Paslahepevirus balayani
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA490248 | 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 (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: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:Primary objectives: The primary objective is to investigate circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
Primary endpoints: circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
| 2533916 | ecrin-mdr-crc
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