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ABSTRACT:
PROVIDER: PRJNA490839 | ENA |
REPOSITORIES: ENA
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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.
2022-05-19 | PXD030318 | Pride
Project description:Rabbit haemorrhagic disease virus (RHDV) belongs to the family Caliciviridae, genus Lagovirus and is used in Australia as a biocontrol tool to keep the population of european rabbits low. This virus has a positive-sense single-stranded RNA genome that encodes structural (capsid) and non-structural proteins. Due to the lack of an established cell culture system for this virus, some of the non-structural proteins are yet awaiting characterisation and their function is unknown. This work attempted to characterise the process of RHDV infection and identify pathways that alterate in RHDV-infected rabbit liver at the proteome level. Young rabbits were infected with RHDV2 (genotype GI.1bP-GI.2) and humanely killed 24 hours post-infection. 25% liver homogenates were prepared in RNAlater buffer and stored at -20C. Uninfected rabbit liver samples served as a control. Samples from three RHDV2-infected animals (K375, K376, K378) and three uninfected animals (K3, K14, K12) were used in this study.
2022-10-14 | PXD031027 | Pride
Project description:Rabbit hemorrhagic disease virus 2 Genome sequencing and assembly
| PRJNA590640 | ENA
Project description:Rabbit hemorrhagic disease is an acute and highly fatal infectious disease caused by rabbit hemorrhagic disease virus. The mortality rate of adult rabbits is more than 90 %, but 2-week-old young rabbits are not affected. Based on the differences in the susceptibility of young rabbits and adult rabbits to RHDV, TMT proteomics technology was used to detect and quantitatively analyze the liver tissue proteins of young rabbits (2 weeks old) and adult rabbits (6 months old). 4353 proteins were quantitatively obtained from the liver tissues of young rabbits and adult rabbits, and 821 differential proteins were screened. Among them, 294 proteins were significantly upregul-ated and 527 proteins were significantly down-regulated in the liver tissues of adult rabbits compared with young rabbits.
2022-11-30 | PXD045206 | iProX
Project description:Kyasanur Forest disease virus (KFDV) and the closely related Alkhurma hemorrhagic disease virus (AHFV) are emerging flaviviruses that cause severe viral hemorrhagic fevers in humans. Increasing geographical expansion and case numbers, particularly of KFDV in southwest India, class these viruses as a public health threat. Viral pathogenesis is not well understood and additional vaccines and antivirals are needed to effectively counter the impact of these viruses. However, current animal models for KFDV do not accurately reproduce viral tissue tropism or clinical outcomes observed in humans. Here, we show pigtailed macaques (Macaca nemestrina) infected with KFDV or AHFV develop viremia that peaks 2 to 4 days following inoculation. Over the course of infection, animals developed lymphocytopenia, thrombocytopenia, and elevated liver enzymes. Infected animals exhibited hallmark signs of human disease characterized by a flushed appearance, piloerection, dehydration, loss of appetite, weakness, and hemorrhagic signs such as epistaxis. Virus was commonly present in the gastrointestinal tract, consistent with human disease caused by KFDV and AHFV where gastrointestinal symptoms (hemorrhage, vomiting, diarrhea) are common. This work characterizes a nonhuman primate model for KFDV and AHFV that closely resembles human disease for further utilization in understanding host immunity and development of antiviral countermeasures.
2021-10-22 | GSE185797 | GEO
Project description:Rabbit hemorrhagic disease virus strain:Turretfield 2009 Genome sequencing and assembly
| PRJNA360155 | ENA
Project description:Zaire ebolavirus (ZEBOV) is among the deadliest known human pathogens, causing severe hemorrhagic fever with high case fatality rates ranging from 70-90%. The lack of effective vaccines or treatment available for ZEBOV renders this pathogen as a significant global biodefense threat, as evidenced by the current, highly lethal outbreak of a novel ZEBOV variant in western Africa. Existing mouse models of lethal ZEBOV infection do not reproduce hallmark symptoms of Ebola hemorrhagic fever (EHF) including prolonged blood coagulation, acute hepatitis, disseminated intravascular coagulation (DIC), and death from hemorrhagic shock, thus restricting pathogenesis studies to non-human primates (NHP). This has prevented rapid evaluation of countermeasures in outbreak scenarios, and impeded a comprehensive understanding of how host responses to infection contribute to severe EHF disease. Here we demonstrate that mice from the Collaborative Cross (CC), a panel of reproducible, recombinant inbred animals that span the genetic breadth of three murine subspecies, are susceptible to a spectrum of disease phenotypes following ZEBOV infection. In contrast to C57Bl6/J mice, which develop lethal disease without symptoms of EHF, CC recombinant inbred intercrossed (CC-RIX) lines develop either complete resistance to lethal disease or severe EHF characterized by prolonged coagulation times and 100% mortality. Disease resistance and survival is not dependent on viral tropism, as both resistant and EHF-susceptible lines show similar inflammation and cytopathic effect in target organs. Transcriptomics reveal potential mechanisms for both induction of severe hemorrhage in EHF mediated by IL-6 and vascular activation, and resistance to lethal infection by induction of lymphocyte differentiation and cellular adhesion. These data demonstrate that host responses specific to unique genetic backgrounds determine susceptibility to hemorrhagic syndrome independent of virus replication. The CC represents a novel mouse model for studying EHF pathogenesis, and we anticipate that it will be applied immediately to developing and evaluating therapeutic countermeasures. Microarrays were performed on liver and spleen samples from mice collected at days 1, 3, and 5 post-infection with mouse adapted Zaire ebolavirus or from time-matched mock-infected animals.
