Immunological mechanisms controlling hepatitis C virus infection

Hepatitis C virus (HCV) infection is a significant global health problem, affecting over 150 million people worldwide. There is increasing evidence that a small percentage of individuals exposed to the HCV have the capacity to generate a strong cellular as well as humeral immune response against the virus and avoid persistent infection, and perhaps do so repeatedly after re-exposure. While the critical role of the adaptive immune system in HCV infection is well-established, the importance of the innate immune system has been recognized in more recent years. The immune system has many weapons to combat the HCV infection. These include type I interferons, HCV specific CD4+ cells and CD8+ T cells, cytokine production, natural killer cells, dentritic cells, and the production of anti-HCV neutralizing antibodies. Toll-like receptors form an important element of the innate immune response, and there is considerable evidence for their crucial role in HCV infection. In order to limit the availability of the cellular components for viral amplification, apoptosis occurs. It involves caspases, the key effectors of apoptotic cell death. This article reviews what the immune system does, when HCV attacks the body.