This review summarizes the unique genome organization and replication strategy of the Hepatitis A virus, distinguishing it from other mammalian picornaviruses.
HAV's distinct capsid, IRES, and replication distinguish it from other picornaviruses; leaves open targeted antiviral strategies.
It is an ancient virus with a long evolutionary history and multiple features of its capsid structure, genome organization, and replication cycle that distinguish it from other mammalian picornaviruses. HAV proteins are produced by cap-independent translation of a single, long open reading frame under direction of an inefficient, upstream internal ribosome entry site (IRES). Genome replication occurs slowly and is noncytopathic, with transcription likely primed by a uridylated protein primer as in other picornaviruses. Newly produced quasi-enveloped virions (eHAV) are released from cells in a nonlytic fashion in a unique process mediated by interactions of capsid proteins with components of the host cell endosomal sorting complexes required for transport (ESCRT) system.
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McKnight et al. (2018) studied this question.
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