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首页> 外文期刊>AIDS Research and Human Retroviruses >A novel chemokine-receptor-5 (CCR5) blocker, SCH532706, has differential effects on CCR5+CD4+ and CCR5+CD8+ T cell numbers in chronic HIV infection.
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A novel chemokine-receptor-5 (CCR5) blocker, SCH532706, has differential effects on CCR5+CD4+ and CCR5+CD8+ T cell numbers in chronic HIV infection.

机译：新型趋化因子受体5（CCR5）阻滞剂SCH532706对慢性HIV感染的CCR5 + CD4 +和CCR5 + CD8 + T细胞数量具有不同的影响。

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摘要

HIV treatment with CCR5 receptor blockers may impact CCR5(+) cell distribution. T cell subsets, plasmacytoid dendritic cells (PDC), and antigen-specific [Mycobacteria tuberculosis/avium (M.TB/MAI), cytomegalovirus (CMV), Herpes simplex (HSV), HIV-Gag] CD4(+) T cells were measured in untreated R5-tropic-HIV-infected adults receiving 10 days of SCH532706 (Phase 1), 15 days no therapy, then 10 days of cART (without SCH532706) (Phase 2). Ten males were enrolled with median cells/microl (range) of CD4(+) 310 (92-848), CCR5(+)CD4(+) 57 (17-118), CD8(+) 895 (459-1666), and CCR5(+)CD8(+) 392 (250-983), and median plasma HIV RNA of 4.6 log(10) copies/ml. At baseline, proportions of M.TB, MAI, CMV, HSV, and HIV-Gag-specific CD4(+) T cells were 0.3%, 3.0%, 6.0%, 2.0%, and 1.6%, respectively. Median log(10) HIV RNA copies/ml declines were 1.5 (Phase 1) and 1.75 (Phase 2) (p = 0.7). Median CD4(+) and CD8(+) changes, respectively, during Phases 1 (+16; +91) and 2 (+28; -71) were similar (p = 0.7 both). However, CCR5(+)CD8(+) T cell fluctuations were significantly different (p = 0.02) during Phase 1 (+147 cells) vs. Phase 2 (-35 cells). PDC increased significantly more during Phase 1 (p = 0.04). Declines in antigen-specific cells were similar except for M. avium, which declined significantly during Phase 2 (p = 0.04). Similar declines in activation and proliferation of T cell subsets were observed during both treatment phases. For equivalent HIV RNA declines, CCR5-receptor blockade differentially increased CD8(+) T cell and PDC numbers in the circulation. These results confirm that cell surface CCR5 expression on these cells constantly directs trafficking during HIV infection. The persistence and clinical meaning of these immunological changes during long-term exposure to this class of anti-HIV drugs are unknown, but may have implications for immunosurveillance of inflammation.
机译：用CCR5受体阻滞剂进行HIV治疗可能会影响CCR5（+）细胞分布。 T细胞亚群，浆细胞样树突状细胞（PDC）和抗原特异性[结核分枝杆菌/禽（M.TB / MAI），巨细胞病毒（CMV），单纯疱疹（HSV），HIV-Gag] CD4（+）T细胞是在未经治疗的R5-tropic-HIV感染的成年人中测量10天的SCH532706（阶段1），15天不进行治疗，然后10天的cART（无SCH532706）（阶段2）。十名男性接受了CD4（+）310（92-848），CCR5（+）CD4（+）57（17-118），CD8（+）895（459-1666），和CCR5（+）CD8（+）392（250-983），中位数血浆HIV RNA为4.6 log（10）拷贝/ ml。在基线时，M.TB，MAI，CMV，HSV和HIV-Gag特异性CD4（+）T细胞的比例分别为0.3％，3.0％，6.0％，2.0％和1.6％。 log（10）HIV RNA拷贝/ ml下降的中位数为1.5（第1阶段）和1.75（第2阶段）（p = 0.7）。在第1阶段（+16; +91）和第2阶段（+28; -71）期间，CD4（+）和CD8（+）的中位数变化分别相似（p均为0.7）。但是，CCR5（+）CD8（+）T细胞的波动在第1阶段（+147个细胞）与第2阶段（-35个细胞）之间显着不同（p = 0.02）。在阶段1中，PDC显着增加（p = 0.04）。抗原特异性细胞的下降相似，只是鸟分枝杆菌在第二阶段显着下降（p = 0.04）。在两个治疗阶段均观察到类似的T细胞亚群激活和增殖下降。对于等效的HIV RNA下降，CCR5受体阻滞在循环中差异地增加了CD8（+）T细胞和PDC数量。这些结果证实在这些细胞上的细胞表面CCR5表达在HIV感染期间不断指导运输。长期暴露于此类抗HIV药物期间，这些免疫学改变的持久性和临床意义尚不清楚，但可能会对炎症的免疫监测产生影响。

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