Susceptibility and humoral response of brown trout X lake trout hybrids to infectious hematopoietic necrosis virus: a model for examining disease resistance mechanisms

LaPatra, Scott E.; Lauda, K. A.; Jones, G. R.; Shewmaker, W.; Groff, J. M.; Routledge, D.

doi:10.1016/s0044-8486(96)01381-6

Cited by 19 publications

(14 citation statements)

References 20 publications

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“…Garver, unpublished data). These results contrast with previous studies of IHNV M genogroup virus in rainbow trout, where injection challenge resulted in much more rapid and higher mortality relative to immersion challenge (LaPatra, Lauda, Jones, Shewmaker, Groff & Routledge 1996).…”

Section: Discussioncontrasting

confidence: 99%

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

Purcell

Garver²,

Conway

et al. 2009

Journal of Fish Diseases

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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.

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Section: Discussioncontrasting

confidence: 99%

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

Purcell

Garver²,

Conway

et al. 2009

Journal of Fish Diseases

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“…Our assumption was that injection bypassed the host entry stage of the virus by skirting skin mucosal defenses, an important component of the fish immune system (12). This assumption is supported by findings that injection challenges typically induce higher levels of mortality than immersion challenges in rainbow trout (12,35,45,48). However, the work presented here did not examine cellular entry, which is a completely separate phenomenon based largely on viral receptors.…”

Section: Discussionmentioning

confidence: 79%

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

Wargo

Kurath

2011

J Virol

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The relationship between pathogen fitness and virulence is typically examined by quantifying only one or two pathogen fitness traits. More specifically, it is regularly assumed that within-host replication, as a precursor to transmission, is the driving force behind virulence. In reality, many traits contribute to pathogen fitness, and each trait could drive the evolution of virulence in different ways. Here, we independently quantified four viral infection cycle traits, namely, host entry, within-host replication, within-host coinfection fitness, and shedding, in vivo, in the vertebrate virus Infectious hematopoietic necrosis virus (IHNV). We examined how each of these stages of the viral infection cycle contributes to the fitness of IHNV genotypes that differ in virulence in rainbow trout. This enabled us to determine how infection cycle fitness traits are independently associated with virulence. We found that viral fitness was independently regulated by each of the traits examined, with the largest impact on fitness being provided by within-host replication. Furthermore, the more virulent of the two genotypes of IHNV we used had advantages in all of the traits quantified. Our results are thus congruent with the assumption that virulence and within-host replication are correlated but suggest that infection cycle fitness is complex and that replication is not the only trait associated with virulence.Despite a recent surge in research, the evolution of viral virulence remains a controversial issue (1,7,10,18,22,37,50,60). Some studies have suggested a positive link between viral fitness and virulence (6, 13, 17, 39, 42, 49, 52-54, 58, 59), whereas others found no evidence of such an association (20,24,27) or even indicated that the converse, that virulence is negatively associated with viral fitness, is true (36, 43). Despite the fact that these studies span a wide range of virus and host taxa, a limitation of many of these studies is that viral fitness was typically estimated from only one or two virus traits, at one stage of the viral infection cycle. In reality, viral fitness is likely shaped by multiple traits at each of the viral infection stages, i.e., entry into the host, replication in the host, and shedding from the host, all of which could differentially impact selection for virulence (5).Most estimates of viral fitness come from examinations of the within-host replication stage of the viral infection cycle. 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 verteb...

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“…, 2001). In contrast, triploid hybrids in trout are more resistant to a virus, and they have lower antibody production against the virus when compared with nonhybrid diploids (LaPatra et al. , 1996).…”

Section: Discussionmentioning

confidence: 98%

Host ploidy, parasitism and immune defence in a coevolutionary snail–trematode system

Osnas

Lively

2006

Journal of Evolutionary Biology

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We studied the role of host ploidy and parasite exposure on immune defence allocation in a snail–trematode system (Potamopyrgus antipodarum‐Microphallus sp.). In the field, haemocyte (the defence cell) concentration was lowest in deep‐water habitats where infection is relatively low and highest in shallow‐water habitats where infection is common. Because the frequency of asexual triploid snails is positively correlated with depth, we also experimentally studied the role of ploidy by exposing both diploid sexual and triploid asexual snails to Microphallus eggs. We found that triploid snails had lower haemocyte concentrations than did diploids in both parasite‐addition and parasite‐free treatments. We also found that both triploids and diploids increased their numbers of large granular haemocytes at similar rates after parasite exposure. Because triploid P. antipodarum have been shown to be more resistant to allopatric parasites than diploids, the current results suggest that the increased resistance of triploids is because of intrinsic genetic properties rather than to greater allocation to defence cells. This finding is consistent with recent theory on the advantages of increased ploidy for hosts combating coevolving parasites.

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Susceptibility and humoral response of brown trout X lake trout hybrids to infectious hematopoietic necrosis virus: a model for examining disease resistance mechanisms

Cited by 19 publications

References 20 publications

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

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

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

Host ploidy, parasitism and immune defence in a coevolutionary snail–trematode system

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