SUPPRESSIVE LONG-TERM ANTIVIRAL MANAGEMENT OF HEPATITIS C VIRUS (HCV) AND HIV

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 具体目标 首要目标 在HIV-1和丙型肝炎病毒(丙型肝炎病毒)混合感染的患者中，比较从进入第二步到终止研究的组织学纤维化进展速度的减少，这些患者接受了聚乙二醇化干扰素治疗，而未接受治疗的对照组对聚乙二醇化干扰素加利巴韦林治疗12周无效。 次要目标 [目的]评价长期应用聚乙二醇干扰素对合并感染者的生活质量的影响。 [目的]确定长期使用聚乙二醇干扰素对丙型肝炎病毒进化和宿主免疫应答的影响。 [目的]探讨ALT、AST、胆红素、白蛋白和蛋白等非侵入性纤维化标志物在预测组织学反应中的作用。 ？确定长期服用聚乙二醇干扰素与未经治疗的对照组对CD4T细胞计数和艾滋病定义疾病的影响。 [目的]确定长期服用聚乙二醇干扰素对代谢参数的影响，包括体重、血脂谱、高血糖和胰岛素抵抗。 评估治疗对艾滋病毒疾病控制的影响。 [目的]探讨宿主细胞因子和纤维化相关基因的遗传多态性对基础组织学和疾病组织学进展的影响。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. SPECIFIC AIMS Primary Objective To compare the reduction in the rate of histologic fibrosis progression from Step 2 entry to study termination between subjects treated with PEG-IFN and untreated controls in subjects with HIV-1 and hepatitis C virus (HCV) coinfection who have failed to respond to 12 weeks of PEG-IFN plus ribavirin. Secondary Objectives ¿ To evaluate the quality of life associated with long-term PEG-IFN in coinfected subjects. ¿ To determine the impact of long-term PEG-IFN use on HCV viral evolution and host immunologic response. ¿ To investigate the role of noninvasive markers of fibrosis in predicting histologic response, including ALT, AST, bilirubin, albumin, and protein. ¿ To determine the effect of long-term PEG-IFN versus untreated controls on CD4+ T-cell counts and AIDS-defining illnesses. ¿ To determine the effect of long-term PEG-IFN therapy on metabolic parameters, including body weight, lipid profile, hyperglycemia, and insulin resistance. ¿ To assess the impact of treatment on HIV disease control. ¿ To determine the influence of host genetic polymorphisms on cytokine and fibrosis-related genes on baseline histology and on histologic progression of disease.