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Hepatitis C virus and human immunodeficiency virus: clinical issues in coinfection
1Department of Medicine, New York University School of Medicine, New York 10016, USA.
Insights
Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) coinfection significantly worsens liver disease progression. Treating HCV in coinfected patients can improve liver health and immune response.
Area of Science:
- Hepatology
- Virology
- Immunology
Background:
- Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) coinfection is prevalent, affecting 30-50% of certain populations.
- Shared transmission routes and effective HIV treatment have increased HCV's impact in HIV-positive individuals.
- HIV coinfection exacerbates HCV, leading to more severe liver fibrosis, cirrhosis, and liver-related mortality.
Purpose of the Study:
- To review the impact of HIV coinfection on HCV progression.
- To examine the effects of antiretroviral therapy on HCV.
- To discuss the benefits of treating HCV in coinfected patients.
Main Methods:
- Literature review of studies on HCV/HIV coinfection.
- Analysis of disease progression and treatment outcomes.
- Evaluation of viral load and liver enzyme changes.
Main Results:
- HIV coinfection accelerates liver fibrosis and increases mortality.
- Highly active antiretroviral therapy (HAART) does not impact HCV infection directly but may affect liver enzymes.
- HCV treatment in coinfected patients shows promise in reducing fibrosis and improving immune response.
Conclusions:
- Treating chronic hepatitis C in HIV-coinfected individuals can decrease liver fibrosis and enhance T-cell responses.
- Interferon-alpha, alone or with ribavirin, may be a viable treatment option.
- Managing HCV in coinfected patients can lower viral load and facilitate protease inhibitor therapy.
Abstract:
The prevalence of hepatitis C virus (HCV) and human immunodeficiency virus (HIV) coinfection ranges from nearly 30% to over 50%, depending on the population. Shared modes of transmission and the success of current antiretroviral regimens have contributed to the emergence of HCV as a significant pathogen in the HIV-positive population. HIV coinfection appears to worsen HCV infection, with studies showing more severe fibrosis, a higher frequency of cirrhosis, and increased deaths from liver disease. HIV coinfection may also increase the rate of maternal-fetal transmission of HCV. Similarly, studies suggest a more rapid progression to AIDS or death for HCV genotypes 1a and 1b than for other genotypes in HIV-infected patients with hemophilia. Highly active antiretroviral therapy (HAART), such as HIV protease inhibitors, has no effect on HCV infection and may transiently increase ALT, AST, and hepatitis C viral load. Hepatotoxicity associated with HAART may or may not be related to the presence of HCV and may depend on the specific agents used. Data suggest that treating chronic hepatitis C in HIV-co-infected patients can decrease fibrosis, increase T-cell responsiveness to HCV antigens, and decrease the rate of fatal hepatomas. Interferon alpha may provide sustained biochemical or virologic responses in HIV/HCV-coinfected patients. The combination of interferon-alpha and ribavirin may also be a treatment option but is more complex, and additional research is needed. Treating HCV infection in HIV/HCV-coinfected individuals may help lower the hepatitis C viral load and permit treatment with protease inhibitors.