Viral Nervous Necrosis (VNN) an Emerging Disease Caused by Nodaviridae in Aquatic Hosts: Diagnosis, Control and Prevention: a Review

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Viral Nervous Necrosis (VNN) an Emerging Disease Caused by Nodaviridae in Aquatic Hosts: Diagnosis, Control and Prevention: a Review Viral nervous necrosis (VNN) an emerging disease caused by Nodaviridae in aquatic hosts: Diagnosis, control and prevention: A review Item Type article Authors Zorriehzahra, M.J.; Adel, M.; Dadar, M.; Ullah, S.; Ghasemi, M. DOI 10.22092/ijfs.2018.117849 Download date 29/09/2021 22:12:15 Link to Item http://hdl.handle.net/1834/40692 Iranian Journal of Fisheries Sciences 18(1) 30-47 2019 DOI: 10.22092/ijfs.2018.117849 Viral nervous necrosis (VNN) an emerging disease caused by Nodaviridae in aquatic hosts: Diagnosis, control and prevention: A review Zorriehzahra M.J.1*; Adel M.1; Dadar M.2; Ullah S.3; Ghasemi M.4 Received: June 2016 Accepted: September 2016 Abstract Betanodavirus is one of the two genera making up the family Nodaviridae and is the etiological agent of viral nervous necrosis (VNN, also known as viral encephalopathy and retinopathy or VER). The virus infects a large range of host species in more than 50 species of marine and freshwater fish worldwide from different geographical areas and the known host range continues to expand as new species of fish are used for aquaculture. The disease is characterized by vacuolating necrosis of neural cells of the brain, retina and spinal cord and causes up to 100% mortality in larval and juvenile fish, and can cause significant losses in older fish. The lack of knowledge about control and prevention of the disease makes the problem serious and impedes development of management approaches. Therefore this review focuses on current knowledge and future perspectives of viral nervous necrosis in the aquaculture industry with special focus on the type of diagnosis, control and prevention of the disease. Keywords: Viral nervous necrosis, Betanodavirus, Diagnosis, Control and prevention Downloaded from jifro.ir at 15:23 +0430 on Wednesday April 17th 2019 1-Aquatic Animal Health and Diseases Department, Iranian Fisheries Science Research Institute (IFSRI), Agricultural Research Education and Extension Organization (AREEO), Tehran, I.R. Iran. 2-Razi Vaccine and Serum Research Institute, Agricultural Research, Education and Extension Organization (AREEO), Karaj, I.R. Iran. 3-Fisheries and Aquaculture Lab, Department of Animal Sciences, Quaid-i-Azam University, Islamabad, Pakistan. 4-Iranian Fisheries Science Research Institute (IFSRI), Inland Water Aquaculture Research Center, Bandar Anzali, I.R. Iran. *Corresponding author's Email: zorrieh@yahoo.com 31 Zorriehzahra et al., Viral nervous necrosis (VNN) an emerging disease caused by… Introduction strands known as RNA1 and RNA2. Viral nervous necrosis (VNN) is a RNA1 encodes RNA dependent RNA disastrous fish disease and one of the polymerase (RdRp), a mitochondrial main reasons for great economic losses enzyme, and is responsible for viral in marine fish and the aquaculture replication (Nopadon et al., 2009; Jia et industry. The agent of VNN is a virus al., 2015). On the other hand, RNA2 belonging to the genus Betanodavirus encodes the capsid protein (Wu et al., and family Nodaviridae (Peducasse et 2016). The existence of four genotypes al., 1999; Mu et al., 2013; Jia et al., characterized by high homology has 2015; Pascoli et al., 2016). Actually been approved on the basis of the viral the first documented nodavirus genome analysis, designated bar fin infection was detected in Japanese flounder nervous necrosis virus parrotfish (Oplegnathus fasciatus) in (BFNNV), tiger puffer NNV(TPNNV), Japan (Yoshikoshi and Inoue, 1990). striped jack NNV (SJNNV), and red Then the disease was reported in spotted grouper NNV (RGNNV) barramundi (Lates calcarifer) farmed in (Nishizawa et al., 1997; Shetty et al., Australia (Glazebrook et al., 1990), and 2012). The main target tissues are the then a year later in turbot, Scopthalmus nerve tissues especially the central maximus (Bloch et al., 1991), European nervous system (CNS) and the eye sea bass Dicentrarchus labrax (Breuil (retina). The characteristic lesions of et al., 1991), red spotted grouper, VNN are necrosis and vacuolation of Epinephalus akaara (Mori et al., 1992) the central nervous system and retina of striped jack, Pseudocaranx dentex the affected larvae and juvenile fishes (Mori et al., 1992) and several other showing abnormal swimming behavior species such as the golden grey mullet, (Liu et al., 2015). To date, the disease Downloaded from jifro.ir at 15:23 +0430 on Wednesday April 17th 2019 Liza aurata (Zorriehzahra et al., 2005). has been reported in more than 120 Currently occurrence of VNN is species belonging to 30 families from reported in some African countries 11 different orders, mainly marine fish including: Tunisia (Chérif et al., 2009) being susceptible to infection (Munday and Algeria (Kara et al., 2014). It et al., 2002; Su et al., 2015; Costa et revealed that early unknown mortality al., 2016). On the other hand, several occurred in fry and juveniles of some freshwater fish species such as Chinese marine fish in decade of 1980-1990 in catfish (P. asotus); Australia catfish the world. Now this virus has been (Tandanus tandanus); Barramundi (L. recognized as a major problem and has calcarifer); Medaka (Oryzias latipes); been increasing in importance in Guppy (Poicelia reticulata) and Mediterranean and Asian marine Zebrafish (Danio rerio) showed aquaculture (Costa and Thompson, outbreaks of the disease (Hegde et al., 2016; Vendramin et al., 2016). 