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The host-Pathogen Interactions of Chinook Salmon (Oncorhynchus tshawytscha) and the Aquatic Rhabdoviral Pathogen Infectious Hematopoietic Necrosis Virus.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	The host-Pathogen Interactions of Chinook Salmon (Oncorhynchus tshawytscha) and the Aquatic Rhabdoviral Pathogen Infectious Hematopoietic Necrosis Virus./
作者:	Hernandez, Daniel G.
出版者:	Ann Arbor : ProQuest Dissertations & Theses, : 2019,
面頁冊數:	196 p.
附註:	Source: Dissertations Abstracts International, Volume: 81-04, Section: B.
Contained By:	Dissertations Abstracts International81-04B.
標題:	Virology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=13903850
ISBN:	9781088330791

The host-Pathogen Interactions of Chinook Salmon (Oncorhynchus tshawytscha) and the Aquatic Rhabdoviral Pathogen Infectious Hematopoietic Necrosis Virus.
Hernandez, Daniel G.

The host-Pathogen Interactions of Chinook Salmon (Oncorhynchus tshawytscha) and the Aquatic Rhabdoviral Pathogen Infectious Hematopoietic Necrosis Virus. - Ann Arbor : ProQuest Dissertations & Theses, 2019 - 196 p.

Source: Dissertations Abstracts International, Volume: 81-04, Section: B.

Thesis (Ph.D.)--University of Washington, 2019.

This item must not be sold to any third party vendors.

Infectious hematopoietic necrosis virus (IHNV) is an aquatic rhabdovirus that causes acute disease in Pacific salmon and trout populations in aquaculture facilities and freshwater conservation hatcheries across the northern hemisphere. While disease occurs primarily in juvenile fish, assessment of IHNV surveillance records across the US Pacific Northwest revealed a great majority of IHNV detections to be in adult fish at spawning. This investigation was premised on the high prevalence of IHNV infection in adult CRB Chinook salmon in the absence of disease in juvenile fish. Here, we evaluated field occurrence patterns of IHNV prevalence in Chinook salmon populations and conducted controlled virus exposures to characterize intraspecific variation in IHNV infection, disease and viral shedding in diverse Chinook salmon populations of the US Pacific Northwest. Our goal was to define the unique host-pathogen interactions of Columbia River Basin Chinook salmon and their interactions with the two genogroups (U and M) of IHN viruses prevalent in the CRB to better understand the role that Chinook salmon may have in the ecology and epidemiology of IHNV across the Columbia River watershed. Throughout this work, L genogroup IHNV was included as a positive control virus known to cause disease and mortality in California Chinook salmon. In the first stage of this work, experimental exposures of two genetically distinct populations of Chinook salmon from Washington State to U, M and L genogroup strains of IHNV showed observable differences in host susceptibility to infection and mortality at 1g. While not statistically significant, infection prevalence was higher in the stream-type population with each of the U and M viruses when compared to the ocean-type population. Similarly, mortality was also higher in the stream-type population when compared to the ocean-type population. While differences in host susceptibility were initially attributed to differences in life history phenotype, these findings may instead be linked to more fundamental differences in the origin of each host population. In this initial set of controlled virus exposures, one host population was sourced from outside of the CRB and the other was sourced from within the CRB. Assessment of field surveillance data for the prevalence of IHNV infection in Chinook salmon populations from the CRB and coastal watersheds of Washington and Oregon showed a disproportionally low prevalence of IHNV detection in Chinook salmon populations outside of the CRB. While differences in host susceptibility to IHNV infection and mortality between the stream- and ocean-type populations tested were consistent with field occurrence patterns, additional experimentation with Chinook salmon populations of the CRB showed juvenile susceptibility to IHNV infection to be less likely linked to life history phenotype. To comprehensively characterize intraspecific variation in juvenile Chinook salmon susceptibility to IHNV infection and disease, four populations of CRB Chinook salmon were experimentally exposed to U, M and L genogroup strains of IHNV. These controlled laboratory studies showed little variation in the overall susceptibility of CRB Chinook salmon to IHNV infection. Each host population became infected with the U and M genogroup viruses, at comparable levels observed with the positive control L genogroup virus. While infection prevalence and viral loads were comparably high among the four host populations, mortality was observably low following exposure to the U and M genogroup viruses relative to the L virus. Together, these experimental exposures empirically showed that juvenile Chinook salmon of the CRB can acquire U and M IHNV infections without the virulence observed with these virus types in juvenile sockeye salmon or rainbow and anadromous steelhead trout. These findings suggest that the absence of epizootic events in juvenile Chinook salmon of the CRB is not driven by the inability for U and M viruses to enter these host, but rather the ability of juvenile Chinook salmon to effectively control viral infections. In an effort to empirically test the hypothesis that subclinically infected Chinook salmon serve as vectors of IHNV, controlled laboratory exposures were conducted to characterized the shedding kinetics of U, M and L genogroup strains of IHNV in two diverse Chinook salmon populations of the CRB. A proportion of fish from each host population shed detectable quantities of U, M and L IHNV, where virus shedding peaked between 2-3 days post exposure and was no longer detected after day 5. While each host population shed comparable quantities of M and L IHN virus, a notable difference in the number of fish shedding U virus was observed. A disproportionately low number of lower CRB ocean-type (fall-run) Chinook salmon shed detectible U virus relative to the upper CRB stream-type (spring-run) population. Moreover, the stream-type population shed approximately 1 log more U virus consistently over the course of the infection, relative to the M and L IHN viruses. While our infectivity studies showed the U and M viruses to be equivalently infectious in four diverse populations of CRB Chinook salmon, results of our shedding studies revealed intraspecific variation in the shedding of U virus in CRB Chinook salmon. Our investigational approach made it possible to assess results of our controlled laboratory exposures relative to field occurrence patterns of U and M IHNV infection in Chinook salmon with diverse life history phenotypes. Assessment of the spatial and temporal distributions of spring-run (stream-type) and fall-run (ocean-type) Chinook salmon were observed to coincide with the geographic distributions and prevalence patterns of U and M IHNV across Chinook salmon populations of the CRB. Together, results of this investigation suggest that CRB Chinook salmon populations of the spring-run (stream-type) life history phenotype may be differentially contributing to the successful maintenance of IHNV across the Columbia River watershed.

