Shared human/rabbit ligands for rabbit hemorrhagic disease virus.
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ABSTRACT:
SUBMITTER: Nystrom K
PROVIDER: S-EPMC3309641 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The rabbit hemorrhagic disease virus (RHDV) represents the causative agent of a highly contagious disease in rabbits that is often associated with high mortality. Because of the lack of a suitable cell culture system for RHDV, the pathogenic mechanism and replication of RHDV remains unclear. In order to analyze the pathogenic mechanism of RHDV to rabbits, we used New Zealand white rabbits infected with RHDV, collected liver tissues 32 hours after infection, and used TMT labeling for LC-MS analysis. Subsequently, it was compared and analyzed with the protein data of the liver tissue of the uninfected rabbits. Perform bioinformatics analysis on significantly different proteins. Finally, comprehensively analyze the influence of RHDV on host protein and pathway expression levels. This study provides clues to clarify the pathogenic mechanism of RHDV in rabbits.
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Project description:In September 2019, high mortality in commercial rabbits was reported in the Greater Accra Region of Ghana. Rabbit hemorrhagic disease virus 2 phylogenetically related to isolates from 2015-2017 outbreaks in the Netherlands was confirmed as the causative agent. The virus has not yet been detected in native rabbits in Ghana.
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Project description:Twenty-three of 42 European rabbits (Oryctolagus cuniculus), belonging to the same rabbit colony, died in March 2020 (55% mortality) in Chiba prefecture, Japan. The disease course was extremely acute without indicators of death or hemorrhage. Necropsy revealed liver swelling, discoloration, cloudiness and fragility, and pulmonary edema. Histologically, severe hepatocellular necrosis (mainly peripheral) and intra-glomerular capillary hyalin thrombi were observed. On molecular-biological examination, reverse transcription polymerase chain reaction analysis of RNA from tissues detected a rabbit hemorrhagic disease virus, confirmed as a RHDV-2 VP60 fragment, which shared 99.42% nucleotide identity with the homologous fragment of RHDV-2 German isolate by nucleotide sequence analysis. This report shows the outbreak of rabbit hemorrhagic disease caused by RHDV-2, an emerging infectious disease, in Japan.
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Project description:Rabbit hemorrhagic disease (RHD) is a highly contagious disease caused by rabbit hemorrhagic disease virus (RHDV). Previous research has shown that RHDV induces apoptosis in numerous cell types, although the molecular mechanisms underlying the apoptosis induced by RHDV are not well understood. One possible factor is non-structural protein 6 (NSP6), a 3C-like protease that plays an important role in processing viral polyprotein precursors into mature non-structural proteins. To fully establish a role for NSP6, the present study examined the effects of ectopic expression of the protein in rabbit (RK13) and human (HeLa and HepG2) cells. We found that NSP6 suppressed cell viability and promoted apoptosis in all three cell types in a dose-dependent manner. We also identified increased caspase-3, -8, and -9 activities in RK13 cell, and an increased Bax to Bcl2 mRNA ratio. Mechanistically, the ability of NSP6 to induce apoptosis was impaired by mutation of the catalytic His27 residue. Our study has shown that RHDV NSP6 can induce apoptosis in host cells and is likely an important contributor to RHDV-induced apoptosis and pathogenesis.
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