Pathogenesis of HBV infection Jacek Juszczyk Medical Science Review - Hepatologia 2010; 10 7-12 aaICID: 911662
Article type: Review article
IC™ Value: 3.34
Abstract provided by Publisher
Approximately 5–10% of acutely HBV infected immunocompetent adults develop a chronic hepatitis with different patterns of severity and course. Viral and host factors causing HBV persistence are not completely understood, but it is widely accepted that this virus is not directly cytopathic. The response to HBV is influenced by the immunological events during the initial phase of HBV replication. Many data has revealed that HBV fails to activate early immunological respponses. The control of HBV infection was thought to be dependent on the destruction of infected cells, as well as by cytokine-dependent curative mechanis, without hepatocyte necrosis. The ability to mount an efficient, virus-specific helper and cytotoxic T-cell response is essential for control of HBV infection. Chronic hepatitis appears to be due to a suboptimal cellular immune response and consequently unuseful, thereby permitting the persisting virus to trigger a chronic necroinflammatory liver disease. The template of HBV transcription, the covalently closed circular DNA (cccDNA) plays a key role in the virus replication and as factor of persistence of infection. The size of cccDNA pool under influence of new anti-viral drug may be only reduced, but not eliminated.