Abstract

Hepatitis B virus (HBV) is an enveloped virus with an icosahedral nucleocapsid. The constituent of the capsid is the Core protein, whose 149 N-terminal residues (Cp149) can self-assemble in vivo but also in vitro into capsids containing mainly 120 dimers. CpAMs (for Capsid Assembly Modulators), which are new antiviral molecules currently in clinical trials, can disrupt HBV capsid assembly. They can either lead to the formation of seemingly normal icosahedral capsids (class I CpAMs, e.g., JNJ-632), or to the formation of aberrant (larger and malformed) assemblies (class II CpAMs, e.g., BAY 41-4109).

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