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的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 中心，不一定是研究者的机构。 具体目标 主要目的 在接受12周PEG-IFN+利巴韦林治疗无效的HIV-1和丙型肝炎病毒（HCV）合并感染受试者中，比较接受PEG-IFN治疗的受试者和未接受治疗的对照组之间从第2步入组至研究终止的组织学纤维化进展率降低。 次要目的 ¿ 评价合并感染受试者长期使用PEG-IFN相关的生活质量。 ¿ 确定长期使用聚乙二醇干扰素对HCV病毒进化和宿主免疫应答的影响。 ¿ 研究非侵入性纤维化标志物在预测组织学反应中的作用，包括ALT、AST、胆红素、白蛋白和蛋白质。 ¿ 确定长期PEG-IFN与未经治疗的对照组相比对CD 4 + T细胞计数和AIDS定义疾病的影响。 ¿ 确定长期PEG-IFN治疗对代谢参数的影响，包括体重、血脂、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。 ¿ 确定宿主基因多态性对细胞因子和纤维化相关基因对基线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.