Gulf of Alaska | Fishes and Fish Habitats
Elevated temperature increases disease progression and host response of Pacific herring to erythrocytic necrosis virus Presenter: Joanne Salzer, jsalzer@usgs.gov Paul Hershberger , phershberger@usgs.gov, USGS - Western Fisheries Research Center Justin Greer , jgreer@usgs.gov Maya Groner , mgroner@biglow.org Ashley MacKenzie , amackenzie@usgs.gov Jacob Gregg , jgregg@usgs.gov Controlled laboratory exposure studies provided evidence for a direct relationship between temperature and the progression of viral erythrocytic necrosis (VEN) in Pacific herring. Waterborne exposure of Pacific herring to kidney homogenates containing the causative iridovirus (erythrocytic necrosis virus - ENV) resulted in the establishment of infections, characterized by high infection prevalence (89%; 40/45) and mean viral loads (5.5 log10- gene copies / ug DNA) in kidney tissues at 44 d post exposure. Viral loads were higher in herring from the ambient (9.0 °C) and warm (13.5 °C) treatments (6.1 - 6.2 log10- gene copies / total DNA) than in the cool (6.9 °C) treatment (4.3 log10- gene copies / total DNA). Similarly, disease signs were temperature dependent, with cytoplasmic inclusion bodies occurring in 20% of herring in the cool, 47% in the ambient, and 60% in the warm treatments. The mean disease load in each fish (enumerated as the percent of erythrocytes with cytoplasmic inclusions), increased with temperature from 13% in the cool, 47% in the ambient, and 32% in the warm treatments at 44 days post exposure. Transcriptional analysis indicated that the number of differentially expressed genes among ENV-exposed herring also increased with temperature, time post exposure, and viral load. Correlation network analysis of transcriptomic data showed robust activation of interferon and viral immune responses in hepatic tissue of infected individuals independent of other experimental variables.
Alaska Marine Science Symposium 2023 191
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