Variable region of betanodavirus RNA2 is sufficient to determine host specificity

Abstract

Betanodaviruses, the causative agents of viral nervous necrosis in marine fish, have bipartite positive-sense RNA genomes. The viruses have been classified into 4 distinct types based on nucleotide sequence similarities in the variable region (the so-called T4 region) of the smaller genomic segment RNA2 (1.4 kb). Betanodaviruses have marked host specificity, although the primary structures of the viral RNAs and encoded proteins are similar among the viruses. We have previously demonstrated, using reassortants between striped jack nervous necrosis virus (SJNNV) and redspotted grouper nervous necrosis virus (RGNNV), that RNA2, which encodes the coat protein, strictly controls host specificity. However, because RNA2 is large, we were unable to propose a mechanism underlying this RNA2-based host specificity. To identify the RNA2 region that controls host specificity, we constructed RNA2 chimeric viruses from SJNNV and RGNNV and tested their infectivity in the original host fish, striped jack Pseudocaranx dentex and sevenband grouper Epinephelus septemfasciatus. Among these chimeric viruses, SJNNV mutants containing the variable region of RGNNV RNA2 infected sevenband grouper larvae in a manner similar to RGNNV, while RGNNV mutants containing the variable region of SJNNV RNA2 infected striped jack larvae in a manner similar to SJNNV. Immunofluorescence microscopic studies using anti-SJNNV polyclonal antibodies revealed that these chimeric viruses multiplied in the brains, spinal cords and retinas of the infected fish, as in infections by the parental viruses. These results indicate that the variable region of RNA2 is sufficient to control host specificity in SJNNV and RGNNV.

Comparative analysis of both genomic segments of betanodaviruses isolated from epizootic outbreaks in farmed fish species provides evidence for genetic reassortment

“…The existence of these two changes was also observed in the 16 reassortant isolates that were partially sequenced. These results confirmed that C-terminal protruding domains of the capsid protein are involved in host specificity, as reported previously (Iwamoto et al, 2004;Ito et al, 2008). However, the other change was observed in the N-terminal one-third of the protein.…”

“…All of the reassortant strains exhibited a slightly modified SJNNV capsid, with three different amino acid positions in all strains (the differences increased to a maximum of six in some strains). One of these changes observed in residue 247 was encoded by the nucleotide triplet 737-739, included in the sequence nt 695-765, described by Ito et al (2008) as a hostspecific determinant. Another change in the amino acid sequence (aa 270) was also observed on the C-terminal side of the capsid protein.…”

Pathogenicity of Striped Jack Nervous Necrosis Virus (SJNNV) Isolated from Asymptomatic Wild Japanese Jack Mackerel <i>Trachurus japonicus</i>

“…Considering that even striped jack has a strict age-dependent resistance against SJNNV (Arimoto et al, 1993), less susceptible Japanese jack mackerel might be more resistant at juvenile or older stages and thus possibly develop into subclinical infection. We previously reported that RNA2 determines the host-specificity of betanodaviruses (SJNNV and RGNNV) and the T4 region in RNA2 is particularly important for pathogenicity (Iwamoto et al, 2004;Ito et al, 2008). After the first report on SJNNV of striped jack larvae in 1992 (Mori et al, 1992), the SJNNV genotype was detected by cell culture isolation or PCR from cultured Senegalese sole Solea senegalensis, sea bass Dicentrarchus labrax, and gilthead sea bream Sparus aurata in southern Europe, and these European SJNNVs are phylogenetically different from Japanese SJNNVs all of which were isolated from diseased striped jack larvae (Thiéry et al, 2004;Cutrín et al, 2007;Toffolo et al, 2007;Olveira et al, 2009;Cherif et al, 2011;Panzarin et al, 2012).…”

Genetic Characterization of Viral Nervous Necrosis Infects Tilapia (Oreochromis sp.) in Indonesia

“…It showed that VNN has the ability to infect across species and adapt to a new host species [19]. A specific host on the most viral infections are usually controlled by the interaction with a viral surface protein receptors on the surface of target cells precisely [31], so long as the tilapia have receptors that can bind to the attachment site (s) virus particles, then certainly virus will entry into host cells (tilapia), because it does not directly host cell have facilitated the virus to enter the cell [32]. The tilapia have such receptors HSC70, as well as groupers [33], which specifically alleged that the virus can perform attachment and involved in an interaction that could cause the virus to enter the body tilapia.…”