Grotmol S, Bergh O, Totland G K
Department of Aquaculture, Institute of Marine Research, Bergen, Norway.
Dis Aquat Organ. 1999 May 12;36(2):95-106. doi: 10.3354/dao036095.
The susceptibility of the Atlantic halibut Hippoglossus hippoglossus yolk-sac larvae to viral encephalopathy and retinopathy (VER) was investigated by waterborne challenge experiments with nodavirus. Transfer of VER was indicated by several lines of evidence. A significantly higher cumulative mortality was observed after challenge with virus compared to mock challenge, and increasing doses of virus resulted in shorter incubation periods. When the challenge was performed on the day after hatching, the time from inoculation to the time when 50% of the larvae were dead (LT50) ranged from 26 to 32 d. Postponement of challenge for 13 d reduced the LT50 to 14 d, indicating that the susceptibility of the larvae to the present nodavirus strain was low during the first 2 wk after hatching. The progression of the infection was monitored by sequential immunohistochemistry and electron microscopy. On Day 18 after hatching the initial signs of infection were observed as a prominent focus of immunolabelling in the caudal part of the brain stem. In the same larvae immunolabelled single cell lesions were observed in the stratified epithelium of the cranial part of the intestine. The portal of entry into the larvae may thus have been the intestinal epithelium, while the route of infection to the CNS may have been axonal transport to the brain stem through cranial nerves such as the vagus nerves. Later in the infection, lesions became more severe and widespread and were also found throughout the brain and spinal cord and in the retina, cranial ganglia, intestine, liver, olfactory epithelium, yolk-sac epithelium, gills and pectoral fins. The mortality in all virus-challenged groups was 100%. This study thus demonstrates that the present nodavirus strain is able to replicate and cause VER in Atlantic halibut yolk-sac larvae at temperatures as low as 6 degrees C.
通过用水传播诺达病毒对大西洋庸鲽（Hippoglossus hippoglossus）卵黄囊幼虫进行攻毒实验，研究了其对病毒性脑病和视网膜病（VER）的易感性。多条证据表明VER能够传播。与模拟攻毒相比，病毒攻毒后观察到累积死亡率显著更高，并且病毒剂量增加导致潜伏期缩短。在孵化后第一天进行攻毒时，从接种到50%幼虫死亡的时间（LT50）为26至32天。将攻毒推迟13天可使LT50降至14天，这表明幼虫在孵化后的前2周对当前诺达病毒株的易感性较低。通过连续免疫组织化学和电子显微镜监测感染的进展。在孵化后第18天，观察到感染的初始迹象是脑干尾部免疫标记的一个突出焦点。在同一幼虫中，在肠道头部的分层上皮中观察到免疫标记的单细胞病变。因此，进入幼虫的门户可能是肠上皮，而感染中枢神经系统的途径可能是通过迷走神经等脑神经向脑干的轴突运输。在感染后期，病变变得更加严重和广泛，并且在整个脑和脊髓、视网膜、脑神经节、肠道、肝脏、嗅上皮、卵黄囊上皮、鳃和胸鳍中也发现了病变。所有病毒攻毒组的死亡率均为100%。因此，本研究表明，当前的诺达病毒株能够在低至6摄氏度的温度下在大西洋庸鲽卵黄囊幼虫中复制并引起VER。
