Abstract
Hepatitis E virus (HEV) infection is one of the most common causes of acute hepatitis in the world. HEV is an enterically transmitted positive-strand RNA virus found as a non-enveloped particle in bile as well as stool and as a quasi-enveloped particle in blood. Current understanding of the molecular mechanisms and host factors involved in productive HEV infection is incomplete, but recently developed model systems have facilitated rapid progress in this area. Here, we provide an overview of the HEV life cycle with a focus on the host factors required for viral entry, RNA replication, assembly and release. Further developments of HEV model systems and novel technologies should yield a broader picture in the future.
Highlights
Hepatitis E virus (HEV) has been identified as a cause of the waterborne hepatitis outbreaks in the early 1980s [1,2]
The mechanisms driving HEV assembly are poorly understood but early observations showed that RNA and the ORF2 protein can spontaneously assemble into virus-like particles in insect cells [86]
HEV research is a rapidly growing field, our current knowledge of the virus life cycle is still limited by important gaps
Summary
Hepatitis E virus (HEV) has been identified as a cause of the waterborne hepatitis outbreaks in the early 1980s [1,2]. The viral genome is released into the cytoplasm and the host translational machinery produces the ORF1 replicase, which drives viral RNA replication (Figure 1B). RNA viruses, especially those with relatively limited genome size and coding capacity, such as HEV, are dependent on the host cell machinery. The. andunidentified a quasi-enveloped form (eHEV), the entry viral As capsid subsequently interact with an as yet host factor and undergo the pathway of the virus may differ for these two forms. Since both quasi-enveloped and have non-enveloped are host factors involved in the initial attachment to the cell and virus internalization, including internalized in vesicles belonging to the endosomal pathway, it is plausible that they use a common the (GRP78), ATP synthase subunit β (ATPB5).
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