreau, Jean Françoisc,d; Pellegrin, Jean Luce; Blanco, Patrickc,d

Clinical Science

Objective: To analyse immunological markers associated with CD4+ lymphocyte T-cell count (CD4+) evolution during 12-month follow-up after treatment discontinuation.

Method: Prospective observational study of chronically HIV-1 infected patients with CD4+ above 400 × 106 cells/l.

Results: CD4+ changes took place in two phases: an initial rapid decrease in the first month (−142 × 106 cells/l on average), followed by a slow decline (−17 × 106 cells/l on average) The second slope of CD4+ decline was not correlated with the first and only baseline plasma HIV RNA was associated with it. The decline in CD4+ during the first month was steeper in patients with higher CD4+ and weaker plasma HIV RNA baseline levels. Moreover, the decline was less pronounced (P < 10−4) in patients with CD4+ nadir above 350 × 106 cells/l (−65 × 106 cells/l per month) in comparison with those below 350 × 106 cells/l (−200 × 106 cells/l per month). A high number of dendritic cells (DCs) whatever the type was associated with high CD4+ at the time of treatment interruption and its steeper decline over the first month. Moreover, the myeloid DC level was stable whereas the lymphoid DC count, which tended to decrease in association with decrease in CD4+, was negatively correlated with the HIV RNA load slope.

Conclusions: The results support the use of the CD4+ nadir to predict the CD4+ dynamic after treatment interruption and consideration of the CD4+ count after 1-month of interruption merely reflects the 12-month level of CD4+. Although DCs seem to be associated with the CD4+ dynamic, the benefit of monitoring them has still to be defined.

aINSERM E0338

bINSERM U593, ISPED

cCNRS UMR5164 CIRID, Bordeaux 2 University

dDepartment of Virology and Immunology

eDepartment of Internal Medicine and Infectious Diseases, Bordeaux University Hospital, Bordeaux, France

Received 26 May, 2004

Revised 1 October, 2004

Accepted 12 October, 2004

Correspondence to Rodolphe Thiébaut, INSERM E0338 & U593, ISPED, Université Bordeaux 2, Case 11, 146 Rue Léo Saignat, 33076 Bordeaux Cedex, France. E-mail: rodolphe.thiebaut@isped.u-bordeaux2.fr

© 2005 Lippincott Williams & Wilkins, Inc.