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T n p l o~d hybnds were obtained from rainbow trout Oncorhynchus mykiss females crossed w t h sires of brook trout Salvehnus fontinalis arctic char S alpinus and lake trout S namaycush following heat-shock-provoked retention of the second polar body Survlval rates of h y b r~d s obtained were ca 50 % The hybnds and the parental specles were challenged with infect~ous pancreatic necrosls vlrus (IPNV) type Sp viral haemorrhagic septlcaem~a vlrus (VHSV) types 1 and 3 and lnfect~ous h a e m a t o p o~e t~c necrosis vlrus (IHNV) Ra~nbow trout X coho salmon ( 0 h s u t c h ) t n p l o~d hybnds were included in certain infection t i~a l s The results Indicated that brook trout were reslstant to VHSV and brook trout X ralnbow trout hybnds were reslstant to both VHSV and IHNV but suscept~ble to IPNV Arct~c char were susceptible to IPNV and resistant to VHSV The hybnds were suscept~ble to IPNV, but part~ally reslstant to VHSV Lake trout were partially resistant to IPNV but their hybnds w t h ralnbow trout were susceptible Lake trout infected by VHSV showed c l~n~c a l slgns and sign~ficant losses resulted

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Health control is a major issue in animal breeding and a better knowledge of the genetic bases of resistance to diseases is needed in farm animals including fish. The detection of quantitative trait loci (QTL) will help uncovering the genetic architecture of important traits and understanding the mechanisms involved in resistance to pathogens. We report here the detection of QTL for resistance to Viral Haemorrhagic Septicaemia Virus (VHSV), a major threat for European aquaculture industry. Two induced mitogynogenetic doubled haploid F2 rainbow trout (Oncorhynchus mykiss) families were used. These families combined the genome of susceptible and resistant F0 breeders and contained only fully homozygous individuals. For phenotyping, fish survival after an immersion challenge with the virus was recorded, as well as in vitro virus replication on fin explants. A bidirectional selective genotyping strategy identified seven QTL associated to survival. One of those QTL was significant at the genome-wide level and largely explained both survival and viral replication in fin explants in the different families of the design (up to 65% and 49% of phenotypic variance explained respectively). These results evidence the key role of innate defence in resistance to the virus and pave the way for the identification of the gene(s) responsible for resistance. The identification of a major QTL also opens appealing perspectives for selective breeding of fish with improved resistance.

Rainbow trout fry were infected by a pathogenic Sp type of infectious pancreatic necrosis virus isolated in France. Fry held at lO'C and infected at different ages showed a decrease of sensitivity with increasing age and ceased to be susceptible to the disease when 20 weeks old. Mortality was delayed at 6'C and lowered or suppressed at 16'C. When fry were moved from 10 to 16'C before infection mortality was also lowered but not when they were moved from 16 to lO'C. Late infection of sihlings kept at different temperatures before infection suggested a relation between the number of degrees x days and the final mortaUty recorded.

A non-pathogenic cell culture adapted variant was obtained from a normally pathogenic strain of IPN virus (Sp type) after several passages in RTG-2 cells. This cell culture modified (CCA) strain was compared with the original wild (W) strain in various tests. Cross neutralization tests showed no obvious antigenic difference between the two. However the CCA strain was neutralized by a 1:5000 dilution of normal trout serum whereas the W strain was not. In RTG-2 cells, CCA strain gave both large and small plaques, whereas the W strain gave only small ones. Both virus strains were heat sensitive and labile to cyclic freezing and thawing. The CCA virus was more stable in storage at 4°C under different pH conditions and its growth in RTG-2 cells was more rapid. Thert (supraoptimal temperature at which viral yield is depressed by 90%) appeared to be 19-20°C for the CCA strain and 18-19°C for the W strain. Pre-treatment of RTG-2 cells with ultraviolet inactivated CCA virus could inhibit growth of W virus, but had no effect on replication of homologous virus.