Steel Alan, Cox Alison E, Shamji Mohamed H, John Laurence, Nelson Mark, Henderson Don C, Gotch Frances M, Gazzard Brian G, Kelleher Peter
Department of Immunology, Imperial College, Chelsea and Westminster Hospital, London.
Antivir Ther. 2007;12(6):971-5.
To determine if the expression of CD38 on CD8+ T-cells could be used as a marker of viral replication <50 copies/ml in peripheral blood.
In a cross-sectional study of patients attending a single HIV clinic in London, an ultra-sensitive HIV RNA viral load assay, with a limit of detection of 3 copies/ml, was used to determine HIV-1 replication in plasma in 70 patients who had sustained viral suppression <50 copies/ml by bDNA assays. Immune activation using the expression of CD38 on CD8+ T-cells was also assessed in patients on antiretroviral therapy (ART) with sustained viral suppression, individuals with persistent low-level viraemia <400 copies/ml and subjects failing ART (viral load >400 copies/mi).
There was no significant difference in the percentage of CD8+CD38++ T-cells between patients with <50 copies or <3 copies/ml. Immune activation was significantly increased in patients with persistent low-level viraemia and in subjects failing ART. CD4+ T-cell counts in patients on long-term successful ART are inversely associated with CD8+ T-cell activation.
T-cell activation in patients on long-term successful ART is not due to residual low-level viral replication in the blood compartment of HIV-1. CD8+ T-cell activation in this patient group appears to be associated with poor CD4+ T-cell recovery.
确定CD8⁺ T细胞上CD38的表达是否可作为外周血中病毒复制低于50拷贝/毫升的标志物。
在一项针对伦敦一家单一HIV诊所患者的横断面研究中,采用检测限为3拷贝/毫升的超灵敏HIV RNA病毒载量测定法,来确定70例通过分支DNA测定法实现病毒持续抑制低于50拷贝/毫升的患者血浆中的HIV-1复制情况。还对接受抗逆转录病毒治疗(ART)且病毒持续抑制的患者、病毒血症持续处于低水平(低于400拷贝/毫升)的个体以及ART治疗失败(病毒载量>400拷贝/毫升)的受试者,评估了利用CD8⁺ T细胞上CD38表达情况来反映的免疫激活情况。
病毒载量低于50拷贝/毫升或低于3拷贝/毫升的患者之间,CD8⁺CD38⁺⁺ T细胞的百分比无显著差异。病毒血症持续处于低水平的患者以及ART治疗失败的受试者的免疫激活显著增加。长期成功接受ART治疗的患者的CD4⁺ T细胞计数与CD8⁺ T细胞激活呈负相关。
长期成功接受ART治疗的患者的T细胞激活并非由于HIV-1血液 compartment中残留的低水平病毒复制。该患者群体中的CD8⁺ T细胞激活似乎与CD4⁺ T细胞恢复不良有关。