HCV causes chronic infection in the majority of infected patients, which is associated with attenuated adaptive immunity against the virus. Accumulating data suggest that HCV may modulate the adaptive anti-HCV immunity of the host to facilitate the establishment of viral persistence. Potential mechanisms of this modulation include infection of dendritic cells by HCV, as well as binding of HCV envelope or core proteins to cell surface receptors, resulting in perturbation of the functions of different immune cell subsets. These mechanisms may operate predominantly in the liver, the primary site of infection by HCV, where the unique hepatic environment favors tolerance rather than immunity to foreign antigens. Elucidation of these mechanisms may lead to development of novel therapeutic strategies combining both antiviral drugs and immunotherapy agents.
[hepatitis - buku HCV:chapter 14] |