2003; Shetty et al., 2012). Affected fish Betanodavirus is non-enveloped and may reveal different clinical signs icosahedral with a diameter of 20–30 related to species, age and temperature nm, with two positive-sense RNA of the environment; an acute and sub- Iranian Journal of Fisheries Sciences 18(1) 2019 32 acute form characterized by atypical present in the retina and brain of the signs and a chronic form was observed infected fish, ultimately leading to for the first time only in affected fish in abnormal swimming, coloration, sight the Caspian Sea up to now and swim bladder control (Munday et (Zorriehzahra et al., 2016). The most al., 2002; Costa and Thompson, 2016,). specific and common symptoms In general, the clinical signs of VNN observed among the different species is are observed in the specific behavior of an abnormal swimming behavior, affected individuals. These behavioral lethargy and swim bladder changes include: loss of appetite, erratic hyperinflation that lead to abdominal swimming patterns like whirling, spiral, extension. The viral etiology has been looping swimming and belly up at rest, emphasized following the identification loss of equilibrium, minimized nervous of small, non-enveloped, RNA agents coordination, uncoordinated swimming definitively specified to the and alterations in pigmentations Nodaviridae family, genus (Nopadon et al., 2009). These signs are Betanodavirus. Although horizontal accompanied by some general sings transmission surely appears to be the such as anemia, lethargy and anorexia most common transmission route, (Munday et al., 2002). The infected vertical transmission has also been individuals also adopt a peculiar already proved in some species. stationary position, such as vertical According to the OIE protocol, position keeping caudal fin and head VER/VNN is officially diagnosed above the water surface. Some VNN through the isolation of the causative infected fish swim straight forward so agent in susceptible cell line and then swiftly that they are unable to identified with immunological or discontinue their speed and crash into Downloaded from jifro.ir at 15:23 +0430 on Wednesday April 17th 2019 molecular methods such as FAT or by tanks’ walls and they experience real time RT-PCR or nested RT-PCR traumatic and harrowing lesions on (OIE, 2018). The control of the disease their jaws and nose (Maltese and Bovo, is intricate with difficulties in applying 2007; Binesh, 2014; Keawcharoen et biosecurity procedures, emphatic al., 2015). Other changes that coexist hygiene and preventive actions in open are hyperinflation of the swim bladder environments like the ocean and in (Mori et al., 1992; Hellberg et al., selecting brood fish free of pathogen. 2010; Kara et al., 2014; Vendramin et Furthermore, commercial vaccines are al., 2016) (Fig. 1). The presence or currently not available. absence of any of these signs or deviation in pigmentation change may Clinical signs and symptoms be due to species and water temperature The clinical sings of viral nervous (Binesh, 2014). necrosis are linked to the neuro- invasive nature of viruses of the family Nodaviridae, causing this disease, as well as the consequences of the lesions 33 Zorriehzahra et al., Viral nervous necrosis (VNN) an emerging disease caused by… Figure 1: Clinical signs in VNN: hyperinflation of swim bladder (left) and abdominal extension (right) in infected Lisa aurata in the Caspian Sea (Zorriehzahra et al., 2014). Virus isolation al., 1999; Iwamoto et al., 2001). These A number of cell lines are now observations were highly reproducible available for the culture of and formed the basis for a successful betanodaviruses (Qin et al., 2006). The virus titration system. Quantitative striped snakehead cell line (SSN-1) analysis using the cloned E-11 cell line originally developed by Frerichs et al., clearly revealed differences in the (1996) has been shown to be permissive optimal growth temperatures among the for 17 isolates of fish nodaviruses, 4 genotypic variants: 25 to 30° C for encompassing the RGNNV, SJNNV, strain SGWak97 (RGNNV), 20 to 25 TPNNV and BFNNV types (Iwamoto degrees C for strain SJNag93 (SJNNV), et al., 2000; Dalla Valle et al., 2001; 20 degrees C for strain TPKag93 Iwamoto et al., 2001; Chi et al., 2003). (TPNNV), and 15 to 20° C for strain Iwamoto et al., (2000) reported that six JFIwa98 (BFNNV) (Iwamoto et al., cell clones were derived from the SSN- 2001). Electron microscopy Downloaded from jifro.ir at 15:23 +0430 on Wednesday April 17th 2019 1 cell line, which is composed of a demonstrated SnRV retrovirus particles mixed cell population and persistently only in A-6 and E-9 cells, but PCR infected with a C-type retrovirus amplification for the pool gene and (SnRV).
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