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Vertebrates such as humans serve as the natural hosts. Transmission routes are fecal-oral and blood.<ref name=ViralZone />
Following ingestion, HAV enters the bloodstream through the [[epithelium]] of the [[oropharynx]] or intestine.<ref name="Murray, P. r. 2005">Murray, P.R., Rosenthal, K.S. & Pfaller, M.A. (2005). Medical Microbiology 5th ed., Elsevier Mosby.</ref> The blood carries the virus to its target, the liver, where it multiplies within [[hepatocytes]] and [[Kupffer cells]] (liver macrophages). Viral replication is cytoplasmic. Entry into the host cell is achieved by attachment of the virus to host yeag receptors, which mediates [[endocytosis]]. Replication follows the positive-stranded RNA virus replication model. Translation takes place by viral initiation. The virus exits the host cell by lysis and [[viroporin]]s. [[Virions]] are secreted into the bile and released in stool. HAV is excreted in large numbers about 11 days prior to the appearance of symptoms or anti-HAV [[IgM]] [[antibodies]] in the blood. The [[incubation period]] is 15–50 days and risk of death in those infected is less than 0.5%.{{citation needed|date=June 2021}}
Within the liver hepatocytes, the [[RNA genome]] is released from the protein coat and is translated by the cell's own [[ribosome]]s. Unlike other picornaviruses, this virus requires an intact [[eukaryotic initiation factor 4G]] (eIF4G) for the initiation of translation.<ref name=aragones2010>{{cite journal |vauthors = Aragonès L, Guix S, Ribes E, Bosch A, Pintó RM |title=Fine-tuning translation kinetics selection as the driving force of codon usage bias in the hepatitis A virus capsid |journal=PLOS Pathog. |volume=6 |issue=3 |page=e1000797 |date=March 2010 |pmid=20221432 |pmc=2832697 |doi=10.1371/journal.ppat.1000797 |editor1-last=Andino |editor1-first=Raul |doi-access=free }}</ref> The requirement for this factor results in an inability to shut down host [[protein synthesis]], unlike other picornaviruses. The virus must then inefficiently compete for the cellular translational machinery, which may explain its poor growth in [[cell culture]]. Aragonès et al. (2010) theorize that the virus has evolved a naturally highly deoptimized codon usage with respect to that of its cellular host in order to negatively influence viral protein translation kinetics and allow time for capsid proteins to fold optimally.<ref name=aragones2010/>
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