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. The purpose of this protocol is to define the immunologic (immune function) spectrum of hepatitis C disease in co-infected HIV individuals. Since its discovery in 1989, hepatitis C virus (HCV) has been recognized as a major cause of chronic hepatitis and hepatic fibrosis that progresses in many patients to cirrhosis and hepatocellular cancer. In the United States, approximately 4 million people have been infected with HCV annually and there are around 10,000 HCV-related deaths each year. Due to shared routes of transmission, HCV and HIV co-infection is common, affecting 60-95% of those with parental exposures, such as injection drug users. As a result, the HCV disease burden among HIV-infected adults is substantial. Similar to HIV, most persons do not experience symptoms early in the course of HCV infection. However, natural history studies indicate that HCV infection can cause progressive inflammation and scarring, which may lead to cirrhosis, cancer, and liver failure in up to 20% of infected individuals in a period of 20-30 years. Among HIV-infected persons, the progression of HCV-related liver disease may be quite rapid (less than 10 years). In the United States, many co-infected patients who were infected with HCV in the 1970s or 1980s are now experiencing progressive HCV-related liver disease. Thus, as deaths from AIDS declines, HCV co-infection is an increasingly important problem. Effective HCV treatment for co-infected individuals is urgently needed. The severity of HCV in patients co-infected with HIV appears to be more severe and aggressive that in patients with HCV alone. This is most likely due to the individual's decreased immune factors. Despite this suspicion, the interactions between the immune system and HCV in these patients remains unknown. Because abnormal CD4 cell numbers and function are the hallmark of HIV infection, the investigators suspects that these abnormalities are associated with the increased severity of HCV infection in co-infected individuals. This study proposes to collect prospective data on HCV-HIV co-infected individuals to determine the relationship of HCV infection and severity with immune response. Patients who are participating in the 'PEG-Interferon Alpha 2-b+ Ribavirin for he Treatment of Chronic Hepatitis C Infection in HIV-Infected Persons Not Previously Treated with Interferon' will be eligible to complete this secondary study. Additional blood samples will be collected from consenting patients during their regular baseline, 24, 48 and cessation visits. The additional blood samples will be evaluated for immunologic factors. In addition, patients who have HCV but do not have HIV, and patients with only HIV, will be recruited in order to serve as control populations for this study.
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