Paslahepevirus balayani
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ABSTRACT:
PROVIDER: PRJNA494038 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Paslahepevirus balayani Genome sequencing
| PRJNA517081 | ENA
Project description:Paslahepevirus balayani Raw sequence reads
| PRJNA483408 | ENA
Project description:Paslahepevirus balayani Genome sequencing and assembly
| PRJNA490248 | ENA
Project description:Paslahepevirus balayani (HEV) sequencing
| PRJEB107200 | ENA
Project description:Paslahepevirus balayani strain:FR-HuHEVF3f | isolate:HEV3f-P7H Genome sequencing and assembly
| PRJNA685626 | ENA
Project description: Not available
| S-EPMC10288091 | biostudies-literature
Project description:The Paslahepevirus balayani hepatitis E virus (HEV) and the distantly related Rocahepevirus ratti rat HEV pose a risk for zoonotic transmission to humans. However, the molecular determinants for HEV transmission between species remain unknown. Despite the broad host range including its ability to infect certain rodent species, infections of animals of the genus Mus within the subfamily Murinae are rarely documented. To dissect the molecular mechanisms underlying species barriers to HEV infection, this study aimed to investigate the virus replication cycle and immune-related determinants responsible for restricted HEV infection in murine hepatocytes. Murine hepatic cell lines supported moderate levels of zoonotic HEV replication and infectious virion production upon transfection of in vitro transcribed viral RNA. Notably, viral replication was not restricted by innate immune responses or presence of dominant restriction factors but was limited by absence of host-specific dependency factors. While successful attachment to murine hepatic cells was detected, mechanisms of viral entry differed between human and murine hepatocytes, correlating with murine cell lines and primary murine hepatocytes being refractory to HEV infection. In summary, the murine barrier to HEV infection is defined at the viral entry stage, specifically by a block post attachment and before viral replication is initiated. These findings shed new light on the fundamental role of viral entry mechanisms in defining HEV species tropism.
2026-08-07 | GSE319021 | GEO
Project description:A significant number of pandemics, endemics and even sporadic outbreaks trace back to zoonotic spillovers of emerging RNA viruses. Especially, zoonotic infections with the distantly related hepatitis E virus (HEV, species Paslahepevirus balayani) from various animal origins, such as pigs, deer, wild boar, rabbits and camelids, are well-documented and account for 20 million acute hepatitis cases each year. The detection of HEV RNA in rats surrounding pig farms suggest that they serve as an additional reservoir and source of zoonotic HEV infection. Moreover, the rising number of zoonotic spillover events with the distantly related rat hepatitis E virus (ratHEV, species Rocahepevirus ratti) underscores the urgent need to elucidate the role of rats as a reservoir for HEV infection and in the transmission dynamics of viruses within the family Hepeviridae. Herein, we introduce a novel HEV reverse zoonosis model based on the infection of rat liver cells, which supports completion of the entire HEV replication cycle. RNA sequencing analyses unraveled distinct host responses to HEV infection characterized by minimal activation of innate immune responses. Importantly, host-directed antivirals targeting entry factors previously identified in human host cells effectively restricted HEV infection in rat liver cells. Furthermore, human-specific genomic rearrangements conferred increased fitness across human and rat hepatoma cells. In conclusion, our study indicates conserved viral replication mechanisms of HEV between rats and humans, providing valuable insights into the molecular mechanisms of zoonotic spillover across species.
2026-05-01 | GSE329031 | GEO
Project description:The hepatitis E virus (HEV; species Paslahepevirus balayani) is a common human pathogenic and zoonotic virus that can cause both acute fulminant and chronic hepatitis. Despite its reputation as a hepatotropic virus, HEV infection is also associated with a number of extrahepatic diseases, including kidney disorders. However, the extent to which HEV replicates in kidney cells remains unclear. The present study aims to investigate the capacity of HEV to propagate in kidney cells in vitro and to assess whether HEV displays mutational signatures that correlate with compartmentalisation in vivo. We use HEV cell culture models to study the replication cycle and the effect of antivirals in human kidney cell lines and primary cells. In addition, we identified patients with chronic HEV infection (n = 9) from which we then sequenced viral RNA of urine, stools and plasma to analyse the viral sequence composition, to assessintra-host diversity and compartmentalisation(n = 2). A wide range of human kidney cell lines as well as primary cells supports viral entry, replication and propagation of HEV in vitro. Interestingly, the broad-spectrum antiviral ribavirin was less effective in inhibiting HEV replication in some kidney cells. Sequencing of HEV RNA-directed RNA polymerase coding region from plasma, stool and urine and subsequent phylogenetic analysis revealed diversification of HEV into tissue-specific viral subpopulations. In particular, the viruses derived from urine were found to be distinct from those derived from plasma and stool. In conclusion, kidney cells support the propagation of HEV in vitro and exhibit reduced sensitivity to antiviral treatment. Furthermore, HEV patient-derived sequences demonstrated compartmentalisation into distinct clusters that correlated with sample source. Collectively, these data indicate the potential for extrahepatic replication of HEV, which may result in clinically significant disease or serve as a reservoir for patient relapse.
2025-07-02 | GSE300759 | GEO