Characterization of Viral Dynamics in Human Immunodeficiency Virus Type 1–Infected Patients Treated with Combination Antiretroviral Therapy: Relationships to Host Factors, Cellular Restoration, and Virologic End Points
Author(s) -
Hulin Wu,
Daniel R. Kuritzkes,
Daniel McCler,
Harold A. Kessler,
Elizabeth Connick,
Alan Landay,
Greg T. Spear,
Margo HeathChiozzi,
Franck Rousseau,
Lawrence Fox,
John Spritzler,
John M. Leonard,
Michael M. Lederman
Publication year - 1999
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/314670
Subject(s) - cd38 , ritonavir , zidovudine , cd8 , viral load , virology , lamivudine , immunology , virus , lymphocyte , lentivirus , biology , indinavir , viral disease , medicine , antiretroviral therapy , immune system , genetics , hepatitis b virus , stem cell , cd34
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). Viral 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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