Shedding Kinetics of Infectious Hematopoietic Necrosis Virus (IHNV) in Juvenile Spring- and Fall-Run Chinook Salmon of the Columbia River Basin.

Abstract

Simple SummaryWhen a virus infects a host it reproduces in that host and then sheds from the host in order to find new hosts for more rounds of reproduction. Thus, virus shedding is a critical step in the host-to-host transmission cycles that allow a virus to spread across a landscape and persist over time. In Pacific salmon and trout the virus infectious hematopoietic necrosis virus (IHNV) causes significant disease, with up to 50% mortality in outbreaks in some conservation hatcheries. Chinook salmon have evolved as two distinct life-history types, referred to as spring- and fall Chinook salmon, and they are the most abundant host of IHNV in the Columbia River basin (CRB) of Washington, Oregon, and Idaho. Here we examined the timing and quantity of virus shedding from both spring-run and fall-run CRB Chinook salmon after controlled exposures to three IHNV strains representing different virus subgroups. We observed rapid shedding kinetics with similar timing for two virus strains in both host types. However, spring Chinook salmon shed much more virus from the UC subgroup than fall fish, suggesting that spring Chinook salmon may play a dominant role in the ecology and maintenance of IHNV in the CRB.This investigation sought to characterize the shedding of infectious hematopoietic necrosis virus (IHNV) in two populations of Columbia River Basin (CRB) Chinook salmon (Oncorhynchus tshawytscha). Juvenile spring- and fall-run Chinook salmon were exposed by immersion to each of three IHN virus strains from the UC, MD, and L subgroups, and then monitored for viral shedding from individual fish for 30 days. Detectable quantities of UC, MD and L IHN virus were shed by a subset of fish from each host population (1–9 out of 10 fish total in each treatment group). Viral shedding kinetics were consistent, with a rapid onset of shedding, peak shedding by 2–3 days, and then a rapid decline to below detectable levels by 7 days’ post-exposure to IHNV. Intraspecies variation was observed as spring Chinook salmon shed more UC virus than fall fish: spring Chinook salmon shed UC virus in greater numbers of fish, with 22-fold higher mean peak shedding magnitude, 33-fold higher mean total virus shed per fish, and 900-fold higher total virus shed per treatment group. The L and MD viruses had comparable shedding at intermediate levels in each host population. All viral shedding occurred well before host mortality began, and shedding magnitude did not correlate with virulence differences. Overall, the greater shedding of UC virus from spring Chinook salmon, combined with low virulence, indicates a uniquely high transmission potential that may explain the predominance of UC viruses in CRB Chinook salmon. This also suggests that spring-run fish may contribute more to the ecology of IHNV in the CRB than fall-run Chinook salmon.