The transcriptomic response of Senegalese sole (Solea senegalensis) triggered by two betanodaviruses with different virulence to that fish species has been assessed using an OpenArray® platform based on TaqMan™ quantitative PCR. The transcription of 112 genes per sample has been evaluated at two sampling times in two organs (head kidney and eye/brain-pooled samples). Those genes were involved in several roles or pathways, such as viral recognition, regulation of type I (IFN-1)-dependent immune responses, JAK-STAT cascade, interferon stimulated genes, protein ubiquitination, virus responsive genes, complement system, inflammatory response, other immune system effectors, regulation of T-cell proliferation, and proteolysis and apoptosis. The highly virulent isolate, wSs160.3, a wild type reassortant containing a RGNNV-type RNA1 and a SJNNV-type RNA2 segments, induced the expression of a higher number of genes in both tested organs than the moderately virulent strain, a recombinant harbouring mutations in the protruding domain of the capsid protein. The number of differentially expressed genes was higher 2 days after the infection with the wild type isolate than at 3 days post-inoculation. The wild type isolate also elicited an exacerbated interferon 1 response, which, instead of protecting sole against the infection, increases the disease severity by the induction of apoptosis and inflammation-derived immunopathology, although inflammation seems to be modulated by the complement system. Furthermore, results derived from this study suggest a potential important role for some genes with high expression after infection with the highly virulent virus, such as rtp3, sacs and isg15. On the other hand, the infection with the mutant does not induce immune response, probably due to an altered recognition by the host, which is supported by a different viral recognition pathway, involving myd88 and tbkbp1.

塞内加尔鞋底（的转录响应塞内加尔鳎已使用基于TaqMan™定量PCR的OpenArray®平台评估了由两种与该鱼类具有不同毒力的兽疫病毒触发的）。已在两个器官（头部肾脏和眼/脑池样本）的两个采样时间评估了每个样本中112个基因的转录。这些基因参与了多种作用或途径，例如病毒识别，I型（IFN-1）依赖性免疫应答调节，JAK-STAT级联，干扰素刺激基因，蛋白质泛素化，病毒应答基因，补体系统，炎症应答，其他免疫系统效应子，调节T细胞增殖以及蛋白水解和凋亡。高毒力分离株wss160.3，一种含有RGNNV型RNA1和SJNNV型RNA2片段的野生型重配物，与中等毒性毒株相比，该病毒诱导了两个受试器官中更高数量的基因表达，重组毒株在衣壳蛋白的突出结构域具有突变。用野生型分离株感染后2天，差异表达基因的数量比接种后3天更高。野生型分离物还引起加剧的干扰素1应答，尽管炎症似乎是由补体系统调节的，但它不是通过保护单独的感染，而是通过诱导细胞凋亡和炎症衍生的免疫病理学来增加疾病的严重程度。此外，这项研究得出的结果表明，某些高表达基因在感染高毒力病毒后具有潜在的重要作用，例如 用野生型分离株感染后2天，差异表达基因的数量比接种后3天更高。野生型分离物还引起加剧的干扰素1应答，尽管炎症似乎是由补体系统调节的，但它不是通过保护单独的感染，而是通过诱导细胞凋亡和炎症衍生的免疫病理学来增加疾病的严重程度。此外，这项研究得出的结果表明，某些高表达基因在感染高毒力病毒后具有潜在的重要作用，例如 用野生型分离株感染后2天，差异表达基因的数量比接种后3天更高。野生型分离物还引起加剧的干扰素1应答，尽管炎症似乎是由补体系统调节的，但它不是通过保护单独的感染，而是通过诱导细胞凋亡和炎症衍生的免疫病理学来增加疾病的严重程度。此外，这项研究得出的结果表明，某些高表达基因在感染高毒力病毒后具有潜在的重要作用，例如 尽管炎症似乎是由补体系统调节的，但不是通过保护鞋底免受感染，而是通过诱导凋亡和炎症衍生的免疫病理学来增加疾病的严重程度。此外，这项研究得出的结果表明，某些高表达基因在感染高毒力病毒后具有潜在的重要作用，例如 尽管炎症似乎是由补体系统调节的，但不是通过保护鞋底免受感染，而是通过诱导凋亡和炎症衍生的免疫病理学来增加疾病的严重程度。此外，这项研究得出的结果表明，某些高表达基因在感染高毒力病毒后具有潜在的重要作用，例如rtp3，sacs和isg15。另一方面，突变体的感染不会诱导免疫应答，这可能是由于宿主的识别改变，这是由涉及myd88和tbkbp1的另一种病毒识别途径所支持的。