Relationship between viral dose and outcome of infection in Atlantic salmon, Salmo salar L., post-smolts bath-challenged with salmonid alphavirus subtype 3

Abstract

Salmonid alphavirus subtype 3 (SAV3) causes pancreas disease (PD) and adversely affects salmonid aquaculture in Europe. A better understanding of disease transmission is currently needed in order to manage PD outbreaks. Here, we demonstrate the relationship between viral dose and the outcome of SAV3 infection in Atlantic salmon post-smolts using a bath challenge model. Fish were challenged at 12 °C with 3 different SAV3 doses; 139, 27 and 7 TCID50 L−1 of seawater. A dose of as little as 7 TCID50 L−1 of seawater was able to induce SAV3 infection in the challenged population with a substantial level of variation between replicate tanks and, therefore, likely represents a dose close to the minimum dose required to establish an infection in a population. These data also confirm the highly infectious nature of SAV through horizontal transmission. The outcome of SAV3 infection, evaluated by the prevalence of viraemic fish, SAV3-positive hearts, and the virus shedding rate, was positively correlated to the original SAV3 dose. A maximal shedding rate of 2.4 × 104 TCID50 L−1 of seawater h−1 kg−1 was recorded 10 days post-exposure (dpe) from the highest dose group. The method reported here, for the quantification of infectious SAV3 in seawater, could be useful to monitor PD status or obtain data from SAV3 outbreaks at field locations. This information could be incorporated into pathogen dispersal models to improve risk assessment and to better understand how SAV3 spreads between farms during outbreaks. This information may also provide new insights into the control and mitigation of PD.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-016-0385-2) contains supplementary material, which is available to authorized users.

Immune gene profiles in Atlantic salmon (salmo salar L.) post-smolts infected with SAV3 by bath-challenge show a delayed response and lower levels of gene transcription compared to injected fish

“…There was little difference in the transcription of most of the genes between positive and negative fish at earlier sampling points (S.1) possibly because although the fish were infected, the viral replication had not yet reached a detectable level in heart tissue. Fish which tested negative by RT-qPCR could still have been viraemic, as previously demonstrated [22,32]. Moreover, both infected groups reached 100% prevalence at later time-points indicating that all fish were infected and were responding with individual variance.…”

“…In order to evaluate the immune response in all its complexities it is clearly advantageous to have an infection model with a synchronized time-of-infection which is of sufficient infectivity to achieve 100% prevalence during the initial stage of infection. Lower doses in an infection model cause a staggered rather than a synchronized infection due to infected fish shedding virus and exposing naïve fish not infected at time zero [32]. This makes it difficult to relate the immune response to the time of infection.…”

Time after seawater transfer influences immune cell abundance and responses to SAV3 infection in Atlantic salmon

“…with either 10 4 TCID 50 SAV3 This is based on testing of different doses in the dose range over time while studying infection dynamics with SAV3 in our laboratory over several years, and in particular in two previously published studies. In these earlier studies, both a five times difference in dose (Jarungsriapisit, Moore, Maehle, et al, 2016) and larger fish with a reduced dose (Moore, Nilsen, et al, 2017) had no impact on the progression of histopathological changes, and thus, we could directly compare the two phases. Fish were anaesthetized using both a sedative, 10 mg/l metomidate, and an anaesthetic, 60 mg/l benzocaine, before handling and euthanized with 10 mg/l metomidate and 160 mg/l of Benzocaine before sampling.…”

Method for serial passage of infectious hematopoietic necrosis virus (IHNV) in rainbow trout

“…Empirical and theoretical studies in other systems have suggested that viral infection kinetics and synchrony can be dose dependent (Cummings et al 2012, Littwitz-Salomon et al 2017. Viruses may take longer to initiate infection and reach peak values at lower dosages compared to higher dosages (Chu & Volety 1997, Cummings et al 2012, Abdoli et al 2013, Jarungsriapisit et al 2016. This is further supported by our finding that peak shedding shifted from 48 h post immersion in fish challenged with virus grown in cell culture (P 0 ) to 72 h in fish exposed to virus shed from other fish (P 1 −P 3 ).…”

“…This is further supported by our finding that peak shedding shifted from 48 h post immersion in fish challenged with virus grown in cell culture (P 0 ) to 72 h in fish exposed to virus shed from other fish (P 1 −P 3 ). In addition, host clearance may be faster at lower virus exposure doses (Jarungsriapisit et al 2016).…”