Akademik Veri Yönetim Sistemi
VIRAL HEPATIT DERGISI-VIRAL HEPATITIS JOURNAL, cilt.21, sa.1, ss.1-7, 2015 (ESCI, TRDizin)
Hepatitis B virus (HBV) is still one of the major reasons of the liver disease and it increases the risk of the development of chronic hepatitis, cirrhosis and hepatocellular carcinoma as late-term complications. HBV is partially double-stranded DNA virus that is a member of the Hepadnaviridae virus family. HBV genome contains a small (3.2 kb) covalently closed circular DNA (cccDNA) that is transcribed to generate four known transcripts (3.5 kb, 2.4 kb, 2.1 kb and 0.7 kb size). These transcripts are encoded to produce polymerase, HBcAg, HBeAg, HBsAg (L, M, S surface proteins) and HBx that have defined roles in HBV life cycle and liver injury. Currently, available treatments for chronic hepatitis B are interferon (IFN) monotherapies (conventional IFN-alpha and Peg-IFN-alpha) or nucleos(t) ide analogues (lamivudine, adefovir, telbivudine, entecavir and tenofovir). None of currently approved drugs are curative for HBV infection since they rarely achieve virus eradication. New anti-HBV agents targeting different molecules involved in HBV infection and replication are needed to achieve curative treatments. To understand the HBV biology and life-cycle in detail is of critical importance for developing new anti-HBV agents to identify possible future targets for drugs. The aim of this review was to highlight the HBV replication and life cycle.