Institute of Oceanology, Chinese Academy of Sciences, 7 Nanhai Road, Qingdao 266071, China; East China Sea Fisheries Research Institute, Chinese Academy of Fishery Science, Shanghai 200090, China.
Fish Shellfish Immunol. 2010 Jul;29(1):42-8. doi: 10.1016/j.fsi.2010.02.019. Epub 2010 Feb 25.
The Zhikong Scallop, Chlamys farreri, is one of the most important bivalve mollusks cultured in northern China. However, mass mortality of the cultured C. farreri has posed a serious threat to the maricultural industry in recent years. Acute Viral Necrobiotic Virus (AVNV) is believed as an important etiological agent causing the scallop mass mortalities. To understand the mechanism behind the AVNV associated scallop disease and mortality, we assessed the physiological and immune responses of C. farreri to the virus infection using oxygen consumption rate, ammonium-nitrogen excretion rate, hemocyte copper, zinc superoxide dismutase gene expression, and plasma superoxide dismutase activity and alkaline phosphatase activity as indicators. Scallops challenged by AVNV at 25 degrees C developed typical disease signs 2 days after virus injection. Before the disease manifested, scallop oxygen consumption and NH4+-N excretion rates rose and then fell back. Real-time PCR revealed that the hemocyte cytosol Cu, Zn SOD gene expression was upregulated followed by recovery. The plasma SOD activity, however, augmented consistently following virus injection. Moreover, plasma AKP activity first lowered and then elevated gradually to the highest level at 24 h post virus injection. Scallops challenged by AVNV at 17 degrees C neither developed notable disease nor showed obvious responses that could be associated with the virus infection. While the results suggested a correlation between the elevated seawater temperature and the AVNV infection associated C. farreri mortalities, they also indicated that the viral infection provoked multiple physiological and immune responses in the host scallops.
中国北方养殖的重要双壳贝类之一是栉孔扇贝，Chlamys farreri。然而，近年来，养殖栉孔扇贝的大规模死亡对海水养殖业构成了严重威胁。急性病毒性坏死病毒（AVNV）被认为是导致扇贝大规模死亡的重要病原体。为了了解与 AVNV 相关的扇贝疾病和死亡率的机制，我们使用耗氧量、氨氮排泄率、血细胞铜、锌超氧化物歧化酶基因表达以及血浆超氧化物歧化酶活性和碱性磷酸酶活性作为指标，评估了 C. farreri 对病毒感染的生理和免疫反应。在 25°C 下用 AVNV 攻毒的扇贝在病毒注射后 2 天出现典型的疾病症状。在疾病表现之前，扇贝的耗氧量和 NH4+-N 排泄率先升高后降低。实时 PCR 显示，血细胞胞质 Cu，Zn SOD 基因表达上调，随后恢复。然而，血浆 SOD 活性在病毒注射后持续增加。此外，血浆 AKP 活性首先降低，然后逐渐升高，在病毒注射后 24 小时达到最高水平。在 17°C 下用 AVNV 攻毒的扇贝既没有出现明显的疾病，也没有表现出与病毒感染相关的明显反应。虽然结果表明，升高的海水温度与 AVNV 感染相关的 C. farreri 死亡率之间存在相关性，但它们也表明，病毒感染引发了宿主扇贝的多种生理和免疫反应。
