Chronic Hepatitis B Pathogenesis

Hepatitis B virus (HBV) belongs to the family of hepatophilic DNA viruses (hepadnaviridae), with a genome length of about 3.2kb, and is a partially double-stranded cyclic DNA. HBV is relatively resistant, but it can be inactivated by boiling at 65°C for 10 h, or by high-pressure steam, and is also inactivated by ethylene oxide, glutaraldehyde, peracetic acid, and iodine vapour.HBV is also inactivated by ethylene oxide, glutaraldehyde, peracetic acid and iodine vapour. After the invasion of hepatocytes, part of the double-stranded cyclic HBV DNA in the cell nucleus to the negative chain DNA as a template to extend the positive chain to repair the gap area in the positive chain, the formation of covalent closed-circle DNA (cccDNA); and then cccDNA as a template, transcribed into several different lengths of mRNA, respectively, as the pre-genomic RNA and coding for a variety of antigens of HBV. cccDNA half-life (decay) period is relatively long, it is difficult to completely from the body to the HBV. HBV has been found to have 9 genotypes from A to I, with C and B genotypes predominating in China. HBV genotypes are associated with disease progression and the effectiveness of interferon alpha therapy. Compared with those infected with C genotype, those infected with B genotype have earlier HBeAg seroconversion and are less likely to progress to chronic hepatitis, cirrhosis, and primary hepatocellular carcinoma; and the response rate to interferon alpha therapy is higher in HBeAg-positive patients than in those infected with C genotype; and in patients infected with A genotype, it is higher than that in those infected with D genotype.