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Accession information: (99)00133-7h.htm (shortcode: fig006sjd); 6 December 1999
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A proposed model of hepatitis E virus replication

Shahid Jameel

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Figure 6. A proposed model of hepatitis E virus replication. This model is based on domain homologies between hepatitis E virus (HEV) and other positive-stranded RNA viruses. (a) Following attachment to an as-yet-uncharacterised receptor on the surface of hepatocytes, HEV is internalised and uncoated in the cytoplasm by unknown mechanisms. (b) The genomic positive-strand RNA is translated into nsP, the nonstructural polyprotein encoded by ORF1, which can be processed into individual functional units that might include methyltransferase, protease, helicase and replicase activities. (c) The replicase so generated can use the positive-strand RNA as a template to synthesise the negative-strand replicative intermediates. Because of homology to alphaviral junction sequences (shown as a boxed region on the negative-strand RNA), it is proposed that two classes of positive-strand RNA species, genomic (d) and subgenomic (e), are synthesised from the negative-strand RNA intermediates. (f) The subgenomic RNAs are translated into pORF2 viral structural proteins encoded by ORF2 (and possibly pORF3 encoded by ORF3). (g) The structural protein subunits assemble into a capsid that includes the genomic positive-strand RNA to form progeny virions, which can infect other cells or be shed as infectious virus. The ORF2- and ORF3-encoded proteins might also provide other functions. Experimental proof for most of the steps in this model is awaited. Modified from a diagram in Ref. 2 (fig006sjd).

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