Infectious haematopoietic necrosis virus genogroup‐specific virulence mechanisms in sockeye salmon, Oncorhynchus nerka (Walbaum), from Redfish Lake, Idaho

Abstract

Characterization of infectious haematopoietic necrosis virus (IHNV) field isolates from North America has established three main genogroups (U, M and L) that differ in host-specific virulence. In sockeye salmon, Oncorhynchus nerka, the U genogroup is highly virulent, whereas the M genogroup is nearly non-pathogenic. In this study, we sought to characterize the virus-host dynamics that contribute to genogroup-specific virulence in a captive stock of sockeye salmon from Redfish Lake in Idaho. Juvenile sockeye salmon were challenged by immersion and injection with either a representative U or M viral strain and sampled periodically until 14 days post-infection (p.i.). Fish challenged with each strain had positive viral titre by day 3, regardless of challenge route, but the fish exposed to the M genogroup virus had significantly lower virus titres than fish exposed to the U genogroup virus. Gene expression analysis by quantitative reverse transcriptase PCR was used to simultaneously assess viral load and host interferon (IFN) response in the anterior kidney. Viral load was significantly higher in the U-challenged fish relative to M-challenged fish. Both viruses induced expression of the IFN-stimulated genes (ISGs), but expression was usually significantly lower in the M-challenged group, particularly at later time points (7 and 14 days p.i.). However, ISG expression was comparable with 3 days post-immersion challenge despite a significant difference in viral load. Our data indicated that the M genogroup virus entered the host, replicated and spread in the sockeye salmon tissues, but to a lesser extent than the U genogroup. Both virus types induced a host IFN response, but the high virulence strain (U) continued to replicate in the presence of this response, whereas the low virulence strain (M) was cleared below detectable levels. We hypothesize that high virulence is associated with early in vivo replication allowing the virus to achieve a threshold level, which the host innate immune system cannot control.

Differential virulence mechanisms of infectious hematopoietic necrosis virus in rainbow trout (Oncorhynchus mykiss) include host entry and virus replication kinetics

“…Consistent with data obtained by Purcell et al (2009b) in sockeye salmon, the primary difference between the U and M viral infections was the faster in vivo kinetics and higher level of replication of the high-virulence virus (M IHNV in rainbow trout), which was able to persist even in the presence of a relatively high Mx-1 response. These results fit well with the kinetics hypothesis presented by Purcell et al (2009b), which links high virulence to rapid replication of IHNV. The virus takes advantage of the fact that the host innate immune system requires induction to become active.…”

“…As in previous observations in sockeye salmon (Purcell et al, 2009b), Mx-1 expression mirrored viral load in rainbow trout. This suggests a lagging immune response rather than a causal factor that controls viral load.…”

“…Infection with IHNV is known to rapidly induce a strong host innate IFN response (Trobridge et al, 1997a, b;Purcell et al, 2004;Landis et al, 2008;Purcell et al, 2009b) and, as in other aquatic rhabdoviruses, IHNV is reported to be sensitive to the effects of IFN (Eaton, 1990;RogelGaillard et al, 1993;Ooi et al, 2008). In U IHNV infection, it appeared that the lower level of immune response was sufficient to control the relatively lower level of viral load, resulting in lower fish mortality and eventual virus clearance.…”

“…Conversely, high virulence of U isolates and low virulence of M isolates were observed in sockeye and kokanee salmon. Purcell et al (2009b) recently investigated the virus-host dynamics that contribute to host-specific virulence of U and M IHNV in sockeye salmon. In sockeye salmon, both virus types entered the host, replicated and spread, but the more virulent U IHNV replicated significantly faster, and to higher levels relative to M IHNV.…”

Genotipificacion y relacion hospedador especifica del virus de la necrosis pancreatica infecciosa en Chile

“…Estudios basados en desafíos experimentales con ambas especies y genogrupos han mostrado que esta relación está asociada a una virulencia específica para cada hospedador (i.e., mortalidad causada por la infección), la cual depende principalmente de la capacidad del virus de entrar en el pez hospedador y de replicarse rá- Tapia et al (2015). **Sin considerar virus incluidos en Tapia et al (2015) y Jorquera et al (2016 pidamente (Peñaranda et al, 2009(Peñaranda et al, , 2011Purcell et al, 2009). De igual forma, la relación hospedadorespecífica encontrada en muestras de campo en este estudio podría ser confirmada mediante el desarrollo de un estudio de infección in vivo de ambos genogrupos del virus IPN en salmón del Atlántico y especies del género Oncorhynchus, para determinar si también está asociada al nivel de virulencia que estos genogrupos puedan presentar en cada especie.…”