TY - JOUR
T1 - Characterization of viral dynamics in human immunodeficiency virus type 1-infected patients treated with combination antiretroviral therapy
T2 - Relationships to host factors, cellular restoration, and virologic end points
AU - Wu, Hulin
AU - Kuritzkes, Daniel R.
AU - McClernon, Daniel R.
AU - Kessler, Harold
AU - Connick, Elizabeth
AU - Landay, Alan
AU - Spear, Greg
AU - Heath-Chiozzi, Margo
AU - Rousseau, Franck
AU - Fox, Lawrence
AU - Spritzler, John
AU - Leonard, John M.
AU - Lederman, Michael M.
PY - 1999
Y1 - 1999
N2 - Biphasic plasma viral decays were modeled in 48 patients treated with ritonavir, zidovudine, and lamivudine. Estimated first- and second-phase decay rates were d1 as 0.47/day and d2 as 0.04/day. Interpatient differences in both decay rates were significant. The d1 was directly correlated with baseline CD4+, CD4+CD28+, and CD8+CD28+ T lymphocyte counts (P< .05) and inversely correlated with baseline virus load (P = .044) and the magnitude of CD4+ and CD8+ T lymphocyte recovery (P<.01). The d2 was directly correlated with baseline percentage of CD8+ T lymphocytes (P = .023), the CD8+CD38+ cell number (P = .024), and the level of IgG that binds to human immunodeficiency virus (HIV) type 1 gp120 (P = .02). Vital decay rates were not predictive of treatment failure or durability of viral suppression. These exploratory findings are consistent with a model in which immunologic factors contribute to elimination of HIV-infected cells and suggest a dynamic interplay between regulation of HIV expression and lymphocyte activation and recovery.
AB - Biphasic plasma viral decays were modeled in 48 patients treated with ritonavir, zidovudine, and lamivudine. Estimated first- and second-phase decay rates were d1 as 0.47/day and d2 as 0.04/day. Interpatient differences in both decay rates were significant. The d1 was directly correlated with baseline CD4+, CD4+CD28+, and CD8+CD28+ T lymphocyte counts (P< .05) and inversely correlated with baseline virus load (P = .044) and the magnitude of CD4+ and CD8+ T lymphocyte recovery (P<.01). The d2 was directly correlated with baseline percentage of CD8+ T lymphocytes (P = .023), the CD8+CD38+ cell number (P = .024), and the level of IgG that binds to human immunodeficiency virus (HIV) type 1 gp120 (P = .02). Vital decay rates were not predictive of treatment failure or durability of viral suppression. These exploratory findings are consistent with a model in which immunologic factors contribute to elimination of HIV-infected cells and suggest a dynamic interplay between regulation of HIV expression and lymphocyte activation and recovery.
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U2 - 10.1086/314670
DO - 10.1086/314670
M3 - Article
C2 - 10068574
AN - SCOPUS:0011419832
SN - 0022-1899
VL - 179
SP - 799
EP - 807
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 4
ER -