HIV/HCV混合感染患者肿瘤坏死因子相关凋亡诱导配体水平分析

Analysis of level of tumor necrosis factor-related apoptosis-inducing ligand in HIV/HCV co-infected individuals

目的探讨肿瘤坏死因子相关凋亡诱导配体(TRAIL)及其受体在艾滋病病毒(HIV)/丙型肝炎病毒(HCV)混合感染者发病机制中的作用。方法用流式细胞术检测DR4^+CD4^+T淋巴细胞(CD4^+T淋巴细胞简称CD4细胞)、DR5^+CD4^+T细胞、TRAIL^+CD4^+T细胞的比例,CD4细胞计数;用酶联免疫吸附试验检测血浆可溶性TRAIL(s TRAIL)浓度;用荧光定量聚合酶链反应(PCR)测定血浆HIV、HCV核糖核酸载量。结果混合感染者DR5^+CD4^+T细胞比例高于HCV单纯感染者(P=0.03),与HIV单纯感染者相比无统计学差异(P> 0.05)。未接受高效抗反转录病毒治疗(HAART)的HIV单纯感染者的sTRAIL浓度高于接受HAART的HIV单纯感染者(P <0.01)。sTRAIL浓度与HIV病毒量呈正相关(r=0.631,P <0.01);DR5^+CD4^+T细胞比例与CD4细胞计数呈正相关(r=0.377,P <0.01)。结论在HIV感染状态下,CD4细胞可能对TRAIL诱导的凋亡更加敏感,而混合感染HCV后对CD4细胞凋亡的进一步影响或许并不涉及TRAIL及其受体。

Objective To explore the effect of tumor necrosis factor-related apoptosis-inducing ligand(TRAIL) and its receptors on the pathogenesis of HIV/HCV coinfected individuals. Methods The percentage of DR4^+CD4^+ T cells, DR5^+CD4^+ T cells, TRAIL^+CD4^+ T cells, and the count of CD4^+ T cells were detected by means of flow cytometry;the level of soluble TRAIL(sTRAIL) in plasma was detected by enzyme-linked immuno sorbent assay(ELISA);HIV RNA and HCV RNA were detected by Realtime Fluorescence Quantitative Polymerase Chain Reaction. Results The percentage of DR5^+CD4^+ T cells in HIV/HCV coinfected individuals was higher than that in HCV monoinfected individuals(P =0.03). There was no difference in DR5^+CD4^+ T cells percentage between HIV/HCV coinfected individuals and HIV monoinfected individuals(P > 0.05). The concentration of sTRAIL in plasma of HIV untreated monoinfected individuals was higher than that of HIV treated monoinfected individuals(P < 0.01). There was positive correlation between concentration of sTRAIL and HIV load(r =0.631, P< 0.01), and positive correlation between percentage of DR5^+CD4^+ T cells and the count of CD4^+ T cells(r =0.377, P < 0.01). Conclusion In the state of HIV infection, CD4^+ T cells are probably more sensitive to the apoptosis induced by TRAIL. However, as for coinfection of HIV/HCV, the further changes in apoptosis may not refer to TRAIL and its receptors.