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231227s2024 xx |||||o 00| ||eng c |
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|a 10.1002/aah.10202
|2 doi
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|a pubmed24n1319.xml
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|a (DE-627)NLM366151088
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|a (NLM)38124451
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Salzer, J E
|e verfasserin
|4 aut
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|a Effects of temperature on viral load, inclusion body formation, and host response in Pacific Herring with viral erythrocytic necrosis (VEN)
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|c 2024
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 07.03.2024
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|a Date Revised 07.03.2024
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|a published: Print-Electronic
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|a RefSeq: PRJNA862443, GCF_900700415.2
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|a Citation Status MEDLINE
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|a Published 2023. This article is a U.S. Government work and is in the public domain in the USA.
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|a OBJECTIVE: The primary objective of this study was to determine the effects of temperature on viral erythrocytic necrosis (VEN) progression under controlled conditions. Secondarily, this study was intended to evaluate the combined effects of temperature and VEN on the Pacific Herring Clupea palasii transcriptome
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|a METHODS: The effects of temperature on VEN progression were assessed by waterborne exposure of laboratory-reared, specific-pathogen-free Pacific Herring to tissues homogenates containing erythrocytic necrosis virus (ENV) at 6.9, 9.0, or 13.5°C
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|a RESULT: Exposure of Pacific Herring to ENV resulted in the establishment of infections characterized by high infection prevalence (89%; 40/45) and mean viral loads (5.5 log10 [gene copies/μg genomic DNA]) in kidney tissues at 44 days postexposure. Mean viral loads were significantly higher in fish from the ambient (mean = 9.0°C) and warm (mean = 13.5°C) treatments (6.1-6.2 log10 [gene copies/total genomic DNA]) than in fish from the cool (mean = 6.9°C) treatment (4.3 log10 [gene copies/μg genomic DNA]). Similarly, the peak proportion of diseased fish was directly related to temperature, with cytoplasmic inclusion bodies detected in 21% of fish from the cool treatment, 52% of fish from the ambient treatment, and 60% of fish from the warm treatment. The mean VEN load in each fish (enumerated as the percentage of erythrocytes with cytoplasmic inclusions) at 44 days postexposure increased with temperature from 15% in the cool treatment to 36% in the ambient treatment and 32% in the warm treatment. Transcriptional analysis indicated that the number of differentially expressed genes among ENV-exposed Pacific Herring increased with temperature, time postexposure, and viral load. Correlation network analysis of transcriptomic data showed robust activation of interferon and viral immune responses in the hepatic tissue of infected individuals independent of other experimental variables
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|a CONCLUSION: Results from this controlled laboratory study, combined with previous observations of natural epizootics in wild populations, support the conclusion that temperature is an important disease cofactor for VEN in Pacific Herring
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|a Journal Article
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|a Pacific Herring
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| 650 |
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4 |
|a disease in a changing environment
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| 650 |
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4 |
|a gene expression
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| 650 |
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4 |
|a viral erythrocytic necrosis
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| 650 |
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|a DNA
|2 NLM
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| 650 |
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|a 9007-49-2
|2 NLM
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| 700 |
1 |
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|a Greer, J B
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Groner, M L
|e verfasserin
|4 aut
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| 700 |
1 |
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|a MacKenzie, A H
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Gregg, J L
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Hershberger, P K
|e verfasserin
|4 aut
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| 773 |
0 |
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|i Enthalten in
|t Journal of aquatic animal health
|d 1998
|g 36(2024), 1 vom: 20. März, Seite 45-56
|w (DE-627)NLM098202006
|x 1548-8667
|7 nnns
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| 773 |
1 |
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|g volume:36
|g year:2024
|g number:1
|g day:20
|g month:03
|g pages:45-56
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| 856 |
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|u http://dx.doi.org/10.1002/aah.10202
|3 Volltext
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|d 36
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