Key result
Deletion of the HEV ORF3 protein caused a complete lack of fecal virus shedding and failure to sustain persistent infection in humanized mice, and a 70% reduction in apical viral release in vitro.
Why the study?
No HEV-specific treatments are available, and the poorly understood HEV life cycle hampers the development of antivirals.
The viral ORF3 protein is essential for HEV fecal shedding and persistent infection, providing a potential target for antiviral development.
HEV infections are associated with significant morbidity and mortality. HEV gt3 additionally can cause persistent infection, which can rapidly progress to liver cirrhosis. Currently, no HEV-specific treatments are available. The poorly understood HEV life cycle hampers the development of antivirals for HEV. Here, we investigated the role of the viral ORF3 protein in HEV infection in polarized hepatocyte cultures and human liver chimeric mice. We found that two major aspects of the HEV life cycle require ORF3: fecal virus shedding and persistent infection. These results provide a rationale for targeting ORF3 to treat HEV infection.
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A 2021 study studied Hepatitis E virus (HEV) infection. ORF3-deficient (ORF3null) HEV vs. Wild-type (WT) HEV was evaluated on Fecal virus shedding, persistent liver infection, and apical viral release. Deletion of the HEV ORF3 protein caused a complete lack of fecal virus shedding and failure to sustain persistent infection in humanized mice, and a 70% reduction in apical viral release in vitro.
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