ISBN: 9781088330791Subjects--Topical Terms:

642304
Virology.

The host-Pathogen Interactions of Chinook Salmon (Oncorhynchus tshawytscha) and the Aquatic Rhabdoviral Pathogen Infectious Hematopoietic Necrosis Virus.
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520 $a Infectious hematopoietic necrosis virus (IHNV) is an aquatic rhabdovirus that causes acute disease in Pacific salmon and trout populations in aquaculture facilities and freshwater conservation hatcheries across the northern hemisphere. While disease occurs primarily in juvenile fish, assessment of IHNV surveillance records across the US Pacific Northwest revealed a great majority of IHNV detections to be in adult fish at spawning. This investigation was premised on the high prevalence of IHNV infection in adult CRB Chinook salmon in the absence of disease in juvenile fish. Here, we evaluated field occurrence patterns of IHNV prevalence in Chinook salmon populations and conducted controlled virus exposures to characterize intraspecific variation in IHNV infection, disease and viral shedding in diverse Chinook salmon populations of the US Pacific Northwest. Our goal was to define the unique host-pathogen interactions of Columbia River Basin Chinook salmon and their interactions with the two genogroups (U and M) of IHN viruses prevalent in the CRB to better understand the role that Chinook salmon may have in the ecology and epidemiology of IHNV across the Columbia River watershed. Throughout this work, L genogroup IHNV was included as a positive control virus known to cause disease and mortality in California Chinook salmon. In the first stage of this work, experimental exposures of two genetically distinct populations of Chinook salmon from Washington State to U, M and L genogroup strains of IHNV showed observable differences in host susceptibility to infection and mortality at 1g. While not statistically significant, infection prevalence was higher in the stream-type population with each of the U and M viruses when compared to the ocean-type population. Similarly, mortality was also higher in the stream-type population when compared to the ocean-type population. While differences in host susceptibility were initially attributed to differences in life history phenotype, these findings may instead be linked to more fundamental differences in the origin of each host population. In this initial set of controlled virus exposures, one host population was sourced from outside of the CRB and the other was sourced from within the CRB. Assessment of field surveillance data for the prevalence of IHNV infection in Chinook salmon populations from the CRB and coastal watersheds of Washington and Oregon showed a disproportionally low prevalence of IHNV detection in Chinook salmon populations outside of the CRB. While differences in host susceptibility to IHNV infection and mortality between the stream- and ocean-type populations tested were consistent with field occurrence patterns, additional experimentation with Chinook salmon populations of the CRB showed juvenile susceptibility to IHNV infection to be less likely linked to life history phenotype. To comprehensively characterize intraspecific variation in juvenile Chinook salmon susceptibility to IHNV infection and disease, four populations of CRB Chinook salmon were experimentally exposed to U, M and L genogroup strains of IHNV. These controlled laboratory studies showed little variation in the overall susceptibility of CRB Chinook salmon to IHNV infection. Each host population became infected with the U and M genogroup viruses, at comparable levels observed with the positive control L genogroup virus. While infection prevalence and viral loads were comparably high among the four host populations, mortality was observably low following exposure to the U and M genogroup viruses relative to the L virus. Together, these experimental exposures empirically showed that juvenile Chinook salmon of the CRB can acquire U and M IHNV infections without the virulence observed with these virus types in juvenile sockeye salmon or rainbow and anadromous steelhead trout. These findings suggest that the absence of epizootic events in juvenile Chinook salmon of the CRB is not driven by the inability for U and M viruses to enter these host, but rather the ability of juvenile Chinook salmon to effectively control viral infections. In an effort to empirically test the hypothesis that subclinically infected Chinook salmon serve as vectors of IHNV, controlled laboratory exposures were conducted to characterized the shedding kinetics of U, M and L genogroup strains of IHNV in two diverse Chinook salmon populations of the CRB. A proportion of fish from each host population shed detectable quantities of U, M and L IHNV, where virus shedding peaked between 2-3 days post exposure and was no longer detected after day 5. While each host population shed comparable quantities of M and L IHN virus, a notable difference in the number of fish shedding U virus was observed. A disproportionately low number of lower CRB ocean-type (fall-run) Chinook salmon shed detectible U virus relative to the upper CRB stream-type (spring-run) population. Moreover, the stream-type population shed approximately 1 log more U virus consistently over the course of the infection, relative to the M and L IHN viruses. While our infectivity studies showed the U and M viruses to be equivalently infectious in four diverse populations of CRB Chinook salmon, results of our shedding studies revealed intraspecific variation in the shedding of U virus in CRB Chinook salmon. Our investigational approach made it possible to assess results of our controlled laboratory exposures relative to field occurrence patterns of U and M IHNV infection in Chinook salmon with diverse life history phenotypes. Assessment of the spatial and temporal distributions of spring-run (stream-type) and fall-run (ocean-type) Chinook salmon were observed to coincide with the geographic distributions and prevalence patterns of U and M IHNV across Chinook salmon populations of the CRB. Together, results of this investigation suggest that CRB Chinook salmon populations of the spring-run (stream-type) life history phenotype may be differentially contributing to the successful maintenance of IHNV across the Columbia River watershed.
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