Wu H, Kuritzkes D R, McClernon D R, Kessler H, Connick E, Landay A, Spear G, Heath-Chiozzi M, Rousseau F, Fox L, Spritzler J, Leonard J M, Lederman M M
Phase I Section, SDAC of ACTG, Frontier Science and Technology Research Foundation, Inc., Chestnut Hill, MA 02467, USA. wu@sdac. harvard.edu
J Infect Dis. 1999 Apr;179(4):799-807. doi: 10.1086/314670.
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.
对48例接受利托那韦、齐多夫定和拉米夫定治疗的患者的双相血浆病毒衰减进行了建模。估计的第一阶段和第二阶段衰减率分别为d1 = 0.47/天和d2 = 0.04/天。患者间这两种衰减率的差异均具有显著性。d1与基线CD4 +、CD4 + CD28 +和CD8 + CD28 + T淋巴细胞计数直接相关（P<0.05），与基线病毒载量（P = 0.044）以及CD4 +和CD8 + T淋巴细胞恢复程度呈负相关（P<0.01）。d2与基线CD8 + T淋巴细胞百分比（P = 0.023）、CD8 + CD38 +细胞数量（P = 0.024）以及与1型人类免疫缺陷病毒（HIV）gp120结合的IgG水平直接相关（P = 0.02）。病毒衰减率不能预测治疗失败或病毒抑制的持久性。这些探索性发现与免疫因素有助于清除HIV感染细胞的模型一致，并提示HIV表达调控与淋巴细胞激活和恢复之间存在动态相互作用。
