Abstract
Hepatitis B viruses are DNA viruses characterized by their very small genome size and their unique replication via reverse transcription. The circular genome has been efficiently exploited, thereby limiting genome variation, and leaves no space for genes in addition to those essentially needed during the viral live cycle. Hepatitis B viruses are prototype non-cytopathic viruses causing persistent infection. Human hepatitis B virus (HBV), as well as the closely related animal viruses, most frequently are transmitted vertically from mothers to their offspring. Because infection usually persists for many years, if not lifelong, hepatitis B viruses need efficient mechanisms to hide from the immune response of the host. To escape the immune response, they exploit different strategies. Firstly, they use their structural and non-structural proteins multiplely. One of the purposes is to alter the immune response. Secondly, they replicate by establishing a pool of stable extrachromosomal transcription templates, which allow the virus to react sensitively to changes in its microenvironment by up- or downregulating gene expression. Thirdly, hepatitis B viruses replicate in the liver which is an immunopriviledged site.
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