247和270位的衣壳氨基酸参与了对欧洲鲈鱼的贝塔病毒的毒性。,Scientific Reports

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247和270位的衣壳氨基酸参与了对欧洲鲈鱼的贝塔病毒的毒性。
Scientific Reports ( IF 3.8 ) Pub Date : 2019-10-01 , DOI: 10.1038/s41598-019-50622-1
Patricia Moreno ₁ , Sandra Souto ₂ , Rocio Leiva-Rebollo ₁ , Juan J Borrego ₁ , Isabel Bandín ₂ , M Carmen Alonso ₁

Affiliation

欧洲鲈鱼（Dicentrarchus labrax）受神经坏死病毒（NNV）引起的神经坏死疾病的严重影响。在鲈鱼中检出了该病毒的四种基因型中的两种（红点石斑鱼神经坏死病毒RGNNV；条纹杰克神经坏死病毒SJNNV），尽管对该鱼种表现出不同程度的毒力。因此，鲈鱼极易受到RGNNV的侵害，而尚未报道由SJNNV引起的暴发。已通过在上述位置（Mut247Dl965，Mut270Dl965和Mut247 + 270Dl965）。病毒的体外和体内复制，已经分析了由这些病毒触发的病毒毒力和鱼类免疫反应。突变病毒在E-11细胞上复制，尽管与野生型病毒相比显示出一些差异，这表明该突变可影响病毒细胞的识别和进入。在体内，由突变病毒引起的鱼类死亡率降低了75％，与未突变病毒相比，鲈鱼脑中的病毒复制发生了变化。关于鲈鱼的免疫应答，突变病毒触发了较低的IFN I系统和炎症反应相关基因的诱导。此外，突变引起病毒血清学特性的改变（尤其是氨基酸270中的突变），从而导致更高的血清转化率和改变的抗原识别。尽管与野生型病毒相比显示出一些差异，但这表明该突变会影响病毒细胞的识别和进入。在体内，由突变病毒引起的鱼类死亡率降低了75％，与未突变病毒相比，鲈鱼脑中的病毒复制发生了变化。关于鲈鱼的免疫应答，突变病毒触发了较低的IFN I系统和炎症反应相关基因的诱导。此外，突变引起病毒血清学特性的改变（尤其是氨基酸270中的突变），从而导致更高的血清转化率和改变的抗原识别。尽管与野生型病毒相比显示出一些差异，但这表明该突变会影响病毒细胞的识别和进入。在体内，由突变病毒引起的鱼类死亡率降低了75％，与未突变病毒相比，鲈鱼脑中的病毒复制发生了变化。关于鲈鱼的免疫应答，突变病毒触发了较低的IFN I系统和炎症反应相关基因的诱导。此外，突变引起病毒血清学特性的改变（尤其是氨基酸270中的突变），从而导致更高的血清转化率和改变的抗原识别。与未突变的病毒相比，海鲈脑中的病毒复制发生了变化。关于鲈鱼的免疫应答，突变病毒触发了较低的IFN I系统和炎症反应相关基因的诱导。此外，突变引起病毒血清学特性的改变（尤其是氨基酸270中的突变），从而导致更高的血清转化率和改变的抗原识别。与未突变的病毒相比，海鲈脑中的病毒复制发生了变化。关于鲈鱼的免疫应答，突变病毒触发了较低的IFN I系统和炎症反应相关基因的诱导。此外，突变引起病毒血清学特性的改变（尤其是氨基酸270中的突变），从而导致更高的血清转化率和改变的抗原识别。

"点击查看英文标题和摘要"

Capsid amino acids at positions 247 and 270 are involved in the virulence of betanodaviruses to European sea bass.

European sea bass (Dicentrarchus labrax) is severely affected by nervous necrosis disease, caused by nervous necrosis virus (NNV). Two out of the four genotypes of this virus (red-spotted grouper nervous necrosis virus, RGNNV; and striped jack nervous necrosis virus, SJNNV) have been detected in sea bass, although showing different levels of virulence to this fish species. Thus, sea bass is highly susceptible to RGNNV, whereas outbreaks caused by SJNNV have not been reported in this fish species. The role of the capsid protein (Cp) amino acids 247 and 270 in the virulence of a RGNNV isolate to sea bass has been evaluated by the generation of recombinant RGNNV viruses harbouring SJNNV-type amino acids in the above mentioned positions (Mut247Dl965, Mut270Dl965 and Mut247 + 270Dl965). Viral in vitro and in vivo replication, virus virulence and fish immune response triggered by these viruses have been analysed. Mutated viruses replicated on E-11 cells, although showing some differences compared to the wild type virus, suggesting that the mutations can affect the viral cell recognition and entry. In vivo, fish mortality caused by mutated viruses was 75% lower, and viral replication in sea bass brain was altered compared to non-mutated virus. Regarding sea bass immune response, mutated viruses triggered a lower induction of IFN I system and inflammatory response-related genes. Furthermore, mutations caused changes in viral serological properties (especially the mutation in amino acid 270), inducing higher seroconversion and changing antigen recognition.

更新日期：2019-10-01

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