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Pathogenesis and immune response in Atlantic salmon (Salmo salar L.) parr experimentally infected with salmon pancreas disease virus (SPDV)

机译:实验性感染鲑鱼胰腺疾病病毒(SPDV)的大西洋鲑(Salmo salar L.)parr的发病机理和免疫应答

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Atlantic salmon parr were injected intraperitoneally with salmon pancreas disease virus (SPDV) grown on CHSE-214 cells. The viraemia, the histopathological changes in target organs and some immune parameters were taken at intervals up to 30 days post-infection (dpi), The earliest kind of lesion was necrosis of exocrine pancreas, appearing as soon as 2 dpi. It progressed towards complete tissue breakdown at 9 dpi before resolving gradually. Concurrent to this necrosis, a strong inflammatory response was in evidence from 9 dpi in the pancreatic area for a majority of fish. A necrosis of the myocardial cells of the ventricle occurred in infected fish mainly at 16 dpi and it faded thereafter. The monitoring of the plasma viral load showed a rapid haematogenous spreading of SPDV, peaking at 4 dpi, but also the absence of a secondary viraemia. No interferon (IFN) was detected following the infection of parr with SPDV, probably owing to an IFN activity in Atlantic salmon below the detection level of the technique. Neutralising antibodies against SPDV were in evidence from 16 dpi and they showed a time-related increasing titre and prevalence. The phagocytic activity in head-kidney leucocytes was always significantly higher in the infected fish than in the control fish, being particularly high by 9 dpi. Lysozyme and complement levels were both increased and they peaked significantly in the infected fish at 9 and 16 dpi respectively. These results demonstrated that an experimental infection of Atlantic salmon parr with SPDV provoked a stimulation of both specific and non-specific immunity with regards to the viraemia and the histopathology.
机译:向大西洋鲑鱼腹膜注射在CHSE-214细胞上生长的鲑鱼胰腺疾病病毒(SPDV)。在感染后(dpi)的30天内定期采集病毒血症,靶器官的组织病理学变化和一些免疫参数。最早的一种病变是外分泌胰腺坏死,最早出现在2 dpi时。在逐步解决之前,它以9 dpi的速度完全组织破裂。与此坏死同时发生的是,对于大多数鱼,胰腺区域的9 dpi表现出强烈的炎症反应。受感染的鱼主要在16 dpi时发生心室心肌细胞坏死,此后逐渐消失。血浆病毒载量的监测显示SPDV的快速血源性扩散,在4 dpi时达到峰值,但也没有继发性病毒血症。 SPDV感染parr后未检测到干扰素(IFN),这可能是由于大西洋鲑鱼中的IFN活性低于该技术的检测水平。从16 dpi可以明显看出针对SPDV的中和抗体,它们显示出与时间相关的滴度和患病率增加。被感染鱼的头部肾脏白细胞中的吞噬活性始终显着高于对照鱼,特别是高达9 dpi。溶菌酶和补体水平均升高,在受感染的鱼中分别以9 dpi和16 dpi达到峰值。这些结果表明,用SPDV感染大西洋鲑鱼parr引起了关于病毒血症和组织病理学的特异性和非特异性免疫的刺激。

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