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

Abstract

Host specificity is a phenomenon exhibited by all viruses. For the fish rhabdovirus infectious hematopoietic necrosis virus (IHNV), differential specificity of virus strains from the U and M genogroups has been established both in the field and in experimental challenges. In rainbow trout (Oncorhynchus mykiss), M IHNV strains are consistently more prevalent and more virulent than U IHNV. The basis of the differential ability of these two IHNV genogroups to cause disease in rainbow trout was investigated in live infection challenges with representative U and M IHNV strains. When IHNV was delivered by intraperitoneal injection, the mortality caused by U IHNV increased, indicating that the low virulence of U IHNV is partly due to inefficiency in entering the trout host. Analyses of in vivo replication showed that U IHNV consistently had lower prevalence and lower viral load than M IHNV during the course of infection. In analyses of the host immune response, M IHNV-infected fish consistently had higher and longer expression of innate immunerelated genes such as Mx-1. This suggests that the higher virulence of M IHNV is not due to suppression of the immune response in rainbow trout. Taken together, the results support a kinetics hypothesis wherein faster replication enables M IHNV to rapidly achieve a threshold level of virus necessary to override the strong host innate immune response.

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.…”

First field evidence of the evolution from a non-virulent HPR0 to a virulent HPR-deleted infectious salmon anaemia virus

“…Sequencing and functional characterization further suggest both HPR-deletion and a Q 266 L substitution, or insertion adjacent to the cleavage site in the F protein influences ISAV virulence [22], by promoting viral fusion and the activation of proteolytic cleavage [23,24]. However, other viral functions, for example virus receptor binding [25], virus uptake, replication rate, shedding of new virions [26,27], modulation of the host immune response [28,29] and the ability to spread to new hosts [30], can also influence virulence.…”

In Vivo Fitness Associated with High Virulence in a Vertebrate Virus Is a Complex Trait Regulated by Host Entry, Replication, and Shedding

“…For a few systems, researchers have made an effort to provide a detailed assessment of the importance of within-host dynamics on fitness, by separately quantifying replication in single-genotype infections and the relative abilities of virus genotypes to produce infectious progeny in a coinfection environment, herein referred to as coinfection fitness (15,39,59). However, the connection between within-host fitness and transmission remains elusive (20,24,42,52), partly due to an incomplete understanding of virus investment into shedding and entry (8,45). These limitations are compounded in vertebrate virus systems by the fact that viral fitness is not often quantified in vivo, using intact, immune competent, living hosts (13,29,36,42,43,53,55,59).…”

“…To assess both virus host entry and replication as a combined trait, we infected live rainbow trout with the two IHNV genotypes by the natural route of immersion in water containing virus and then quantified viral loads in individual fish after a 3-day period of in vivo replication (55,59). To independently quantify replication alone, we bypassed the host entry step of the natural infection process by administering the virus through intraperitoneal injection into the trout and subsequently quantified viral loads after a 3-day in vivo replication period (45). Comparison of the results from immersion and injection challenges thus provided an estimate of the contribution of host entry to fitness differences between the genotypes.…”