2014-05-01 | E-GEOD-57214 | biostudies-arrayexpress
Project description:Rhesus macaques (Macaca mulatta) infected with a lethal dose of lymphocytic choriomeningitis virus-strain WE (LCMV-WE) provide a model for Lassa fever virus infection of man. Like Lassa fever in human beings, disease begins with flu-like symptoms but can progress to morbidity fairly rapidly. Previously, we profiled the blood transcriptome of LCMV-infected monkeys (M. Djavani et al. J. Virol. 2007: PMID 17522210) showing distinct pre-viremic and viremic stages that discriminated between virulent and benign infections. In the present study, changes in liver gene expression from macaques infected with virulent LCMV-WE were compared to gene expression in uninfected monkeys as well as to monkeys that were infected but not diseased. We observed gene expression changes that occurred before the viremic stage of the disease, and could potentially serve as biomarkers that discriminate between exposure to a hemorrhagic fever virus and exposure to a benign virus. Based on a functional pathway analysis of differentially expressed genes, virulent LCMV-WE had a much broader effect on liver cell function than non-virulent virus. During the first few days of infection, virulent virus impacted gene expression associated with the generation of energy, such as fatty acid metabolism and glucose metabolism, with the complement and coagulation cascades, and with steroid metabolism, MAPK signaling and cell adhesion. For example, the energy profile resembled that of an organism entering starvation: acetyl-CoA carboxylase, a key enzyme of fatty acid synthesis, was shut down and gene products involved in gluconeogenesis were up-regulated. In conclusion, this study identifies several potential gene markers of LCMV-WE-associated liver disease and contributes to the database of gene expression changes correlated with LCMV pathogenesis in primates. 6 groups: uninfected controls, LCMV-WE infected (pre-viremic; day 1 to day 3), LCMV-WE infected (viremic; day 4 to day 7), LCMV-WE infected (post-viremic; day 8 to day 12), LCMV-Armstrong (LCMV-ARM; non-virulent strain) infected, and LCMV-ARM/LCMV-WE infected but not diseased. Each sample is from the liver of a different rhesus macaque.
2010-06-16 | E-GEOD-12254 | biostudies-arrayexpress
Project description:Genetic analysis of Rabbit hemorrhagic disease virus (RHDV) from Germany, 2013-2020
| PRJEB38327 | ENA
Project description:Rhesus macaques (Macaca mulatta) infected with a lethal dose of lymphocytic choriomeningitis virus-strain WE (LCMV-WE) provide a model for Lassa fever virus infection of man. Like Lassa fever in human beings, disease begins with flu-like symptoms but can progress to morbidity fairly rapidly. Previously, we profiled the blood transcriptome of LCMV-infected monkeys (M. Djavani et al. J. Virol. 2007: PMID 17522210) showing distinct pre-viremic and viremic stages that discriminated between virulent and benign infections. In the present study, changes in liver gene expression from macaques infected with virulent LCMV-WE were compared to gene expression in uninfected monkeys as well as to monkeys that were infected but not diseased. We observed gene expression changes that occurred before the viremic stage of the disease, and could potentially serve as biomarkers that discriminate between exposure to a hemorrhagic fever virus and exposure to a benign virus. Based on a functional pathway analysis of differentially expressed genes, virulent LCMV-WE had a much broader effect on liver cell function than non-virulent virus. During the first few days of infection, virulent virus impacted gene expression associated with the generation of energy, such as fatty acid metabolism and glucose metabolism, with the complement and coagulation cascades, and with steroid metabolism, MAPK signaling and cell adhesion. For example, the energy profile resembled that of an organism entering starvation: acetyl-CoA carboxylase, a key enzyme of fatty acid synthesis, was shut down and gene products involved in gluconeogenesis were up-regulated. In conclusion, this study identifies several potential gene markers of LCMV-WE-associated liver disease and contributes to the database of gene expression changes correlated with LCMV pathogenesis in primates.
2010-06-08 | GSE12254 | GEO