Elevation of temperature and crowding trigger acute viral nervous necrosis in zebra fish, Brachydanio rerio (Hamilton-Buchanan), subclinically infected with betanodavirus.

Abstract

Viral nervous necrosis (VNN) or viral encephalopathy and retinopathy (VER) is an emerging fish disease reported in over 40 species (OIE 2006; Maltese & Bovo 2007). Specific signs include erratic and corkscrew-like swimming behaviour and lethargy. Mortality may reach up to 100% of the fish stock within 2–3 days of disease onset. The disease is caused by a betanodavirus of the family Nodaviridae which is a small, icosahedral (25 nm) RNA virus (Mori et al. 1992). Its bipartite genome consists of two positive RNA strands: RNA1 (3.1 kb) codes for viral RdRP (protein A), while the RNA2 (1.4 kb) codes for coat protein (Mori et al. 1992). A subgenomic RNA3 synthesized from RNA1 during early viral replication codes for protein B2 (Sommerset & Nerland 2004) which acts against host RNA interference (Iwamoto et al. 2005; Fenner et al. 2006). Based on the variable region of coat protein (CP) gene (nt 604–1030), four species have been recognized so far (Nishizawa et al. 1997; Schneemann et al. 2005) which are red spotted grouper nervous necrosis virus (RGNNV), striped jack nervous necrosis virus (SJNNV), tiger puffer nervous necrosis virus (TPNNV) and barfin flounder nervous necrosis virus (BFNNV). They show remarkable temperature preferences (Schneemann et al. 2005). The virus causes acute as well as subclinical infections in fish (Munday, Kwang & Moody 2002). Subclinical infection facilitates vertical/horizontal transmission of the virus (Castric et al. 2001; Breuil et al. 2002) and is described previously in terms of sequestration of the viral particles or low-level multiplication under the influence of interferon system in the host tissues (Chi, Wu & Cheng 2005). It may develop to an acute phase with biological and environmental stress factors like feeding impairment (Johansen et al. 2004), repeated spawning (Mushiake et al. 1993), elevated water temperature (Chi, Shieh & Lin 2003) and elevated levels of CO2 & PO4 (Athanassopoulou, Billinis & Prapas 2004). Infective virions have been isolated from cultured fish 1 year after exposure (Johansen et al. 2004). However, there is no conclusive experimental evidence for the transition or its mechanism. This paper describes a comparative estimation of effect of temperature elevation and crowding on the development of acute viral nervous necrosis in a laboratory model fish, Brachydanio rerio (Hamilton-Buchanan), subclinically infected with betanodavirus. One set each of VNN free (0.29 0.02 g, 3.1 0.2 cm) and subclinically infected but apparently healthy (0.28 0.02 g, 2.98 0.2 cm) zebra fish were collected from commercial ornamental fish culture and trading centres around Chennai, Tamil Nadu, India. The two batches of fish were separately maintained in the laboratory for acclimatization. VNN status was confirmed by specific nested RT-PCR as reported previously (Gomez et al. 2004). Briefly, random samples (n = 5) were collected from both batches of fish and were euthanized in excess concentration Correspondence C P Binesh, Department of Aquaculture, Sacred Heart College, Thevara, Cochin-682013, Kerala, India (e-mail: bineshkanayi@gmail.com)

DOI: 10.1111/jfd.12080

Cite this paper

@article{Binesh2014ElevationOT, title={Elevation of temperature and crowding trigger acute viral nervous necrosis in zebra fish, Brachydanio rerio (Hamilton-Buchanan), subclinically infected with betanodavirus.}, author={C. P. Binesh}, journal={Journal of fish diseases}, year={2014}, volume={37 3}, pages={279-82} }