Betanodavirus of Marine and Freshwater Fish: Distribution, Genomic Organization, Diagnosis and Control Measures

142

115

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.

Section: Distribution and Transmissionmentioning

confidence: 97%

“…Infections caused by NNV have been detected all around the world, with the notable exception of South America (Crane & Hyatt ; Shetty et al . ). It was the cause of mass mortality in Atlantic halibut in Norway and Scotland (Grotmol et al .…”

Section: Distribution and Transmissionmentioning

confidence: 97%

Viral encephalopathy and retinopathy in aquaculture: a review

Doan

Vandeputte

Chatain

et al. 2016

142

115

“…It is frequently fatal and accounts for severe economic losses in the aquaculture industry, particularly in larval and juvenile stages (Doan, Vandeputte, Chatain, Morin, & Allal, ). The causative agent, nervous necrosis virus (NNV), genus Betanodavirus (Thiéry et al., ), can infect a wide range of marine farmed and wild fish species (Doan et al., ) and has also been isolated from freshwater fish (Shetty, Maiti, Shivakumar Santhosh, Venugopal, & Karunasagar, ) and invertebrates (Gomez et al., ; Volpe et al., ). The affected fish commonly display lesions in the central nervous system, with vacuolization and necrosis observed in brain, retina and spinal cord, leading to a range of neurological signs such as abnormal swimming behaviour, anorexia and changes in coloration (Doan et al., ; Maltese & Bovo, ).…”

Section: Introductionmentioning

confidence: 99%

Betanodavirus infection in bath‐challenged Solea senegalensis juveniles: A comparative analysis of RGNNV, SJNNV and reassortant strains

Souto

Olveira

Alonso

et al. 2018

Senegalese sole has been shown to be highly susceptible to betanodavirus infection, although virulence differences were observed between strains. To study the mechanisms involved in these differences, we have analysed the replication in brain tissue of three strains with different genotypes during 15 days after bath infection. In addition, possible portals of entry for betanodavirus into sole were investigated. The reassortant RGNNV/SJNNV and the SJNNV strain reached the brain after 1 and 2 days postinfection, respectively. Although no RGNNV replication was detected until day 3-4 postinfection, at the end of the experiment this strain yielded the highest viral load; this is in accordance with previous studies in which sole infected with the reassortant showed more acute signs and earlier mortality than the RGNNV and SJNNV strains. Differences between strains were also observed in the possible portals of entry. Thus, whereas the reassortant strain could infect sole mainly through the skin or the oral route, and, to a minor extent, through the gills, the SJNNV strain seems to enter fish only through the gills and the RGNNV strain could use all tissues indistinctly. Taken together, all these results support the hypothesis that reassortment has improved betanodavirus infectivity for sole.

“…Betanodavirus affects marine teleost fish of more than 40 species that were identified to be susceptible, and the number of new susceptible host is increasing steadily to include freshwater fish species (Bigarré et al., ; Binesh, ; Bovo et al., ; Furusawa, Okinaka, & Nakai, ; Furusawa, Okinaka, Uematsu, & Nakai, ; Johansen, Amundsen, Dannevig, & Sommer, ; Shetty, Maiti, Santhosh, Venugopal, & Karunasagar, ). These statistics suggest a wide range of susceptible host across saltwater and freshwater fish to nervous necrosis virus, and proposed a potentially low host specificity of the virus.…”

Section: Host and Signsmentioning

confidence: 99%

Betanodavirus: Dissection of the viral life cycle

Low

Nataqain

Chee

et al. 2017

Progressive research has been recently made in dissecting the molecular biology of Betanodavirus life cycle, the causative pathogen of viral encephalopathy and retinopathy in economic important marine fish species. Establishment of betanodavirus infectious clone allows the manipulation of virus genome for functional genomic study, which elucidates the biological event of the viral life cycle at molecular level. The betanodavirus strategizes its replication by expressing anti-apoptosis/antinecrotic proteins to maintain the cell viability during early infection. Subsequently utilizes and controls the biological machinery of the infected cells for viral genome replication. Towards the late phase of infection, mass production of capsid protein for virion assembly induces the activation of host apoptosis pathway. It eventually leads to the cell lysis and death, which the lysis of cell contributes to the accomplishment of viral shedding that completes a viral life cycle. The recent efforts to dissect the entire betanodavirus life cycle are currently reviewed.