Gémez-Mata Juan, Souto Sandra, Bandín Isabel, Alonso María Del Carmen, Borrego Juan José, Labella Alejandro Manuel, García-Rosado Esther
Instituto de Biotecnología y Desarrollo Azul (IBYDA), Departamento de Mi-Crobiología, Facultad de Ciencias, Universidad de Málaga, 29071 Málaga, Spain.
Instituto de Acuicultura, Departamento de Microbiología y Parasitología, Universidade de Santiago de Compostela, 15782 Santiago de Compostela, Spain.
Pathogens. 2021 Oct 27;10(11):1388. doi: 10.3390/pathogens10111388.
Nervous necrosis virus (NNV), genus , the etiological agent of the viral encephalopathy and retinopathy (VER), presents a genome with two positive-sense single-stranded RNA segments. Striped jack nervous necrosis virus (SJNNV) and red-spotted grouper nervous necrosis virus (RGNNV), together with reassortants RGNNV/SJNNV, are the betanodaviruses predominantly isolated in Southern Europe. An RGNNV/SJNNV reassortant isolated from Senegalese sole (wt160) causes high mortalities in this fish species. This virus presents differences in the sequence of the 3' non-coding region (NCR) of both segments compared to RGNNV and SJNNV reference strains. Previously, it has been reported that the reversion of two of these differences (nucleotides 1408 and 1412) in the RNA2 3'NCR to the SJNNV-type (recombinant r1408-1412) resulted in a decrease in sole mortality. In the present study, we have applied an OpenArray to analyse the involvement of sole immune response in the virulence of several recombinants: the r1408-1412 and two recombinants, developed in the present study, harbouring mutations at positions 3073 and 3093 of RNA1 3'NCR to revert them to RGNNV-type. According to the correlation values and to the number of expressed genes, the infection with the RNA2-mutant provoked the most different immune response compared to the immune response triggered after the infection with the rest of the viruses, and the exclusive and high upregulation of genes related to the complement system. The infection with the RNA1-mutants also provoked a decrease in mortality and their replication was delayed at least 24 h compared to the wt160 replication, which could provoke the lag observed in the immune response. Furthermore, the infection with the RNA1-mutants provoked the exclusive expression of and the downregulation of .
神经坏死病毒（NNV），属，是病毒性脑病和视网膜病（VER）的病原体，其基因组由两个正链单链RNA片段组成。条带鰤神经坏死病毒（SJNNV）和红斑石斑鱼神经坏死病毒（RGNNV），以及重组体RGNNV/SJNNV，是在南欧主要分离出的β-诺达病毒。从塞内加尔鳎中分离出的一种RGNNV/SJNNV重组体（wt160）在这种鱼类中导致高死亡率。与RGNNV和SJNNV参考毒株相比，该病毒在两个片段的3'非编码区（NCR）序列上存在差异。此前有报道称，RNA2 3'NCR中这些差异中的两个（核苷酸1408和1412）回复到SJNNV型（重组体r1408-1412）会导致鳎死亡率降低。在本研究中，我们应用了OpenArray来分析鳎免疫反应在几种重组体毒力中的作用：r1408-1412以及本研究中开发的另外两种重组体，它们在RNA1 3'NCR的3073和3093位点发生突变，使其回复到RGNNV型。根据相关性值和表达基因的数量，与感染其他病毒后引发的免疫反应相比，感染RNA2突变体引发的免疫反应差异最大，且与补体系统相关的基因出现了独特且高度上调的情况。与wt160的复制相比，感染RNA1突变体也导致死亡率降低，且其复制至少延迟了24小时，这可能导致免疫反应中出现滞后现象。此外，感染RNA1突变体引发了 的独特表达以及 的下调。
