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Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario

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dc.contributor.advisor Lumsden, John Misk, Ehab 2016-05-12T15:17:38Z 2016-05-12T15:17:38Z 2016-05 2016-05-05 2016-05-12
dc.description.abstract Spring viremia of carp virus (SVCV), an OIE reportable rhabdovirus and fish pathogen, was identified in Canada in 2006 in Hamilton Harbour but has not been reported subsequently. SVCV can have a significant impact on cyprinids, and so the susceptibility of three baitfish species (emerald shiner Notropis atherinoides, fathead minnow Pimpheles promelas, white sucker Catostomus commersonii from the order Cypriniformes was assessed using experimental infection. Millions of baitfish are moved around the province to support the sports fishing industry, and this represents a risk for spread of the virus. Emerald shiner, fathead minnow and koi (43, 53, and 33% mortality, respectively) were highly susceptible, but white sucker or rainbow trout (12.5 and 0% mortality), were not. Infection was confirmed by virus isolation and RT-qPCR and SVCV was immunolocalized in association with histological lesions using immunohistochemistry. A one-step reverse transcription quantitative PCR (RT-qPCR) was adapted and used retrospectively to test samples collected by the Ontario Ministry of Natural Resources for surveillance from 2008 to 2012. A total of 1432 fish from 35 water bodies in Ontario were examined using RT-qPCR, but no additional fish were identified with SVCV. Finally, the pathogenesis of the Rhabdovirus-host interaction at the gill epithelium was investigated using the RTgill-W1 cells. The cell line was pretreated with UV-inactivated (killed) VHSV and recombinant FliC and then infected with viral hemorrhagic septicemia virus (VHSV). The viral load and gene expression was investigated 1, 3, and 6 d post infection (PI) with qPCR. In addition, the transcriptome response of RTgill-W1 cells at 36 h post-treatment with SVCV, VHSV, UV-inactivated VHSV and FliC were tested using microarray and RT-qPCR. Pretreatment of RTgill-W1 cells with killed VSHV induced a reduction in viral load (nucleoprotein copy number by RT-qPCR) after infection. Transcription profiles in VHSV- and SVCV-infected or killed VHSV and FliC pretreated RTgill-W1 cells 36 h post-exposure detected 24, 22, 123 and 190 differentially expressed probes, which contained several important gene candidates with a potentially key role in innate immunity to rhabdovirus infection in gill epithelium. en_US
dc.description.sponsorship OMARFA, NSERC, Egyptian Government en_US
dc.language.iso en en_US
dc.subject Innate immunity en_US
dc.subject SVCV en_US
dc.subject Microarray en_US
dc.title Pathogenesis and Distribution of Spring Viremia of Carp Virus (SVCV) in Ontario en_US
dc.type Thesis en_US Pathobiology en_US Doctor of Philosophy en_US Department of Pathobiology en_US
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