Summary Temperature is considered as the major factor determining virus inactivation in the environment. Food industries, therefore, widely apply temperature as virus inactivating parameter. This review encompasses an overview of viral inactivation and virus genome degradation data from published literature as well as a statistical analysis and the development of empirical formulae to predict virus inactivation. A total of 658 data (time to obtain a first log10 reduction) were collected from 76 published studies with 563 data on virus infectivity and 95 data on genome degradation. Linear model fitting was applied to analyse the effects of temperature, virus species, detection method (cell culture or molecular methods), matrix (simple or complex) and temperature category (<50 and ≥50°C). As expected, virus inactivation was found to be faster at temperatures ≥50°C than at temperatures <50°C, but there was also a significant temperature–matrix effect. Virus inactivation appeared to occur faster in complex than in simple matrices. In general, bacteriophages PRD1 and PhiX174 appeared to be highly persistent whatever the matrix or the temperature, which makes them useful indicators for virus inactivation studies. The virus genome was shown to be more resistant than infectious virus. Simple empirical formulas were developed that can be used to predict virus inactivation and genome degradation for untested temperatures, time points or even virus strains.

Viral encephalopathy and retinopathy (VER), otherwise known as viral nervous necrosis (VNN), is a major devastating threat for aquatic animals. Betanodaviruses have been isolated in at least 70 aquatic animal species in marine and in freshwater environments throughout the world, with the notable exception of South America. In this review, the main features of betanodavirus, including its diversity, its distribution and its transmission modes in fish, are firstly presented. Then, the existing diagnosis and detection methods, as well as the different control procedures of this disease, are reviewed. Finally, the potential of selective breeding, including both conventional and genomic selection, as an opportunity to obtain resistant commercial populations, is examined.

BackgroundEuropean sea bass (Dicentrarchus labrax) is one of the most important species for European aquaculture. Viral nervous necrosis (VNN), commonly caused by the redspotted grouper nervous necrosis virus (RGNNV), can result in high levels of morbidity and mortality, mainly during the larval and juvenile stages of cultured sea bass. In the absence of efficient therapeutic treatments, selective breeding for host resistance offers a promising strategy to control this disease. Our study aimed at investigating genetic resistance to VNN and genomic-based approaches to improve disease resistance by selective breeding. A population of 1538 sea bass juveniles from a factorial cross between 48 sires and 17 dams was challenged with RGNNV with mortalities and survivors being recorded and sampled for genotyping by the RAD sequencing approach.ResultsWe used genome-wide genotype data from 9195 single nucleotide polymorphisms (SNPs) for downstream analysis. Estimates of heritability of survival on the underlying scale for the pedigree and genomic relationship matrices were 0.27 (HPD interval 95%: 0.14-0.40) and 0.43 (0.29–0.57), respectively. Classical genome-wide association analysis detected genome-wide significant quantitative trait loci (QTL) for resistance to VNN on chromosomes (unassigned scaffolds in the case of ‘chromosome’ 25) 3, 20 and 25 (P < 1e06). Weighted genomic best linear unbiased predictor provided additional support for the QTL on chromosome 3 and suggested that it explained 4% of the additive genetic variation. Genomic prediction approaches were tested to investigate the potential of using genome-wide SNP data to estimate breeding values for resistance to VNN and showed that genomic prediction resulted in a 13% increase in successful classification of resistant and susceptible animals compared to pedigree-based methods, with Bayes A and Bayes B giving the highest predictive ability.ConclusionsGenome-wide significant QTL were identified but each with relatively small effects on the trait. Tests of genomic prediction suggested that incorporating genome-wide SNP data is likely to result in higher accuracy of estimated breeding values for resistance to VNN. RAD sequencing is an effective method for generating such genome-wide SNPs, and our findings highlight the potential of genomic selection to breed farmed European sea bass with improved resistance to VNN.Electronic supplementary materialThe online version of this article (10.1186/s12711-018-0401-2) contains supplementary material, which is available to authorized users.

SUMMARY BackgroundFew data are available on the incidence, risk factors and contamination pathways involved in acute indigenous hepatitis E in developed countries.

Viral Nervous Necrosis (VNN) is a major threat for the European sea bass (Dicentrarchus labrax) aquaculture industry. The improvement of disease resistance through selective breeding is a promising option to reduce outbreaks. With the development of high-throughput genotyping technologies, identification of genomic regions involved in the resistance could improve the efficiency of selective breeding. The aim of this study was to identify quantitative trait loci (QTL) involved in VNN resistance and to quantify their effect.Four experimental backcross families comprising 378, 454, 291 and 211 individuals and two commercial populations A and B comprising 1027 and 1042 individuals obtained from partial factorial crosses (59♂ x 20♀ for pop A; 39♂ x 14♀ for pop B) were submitted to a redspotted grouper nervous necrosis virus (RGNNV) challenge by bath. A high-density single nucleotide polymorphism (SNP) chip panel was designed to develop the ThermoFisher Axiom™ 57 k SNP DlabChip, which was used for genotyping all individuals and building a high quality linkage map. In the backcross families, composite interval mapping was performed on 30,917, 23,592, 30,656 and 31,490 markers, respectively. In the commercial populations, 40,263 markers in pop A and 41,166 markers in pop B were used to perform genome-wide association studies (GWAS) using a GBLUP and a BayesCπ approach.Please note that this is an author-produced PDF of an article accepted for publication following peer review. The definitive publisher-authenticated version is available on the publisher Web site.One QTL was identified on chromosome LG12 in three of the four experimental backcross families, and one additional QTL on LG8 was detected in only one family. In commercial populations, QTL mapping revealed a total of seven QTLs, among which the previously mentioned QTL on LG12 was detected in both. This QTL, which was mapped to an interval of 3.45 cM, explained 9.21% of the total genetic variance in pop A, while other identified QTLs individually explained less than 1% of the total genetic variance.The identification of QTL regions involved in VNN resistance in European sea bass, with one having a strong effect, should have a great impact on the aquaculture industry. Future work could focus on the fine mapping of the causal mutation present on LG12 using whole genome sequencing. Highlights► Viral Nervous Necrosis is a major disease for European sea bass. ► A novel SNP array for European sea bass was designed. ► A total of nine QTL were detected. ► One QTL, shared by five over six of the data sets and located on the LG12 explained 9.2% of the total genetic variance.