Abstract
Chronic infection by the Hepatitis B virus (HBV) has no cure and is a major cause of liver damage and liver cancer. According to recent studies, the virus growth can be inhibited by capsid assembly inhibitors (CAMs), which bind in the pockets between the dimer subunits of the HBV capsid protein. This binding alters the orientation of the subunits in the capsid assembly intermediates and can inhibit the virus growth by either accelerating capsid assembly or by misdirecting it. However, the mechanisms of how CAMs affect assembly is presently not well understood, preventing a rational enrichment of their therapeutic potential.
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