Jun Lyu Jin, Jeong Joon Bum, Kim Ju Heon, Nam Jeong Hee, Shin Ki Won, Kim Joong Kyun, Kang Ju-Chan, Jeong Hyun Do
Department of Aquatic Life Medicine, Pukyong National University, Daeyeon 3 dong, Nam-gu, Busan 608-737, South Korea.
Dis Aquat Organ. 2009 Apr 27;84(3):201-8. doi: 10.3354/dao02041.
The effects of various water temperature treatments on the development of red sea bream iridovirus disease (RSIVD) in rock bream Oplegnathus fasciatus challenged with iridovirus Sachun (IVS-1) were determined by measuring the mortality and the viral concentration in the spleen of infected fish. Experimental infections of rock bream with IVS-1 at water temperatures of 18, 21, and 25 degrees C resulted in a cumulative mortality of 100%, but infections at 13 degrees C resulted in 0% mortality, even after 45 d. The disease progressed more rapidly at higher water temperatures; at 25, 21, and 18 degrees C, the mean numbers of days until death were 17, 20, and 30 d, respectively. When the water temperature for fish infected with iridovirus by intramuscular injection was shifted from 13 to 25 degrees C, the cumulative mortality reached 100%, with rapid onset of the disease, independent of the time at which the temperature was shifted, i.e. 7, 14, or 30 d after injection at 13 degrees C. Real-time PCR data revealed that the viral genome copy number in the spleen of rock bream maintained at 13 degrees C increased with time, suggesting the occurrence of viral replication even at 13 degrees C. In the reverse experiment, when the water temperature for fish that were infected at a higher temperature was shifted to 13 degrees C, 3 or 7 d after injection at 25 degrees C, the fish showed 100% cumulative mortality, although the mean number of days until death was higher than that observed for fish maintained at a constant temperature of 25 degrees C. The viral DNA concentration in the spleen of rock bream that had been shifted down to 13 degrees C, 3 or 7 d after injection at 25 degrees C, was not suppressed, but increased and eventually reached levels sufficient to induce mortality at 13 degrees C. However, the level of viral genome copy numbers in the spleen of dead fish at 25 degrees C, regardless of whether those fish were held at a constant temperature of 25 degrees C or shifted up from 13 degrees C, appeared to be greater than the level found in the dead fish shifted down to 13 degrees C after inoculation at 25 degrees C.
通过测量感染虹彩病毒的条石鲷（Oplegnathus fasciatus）的死亡率以及感染鱼脾脏中的病毒浓度，确定了不同水温处理对感染萨春虹彩病毒（IVS-1）的条石鲷患红鳍东方鲀虹彩病毒病（RSIVD）的影响。在18、21和25摄氏度水温下用IVS-1对条石鲷进行实验性感染，累积死亡率达100%，但在13摄氏度水温下感染，即使45天后死亡率仍为0%。在较高水温下疾病进展更快；在25、21和18摄氏度时，直至死亡的平均天数分别为17、20和30天。当通过肌肉注射感染虹彩病毒的鱼的水温从13摄氏度升至25摄氏度时，累积死亡率达100%，疾病迅速发作，与水温变化时间无关，即在13摄氏度注射后7、14或30天。实时PCR数据显示，维持在13摄氏度的条石鲷脾脏中的病毒基因组拷贝数随时间增加，表明即使在13摄氏度也发生了病毒复制。在反向实验中，当在较高温度下感染的鱼在25摄氏度注射后3或7天，水温降至13摄氏度时，鱼的累积死亡率达100%，尽管直至死亡的平均天数高于维持在25摄氏度恒温下的鱼。在25摄氏度注射后3或7天降至13摄氏度的条石鲷脾脏中的病毒DNA浓度未被抑制，反而增加，最终达到足以在13摄氏度诱导死亡的水平。然而，25摄氏度下死亡鱼脾脏中的病毒基因组拷贝数水平，无论这些鱼是维持在25摄氏度恒温还是从13摄氏度升至25摄氏度，似乎都高于在25摄氏度接种后降至13摄氏度的死亡鱼中的水平。
