Department of Aquatic Animal Medicine, College of Fisheries, Huazhong Agricultural University, Wuhan, 430070, People's Republic of China.
Department of Aquatic Animal Medicine, College of Fisheries, Huazhong Agricultural University, Wuhan, 430070, People's Republic of China; Key Lab of Freshwater Animal Breeding, Ministry of Agriculture, Wuhan, 430070, People's Republic of China.
Fish Shellfish Immunol. 2018 Apr;75:58-65. doi: 10.1016/j.fsi.2018.01.053. Epub 2018 Feb 2.
Spring viraemia of carp virus (SVCV) is a deadly pathogen of common carp. SVCV infection is found to be associated with excess reactive oxygen species (ROS) generation and induces oxidative stress in EPC and FHM cells, which contributes to its pathogenesis. In this study, ROS production and mitochondria function as well as antioxidant enzymes in mitochondria were investigated during SVCV infection in EPC cells. Dysfunction of mitochondria and inactivation of mitochondria electron transport chain complex Ⅲ to augment O and HO accumulation were observed in SVCV infected EPC cells. Treatment of Antimycin A reduced the activity of mitochondria complex Ⅲ in EPC cells, which also inhibited the transcription of SVCV glycoprotein gene (SVCV-G) and production of SVCV. Our studies explain the production of ROS following SVCV infection and also suggest that integrate mitochondrial function is important for SVCV infection.
锦鲤疱疹病毒（SVCV）是鲤鱼的一种致命病原体。研究发现，SVCV 感染会导致活性氧（ROS）过度产生，并诱导 EPC 和 FHM 细胞发生氧化应激，这是导致其发病机制的原因之一。在本研究中，我们研究了 SVCV 在 EPC 细胞中感染期间 ROS 的产生、线粒体功能以及线粒体中的抗氧化酶。在感染 SVCV 的 EPC 细胞中，观察到线粒体功能障碍和线粒体电子传递链复合物 III 失活，从而导致 O 和 HO 的积累增加。Antimycin A 的处理降低了 EPC 细胞中线粒体复合物 III 的活性，这也抑制了 SVCV 糖蛋白基因（SVCV-G）的转录和 SVCV 的产生。我们的研究解释了 SVCV 感染后 ROS 的产生，并表明整合线粒体功能对 SVCV 感染很重要。
