Halodesulfovibrio sp. MK-HDV
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA557563 | ENA |
REPOSITORIES: ENA
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Project description:MK: MK-801. Young male C57BL/6J mice received an injection of MK-801 (300 micro-g per g body weight). RNA from control mice were extracted 1hr, 2hr, 4hr, and 6hr after MK experimental mice received their last shock treatment. MK C+S: MK-801 & Context + Shock: Young male C57BL/6J mice received an injection of MK-801 (300 micro-g per g body weight) 1 h prior to contextual fear conditioning that consisted of: Placement into a novel spatial context for 2 min. After 2 min, a 1 sec (0.5 mA) shock was administered through a floor grid. The 2 min-1 sec shock paradigm was repeated for a total of 3 shocks. 1 min after the last shock, animals were removed to their homecage. RNA was extracted 1hr, 2hr, 4hr, and 6hr after the last shock treatment. Keywords: time-course
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Project description:MK: MK-801. Young male C57BL/6J mice received an injection of MK-801 (300 micro-g per g body weight). RNA from control mice were extracted 1hr, 2hr, 4hr, and 6hr after MK experimental mice received their last shock treatment. MK C+S: MK-801 & Context + Shock: Young male C57BL/6J mice received an injection of MK-801 (300 micro-g per g body weight) 1 h prior to contextual fear conditioning that consisted of: Placement into a novel spatial context for 2 min. After 2 min, a 1 sec (0.5 mA) shock was administered through a floor grid. The 2 min-1 sec shock paradigm was repeated for a total of 3 shocks. 1 min after the last shock, animals were removed to their homecage. RNA was extracted 1hr, 2hr, 4hr, and 6hr after the last shock treatment. Keywords: time-course
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Project description:Studying hepatitis delta virus (HDV) and developing new treatments is hampered by the absence limited availability of small animal models. Here a description of a robust mouse model of HDV infection that mimics several important characteristics of the human disease is presented. HDV- and HBV-replication competent genomes were delivered to the mouse liver using adeno-associated viruses (AAV) (AAV-HDV and AAV-HBV). Viral load, antigen expression and genomes were quantified at different time points after AAV injection. Furthermore, liver pathology, genome editing, and the activation of the innate immune response were evaluated. AAV-HDV infection initiated HDV replication in mouse hepatocytes. Genome-editing was confirmed by the presence of small and large-HDV-antigens and sequencing. Viral replication was detected for 45 days, even after the AAV-HDV vector had almost disappeared. In the presence of HBV, HDV infectious particles were detected in serum. Furthermore, as observed in patients, co-infection was associated with the reduction of HBV antigen expression and the onset of liver damage that included the up/down-regulation of genes involved in the development of liver pathologies. HDV replication induced a sustained type-I IFN response, which was significantly reduced in immunodeficient mice and almost absent in MAVS-deficient mice. The animal model described here reproduces important characteristics of human HDV infection and provides a valuable tool for characterizing the viral infection and for developing new treatments. Furthermore, MAVS was identified as a main player in HDV detection and adaptive immunity was found to be involved in the amplification of the innate immune response.
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