Brumme Zabrina L, Chan Keith J, Dong Winnie W, Mo Theresa, Wynhoven Brian, Hogg Robert S, Montaner Julio S, O'Shaughnessy Michael V, Harrigan P Richard
BC Centre for Excellence in HIV/AIDS, St. Paul's Hospital, Vancouver, British Columbia, Canada.
AIDS. 2002 Sep 27;16(14):1929-33. doi: 10.1097/00002030-200209270-00010.
Co-infection with GBV-C ('Hepatitis G' virus) appears to be associated with slower disease progression in HIV-infected, untreated individuals. We wished to determine whether detection of GBV-C RNA was associated with differential response to HIV therapy in a population-based cohort of 461 individuals initiating antiretroviral therapy between June 1996 and August 1998, in British Columbia, Canada.
The presence of GBV-C RNA in plasma was identified by nested RT-PCR, using detection of HIV RNA as a positive control. Time to virological success [achieving HIV plasma viral load (pVL) < or = 500 copies/ml], virological failure (subsequent confirmed pVL > 500 copies/ml) and immunological failure (confirmed CD4 cell count below baseline) were assessed by Kaplan-Meier methods and Cox proportional hazard regression.
Of the 441 individuals for whom results were available, 90 (20.4%) had detectable plasma GBV-C RNA. GBV-C RNA was significantly associated with a lower HIV pVL at baseline (P = 0.004). In univariate and multivariate Cox models, GBV-C RNA positive and negative individuals did not differ with respect to time to virological success [risk ratio (RR), 0.98; 95% confidence interval (CI), 0.75-1.27], time to virological failure (RR, 1.10; 95% CI, 0.74-1.65), or time to immunological failure (RR, 1.09; 95% CI, 0.73-1.63). There was no correlation between detection of GBV-C RNA and mutations in the human chemokine receptors CCR5 and CX CR1, or HIV viral tropism as predicted by the HIV envelope sequence (P > 0.1).
GBV-C viremia is relatively common in individuals seeking treatment for HIV infection; however, it does not appear to have any effect on initial antiretroviral therapy response.
与GBV-C(“庚型肝炎”病毒)合并感染似乎与未接受治疗的HIV感染者疾病进展较慢有关。我们希望确定在1996年6月至1998年8月间于加拿大不列颠哥伦比亚省开始抗逆转录病毒治疗的461名个体组成的基于人群的队列中,GBV-C RNA的检测是否与HIV治疗的不同反应相关。
采用巢式逆转录聚合酶链反应(RT-PCR)鉴定血浆中GBV-C RNA的存在,以HIV RNA检测作为阳性对照。通过Kaplan-Meier方法和Cox比例风险回归评估病毒学成功时间[实现HIV血浆病毒载量(pVL)≤500拷贝/毫升]、病毒学失败(随后确认pVL>500拷贝/毫升)和免疫学失败(确认CD4细胞计数低于基线)。
在可获得结果的441名个体中,90名(20.4%)血浆中可检测到GBV-C RNA。GBV-C RNA与基线时较低的HIV pVL显著相关(P = 0.004)。在单变量和多变量Cox模型中,GBV-C RNA阳性和阴性个体在病毒学成功时间[风险比(RR),0.98;95%置信区间(CI),0.75 - 1.27]、病毒学失败时间(RR,1.10;95%CI,0.74 - 1.65)或免疫学失败时间(RR,1.09;95%CI,0.73 - 1.63)方面没有差异。GBV-C RNA检测与人类趋化因子受体CCR5和CXCR1的突变或HIV包膜序列预测的HIV病毒嗜性之间没有相关性(P>0.1)。
GBV-C病毒血症在寻求HIV感染治疗的个体中相对常见;然而,它似乎对初始抗逆转录病毒治疗反应没有任何影响。