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| Authors||A. Mocroft, A.N. Phillips, B. Ledergerber, C. Katlama, A. Chiesi, F.D. Goebel, B. Knysz, F. Antunes, P. Reiss, J.D. Lundgren|
|Title||Relationship between antiretrovirals used as part of a cART regimen and CD4 cell count increases in patients with suppressed viremia|
|Abstract||Background: It is unknown if the CD4 cell count response differs according to antiretroviral drugs used in combination antiretroviral therapy (cART) in patients with maximal virological suppression [viral load (VL) < 50 copies/ml]. Objectives: To compare the change in CD4 cell count over consecutive measurements with VL < 50 copies/ml at both time-points according to nucleoside backbones and other antiretrovirals used. Methods: Generalized linear models, accounting for multiple measurements within patients, were used to compare CD4 cell Count changes after adjustment for antiretrovirals, time from starting cART, age, CD4 at first VL < 50 copies/ml, prior antiretroviral treatment, and change in CD4 cell count since starting cART. Results: We studied 28418 instances of VL < 50 copies/ml in 4041 patients. The mean annual change in CD4 cell count was +45.5/mu l [95% confidence interval (CI) +39.4 to +51.6/mu l). Comparing two drug nucleoside backbones, there was a lower annual change in CD4 cell count for zidovudine/lamivudine (n = 13038; -15.4/mu l; P = 0.012) and for those on tenofovir (n = 1809; -27.3/mu l; P = 0.029) compared to lamivudine/ stavudine (n = 7339). Compared to the boosted-protease inhibitor regimen (n = 5915), use of an abacavir-based triple-nucleoside regimen was associated with a lower annual change in CD4 cell count (n = 2504 pairs; -26.1/mu l; P = 0.011). Conclusions: A nucleoside backbone of zidovudine/lamivudine or any tenofovir-based backbone was associated with significantly poorer increases in CD4 cell count compared to a nucleoside backbone of stavudine/lamivudine, as was an abacavir-based triple nucleoside regimen compared to a boosted protease inhibitor regimen. Long-term studies are needed to determine whether the differences in immunological response seen here translate into differences in the risk of clinical disease|
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