Established Eurythermic Line of Fish Cells in vitro

Wolf, Ken; Quimby, Megan

doi:10.1126/science.135.3508.1065

Cited by 573 publications

(228 citation statements)

References 6 publications

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“…As IPNV is ubiquitous in Norwegian salmon farming (Melby et al 1991, Jarp et al 1995, the homogenates were treated with a mix of polyclonal neutralising antibodies against IPNV serotype Sp and serotype Ab. The homogenates were then inoculated onto cell cultures from bluegill fry fibroblast (BF)-2 cells (Wolf & Quimby 1966), epithelioma papulosum cyprini (EPC) (Fijan et al 1983), rainbow trout gonad (RTG)-2 (Wolf & Quimby 1962), chinook salmon embryo (CHSE)-214 (Lannan et al 1984) and Atlantic salmon head kidney (ASK) (Devold et al 2000). Inoculated cells were incubated for 1 wk at both 15 and 20°C in parallel and were regularly investigated with an inverted microscope for the occurrence of a cytopathic effect (CPE).…”

Section: Methodsmentioning

confidence: 99%

Experimental transmission of cardiomyopathy syndrome (CMS) in Atlantic salmon Salmo salar

Fritsvold¹,

Kongtorp²,

Taksdal³

et al. 2009

Dis. Aquat. Org.

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Cardiomyopathy syndrome (CMS) is a disease of unknown aetiology, having significant economic impact as it primarily affects large, farmed Atlantic salmon Salmo salar L. in seawater, close to harvest. In the present study, we have demonstrated that CMS is a transmissible disease under experimental conditions. Histopathological lesions consistent with CMS were induced in Atlantic salmon post-smolts after injection of tissue homogenate from farmed fish diagnosed with CMS. Six weeks post-injection (p.i.), experimental fish started developing focal to multi-focal lesions in the atrial endo-and myocardium, with subsequent progression to the ventricle. This proceeded into severe endocarditis and subsequent myocarditis with mononuclear cell infiltration of the atrium and, to a lesser degree, the spongy layer of the ventricle. These lesions were consistent with histopathological findings in field outbreaks of CMS. From Week 33 p.i., lesions also appeared in the compact myocardium, with focal epicarditis adjacent to focal myocardial lesions. In conclusion, these results indicate that CMS has an infectious aetiology and should be treated as a potentially contagious disease.

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Section: Methodsmentioning

confidence: 99%

Experimental transmission of cardiomyopathy syndrome (CMS) in Atlantic salmon Salmo salar

Fritsvold¹,

Kongtorp²,

Taksdal³

et al. 2009

Dis. Aquat. Org.

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“…Briefly, tissue from fry mortalities was homogenized using a sterile mortar, pestle and sand, and diluted (1:10) with Hanks balanced salt solution (Sigma-Aldrich, St Louis, MO, USA) supplemented with 2% fetal bovine serum (Sigma-Aldrich). The homogenate was centrifuged at 2500 g for 15 min at 4 1C and the supernatant filtered through 0.45 mm filter (Whatman, Maidstone, UK) before inoculation at 10 À3 dilution onto a 25 cm 2 tissue culture flask containing a 24-h old confluent monolayer of RTG-2 cells (Wolf and Quimby, 1962) grown on L-15 media (Sigma-Aldrich) supplemented with 2 mM L-glutamine, 2% fetal bovine serum, 100 U ml À1 penicillin and 100 mg ml À1 streptomycin. The virus-inoculated cells were incubated at 15 1C until a full cytopathic effect was evident.…”

Section: Virus Preparationmentioning

confidence: 99%

The susceptibility of Atlantic salmon fry to freshwater infectious pancreatic necrosis is largely explained by a major QTL

et al. 2009

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Infectious pancreatic necrosis (IPN) is a viral disease with a significant negative impact on the global aquaculture of Atlantic salmon. IPN outbreaks can occur during specific windows of both the freshwater and seawater stages of the salmon life cycle. Previous research has shown that a proportion of the variation seen in resistance to IPN is because of host genetics, and we have shown that major quantitative trait loci (QTL) affect IPN resistance at the seawater stage of production. In the current study, we completed a large freshwater IPN challenge experiment to allow us to undertake a thorough investigation of the genetic basis of resistance to IPN in salmon fry, with a focus on previously identified QTL regions. The heritability of freshwater IPN resistance was estimated to be 0.26 on the observed scale and 0.55 on the underlying scale. Our results suggest that a single QTL on linkage group 21 explains almost all the genetic variation in IPN mortality under our experimental conditions. A striking contrast in mortality is seen between fry classified as homozygous susceptible versus homozygous resistant, with QTL-resistant fish showing virtually complete resistance to IPN mortality. The findings highlight the importance of the major QTL in the genetic regulation of IPN resistance across distinct physiological lifecycle stages, environmental conditions and viral isolates. These results have clear scientific and practical implications for the control of IPN.

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“…This virus was provided by Dr. K. Wolf (National Health Research Laboratory, Kearneysville, WV, USA). The IPNV was made to pass 20 times through RTG-2 cells (Wolf and Quimby, 1962). Virus propagation techniques using the RTG-2 cell line were described by Okamoto et al (1983Okamoto et al ( , 1984.…”

Section: Ipn Virus: Sample Collection and Preparationmentioning

confidence: 99%

Identification of Additional Quantitative Trait Loci (QTL) Responsible for Susceptibility to Infectious Pancreatic Necrosis Virus in Rainbow Trout

et al. 2007

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ABSTRACT-Previous typing of microsatellite markers in a BC 1 F 1 backcross rainbow trout Oncorhynchus mykiss revealed two quantitative trait loci (QTL) with a significant impact on susceptibility to infectious pancreatic necrosis. In the present study, additional genetic markers were mapped using the same strain in order to increase QTL resolution. A total of 199 individuals were screened at 226 marker loci (106 microsatellites, 116 amplified fragment length polymorphism markers, classical major histocompatibility complex molecules [MHC class I, nonclassical MHC class I, MHC class II] and tyrosinase) and the QTL were determined by single-point and interval mappings. Seven QTL were distinguished in the linkage groups 12, 17, 23, 26, 29 and 31, in addition to the two already known in RT-3 and 22. The major QTL were those in RT-3, 12 and 22; whereas the classical MHC class I locus Onmy-UBA and the MHC class II locus Onmy-DAB were not associated with any of the QTL, a nonclassical MHC class I region with Onmy-UCA, Onmy-UDA, and Onmy-UEA mapped to the major QTL on RT-3.

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Established Eurythermic Line of Fish Cells in vitro

Abstract: An established line of fish cells has been propagated in vitro for 21 months and 48 subcultivations. Important characteristics of the cells are described.

Cited by 573 publications

References 6 publications

Experimental transmission of cardiomyopathy syndrome (CMS) in Atlantic salmon Salmo salar

Experimental transmission of cardiomyopathy syndrome (CMS) in Atlantic salmon Salmo salar

The susceptibility of Atlantic salmon fry to freshwater infectious pancreatic necrosis is largely explained by a major QTL

Identification of Additional Quantitative Trait Loci (QTL) Responsible for Susceptibility to Infectious Pancreatic Necrosis Virus in Rainbow Trout

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