Open AccessReview
HBV Infection and Host Interactions: The Role in Viral Persistence and Oncogenesis
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Riccardo Nevola, Domenico Beccia, Valerio Rosato, Rachele Ruocco, Davide Mastrocinque, Angela Villani, Pasquale Perillo, Simona Imbriani, Augusto Delle Femine, Livio Criscuolo, Maria Alfano, Marco La Montagna, Antonio Russo, Raffaele Marfella, Domenico Cozzolino, Ferdinando Carlo Sasso, Luca Rinaldi, Aldo Marrone, Luigi Elio Adinolfi and Ernesto Claar
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Abstract
Hepatitis B virus (HBV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Despite the advent of vaccines and potent antiviral agents able to suppress viral replication, recovery from chronic HBV infection is still an extremely difficult goal to achieve.
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Hepatitis B virus (HBV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Despite the advent of vaccines and potent antiviral agents able to suppress viral replication, recovery from chronic HBV infection is still an extremely difficult goal to achieve. Complex interactions between virus and host are responsible for HBV persistence and the risk of oncogenesis. Through multiple pathways, HBV is able to silence both innate and adaptive immunological responses and become out of control. Furthermore, the integration of the viral genome into that of the host and the production of covalently closed circular DNA (cccDNA) represent reservoirs of viral persistence and account for the difficult eradication of the infection. An adequate knowledge of the virus–host interaction mechanisms responsible for viral persistence and the risk of hepatocarcinogenesis is necessary for the development of functional cures for chronic HBV infection. The purpose of this review is, therefore, to analyze how interactions between HBV and host concur in the mechanisms of infection, persistence, and oncogenesis and what are the implications and the therapeutic perspectives that follow.
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