Abstract
Hepatitis E virus (HEV), a major cause of acute hepatitis worldwide, infects approximately 20 million individuals annually. HEV can infect a wide range of mammalian and avian species, and cause frequent zoonotic spillover, increasingly raising public health concerns. To establish a successful infection, HEV needs to usurp host machineries to accomplish its life cycle from initial attachment to egress. However, relatively little is known about the HEV life cycle, especially the functional role(s) of cellular organelles and their associated proteins at different stages of HEV infection. Here, we summarize current knowledge regarding the relation of HEV with the different cell organelles during HEV infection. Furthermore, we discuss the underlying mechanisms by which HEV infection is precisely regulated in infected cells and the modification of host cell organelles and their associated proteins upon HEV infection.
Highlights
Hepatitis E Virus (HEV), a single-stranded, positive-sense RNA virus, is recognized as a significant cause of acute viral hepatitis in both developing and industrialized regions, leading to 20 million infections, more than 3 million cases of hepatitis E, and70,000 deaths annually [1,2]
We summarize the findings that shape our current understanding of host determinants involved in HEV life cycle, including binding, entry, trafficking, replication, assembly, and release
The pORF4 protein is encoded by genotype-1 HEV and directly interacts with eEF1α1 to stimulate RdRp activity, leading to enhanced replication [32]. These results indicate that the endoplasmic reticulum (ER) and ER-resident proteins play essential roles in the HEV life cycle via modulation of virally encoded proteins
Summary
Hepatitis E Virus (HEV), a single-stranded, positive-sense RNA virus, is recognized as a significant cause of acute viral hepatitis in both developing and industrialized regions, leading to 20 million infections, more than 3 million cases of hepatitis E, and. The serves as a template for the transcription of numerous positive-sense RNA genomes for packaging sgRNA is capped at the 5ʹ end and polyadenylated at the 3ʹ end, and translates into the capsid protein (pORF2C), into new virions, well as an kb subgenomic. Given the morphological differences between plates to produce non-structural polyproteins pORF1 and negative-stranded RNA inter non-enveloped virus particles and eHEV, it is believed that they utilize distinct pathways mediates for forming the replication and transcription complex [26]. The non-glycosylated ORF2 protein (pORF2C ) forms naked virions by self-assembling to capsid and packaging of the viral genome, while eHEV formation requires the engagement of pORF3 and the coating of lipid membrane in multivesicular bodies. Secreted particles remain associated with the lipid membrane in the culture supernatant of infected cells, while HEV remains in cells
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