title: Replication and shedding kinetics of infectious hematopoietic necrosis virus in juvenile rainbow trout.
abstract: Viral replication and shedding are key components of transmission and fitness, the kinetics of which are heavily dependent on virus, host, and environmental factors. To date, no studies have quantified the shedding kinetics of infectious hematopoietic necrosis virus (IHNV) in rainbow trout (Oncorhynchus mykiss), or how they are associated with replication, making it difficult to ascertain the transmission dynamics of this pathogen of high agricultural and conservation importance. Here, the replication and shedding kinetics of two M genogroup IHNV genotypes were examined in their naturally co-evolved rainbow trout host. Within host virus replication began rapidly, approaching maximum values by day 3 post-infection, after which viral load was maintained or gradually dropped through day 7. Host innate immune response measured as stimulation of Mx-1 gene expression generally followed within host viral loads. Shedding also began very quickly and peaked within 2days, defining a generally uniform early peak period of shedding from 1 to 4days after exposure to virus. This was followed by a post-peak period where shedding declined, such that the majority of fish were no longer shedding by day 12 post-infection. Despite similar kinetics, the average shedding rate over the course of infection was significantly lower in mixed compared to single genotype infections, suggesting a competition effect, however, this did not significantly impact the total amount of virus shed. The data also indicated that the duration of shedding, rather than peak amount of virus shed, was correlated with fish mortality. Generally, the majority of virus produced during infection appeared to be shed into the environment rather than maintained in the host, although there was more retention of within host virus during the post-peak period. Viral virulence was correlated with shedding, such that the more virulent of the two genotypes shed more total virus. This fundamental understanding of IHNV shedding kinetics and variation at the individual fish level could assist with management decisions about how to respond to disease outbreaks when they occur.
authors: Virginia Institute of Marine Science, College of William and Mary, PO Box 1346, Gloucester Point, VA 23062, United States. Electronic address: arwargo@vims.edu.
authors: Andrew R
authors: AR
authors: Wargo
authors: USGS Western Fisheries Research Center, 6505 NE 65th St., Seattle, WA 98115, United States.
authors: Robert J
authors: RJ
authors: Scott
authors: University of Washington, Department of Biology, Box 351800, Seattle, WA 98195, United States.
authors: Benjamin
authors: B
authors: Kerr
authors: USGS Western Fisheries Research Center, 6505 NE 65th St., Seattle, WA 98115, United States.
authors: Gael
authors: G
authors: Kurath
mesh_terms: D000818:Animals; D005393:Fish Diseases / Q000276:immunology / Q000401:mortality / Q000821:virology*; D005838:Genotype; D054884:Host-Pathogen Interactions / Q000235:genetics / Q000276:immunology; D007113:Immunity, Innate; D029142:Infectious hematopoietic necrosis virus / Q000502:physiology*; D007700:Kinetics; D017686:Oncorhynchus mykiss / Q000821:virology*; D019562:Viral Load; D014779:Virus Replication; D017201:Virus Shedding
keywords: Competition; Fitness; Replication; Shedding; Virus