Health & Environmental Research Online (HERO)


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539750 
Journal Article 
Pathogenesis of hepatitis B virus infection 
Zhang, XD; Zhang, WY; Ye, LH 
2006 
1 
5 
637-647 
English 
Hepatitis B virus (HBV) consists of a circular, partially double-stranded DNA molecule of 3.2 kb in length, which contains four overlapping reading frames that code for surface proteins (HBsAg), core proteins (HBcAg/HBeAg), the viral polymerase and the transcriptional transactivator X protein. HBV infection can lead to chronic carriage of the virus and progressive liver diseases, such as hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC). HBV and hepatitis C virus or HIV coinfections can increase the HCC risk. A great amount of evidence demonstrates that HBV plays an important role in the development of liver diseases. Chronic hepatitis appears to be due to a suboptimal cellular immune response that destroys some of the infected hepatocytes and does not purge the virus from the remaining infected hepatocytes, thereby permitting the persisting virus to trigger a chronic indolent necroinflammatory liver disease that sets the stage for the development of HCC. However, the pathogenesis of HBV-related HCC is incompletely clarified. Hepatitis B virus X protein (HBx), an important transforming inducer, plays a crucial role in HCC occurrence, invasion and metastasis. Monitoring of the HBV genotypes and antibody to hepatitis B x antigen (anti-HBx) are significant for predicting the outcome of antiviral therapy or early diagnosis of liver cirrhosis and HCC. Some molecular approaches, such as antisense, oligonucleoticles, ribozymes, RNA interference targeting HBV mRNA, are available in antiviral therapies. The intracellular antibody technique and immune therapy by dendritic cells could potentially be used in future antiviral therapies. 
hepatitis; hepatitis B virus; hepatitis C virus; hepatocellular; carcinoma; liver cirrhosis; serological markers; promotes hepatocellular growth; x protein hbx; natural-history; gene-expression; centrosome amplification; cellular gene; core protein; risk-factors; viral load; e-antigen