DELTA HEPATITIS AND HEPATITIS C IN HEMOPHILIA

血友病中的三角洲肝炎和丙型肝炎

• 批准号: 7375052
• 负责人: JOAN COX GILL
• 金额: $ 3.8万
• 依托单位: MEDICAL COLLEGE OF WISCONSIN
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-12-01 至 2006-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7375052
• 关键词: DELTA; HEPATITIS; HEMOPHILIA

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. This study will test the hypothesis that hepatitis C virus induces a specific cellular immune deficiency in which CD4 lymphocytes play a central role that precludes HCV clearance by induction of a mechanism that maintains adequate levels of virus-specific antibody but impairs cellular immune clearance. A cohort of hemophilic patients infected with HCV are followed over time; cellulor and humerol immune responses to HCV antigens are characterized and correlated with the extent of liver disease and response to therapy.

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。本研究将验证丙型肝炎病毒诱导特异性细胞免疫缺陷的假设，其中CD4淋巴细胞发挥核心作用，通过诱导维持足够水平的病毒特异性抗体但损害细胞免疫清除的机制来排除HCV清除。一组感染HCV的血友病患者长期随访；细胞和肱骨醇对HCV抗原的免疫反应是有特征的，并与肝脏疾病的程度和对治疗的反应相关。