Morphological changes contribute to apoptotic cell death and are affected by caspase-3 and caspase-6 inhibitors during red sea bream iridovirus permissive replication
Morphological changes contribute to apoptotic cell death and are affected by caspase-3 and caspase-6 inhibitors during red sea bream iridovirus permissive replication
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DOI：
10.1016/j.virol.2004.02.006
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发表时间：
2004-05-01
期刊：
影响因子：
3.7
通讯作者：
Oshima, S
中科院分区：
文献类型：
--
作者：
Imajoh, M;Sugiura, H;Oshima, S
虹彩病毒科的红鱼虹彩病毒(RSIV)是日本西南部许多养殖鱼类致死性感染的病原体。RSIV诱导的细胞凋亡可分为：(1)早期细胞皱缩变圆，(2)中期细胞增大，(3)晚期形成凋亡小体小泡并被邻近细胞吞噬，(4)无吞噬作用的凋亡小体小泡膜完整性丧失。通过亲和标记，RSIV诱导的细胞凋亡包括caspase依赖的细胞凋亡。在caspase-3和-6抑制剂存在的情况下，RSIV感染引起细胞变圆，但不导致细胞增大或形成凋亡体样泡，并进一步限制了部分结构蛋白的合成。这些结果表明，caspase-3和-6参与了RSIV感染后期细胞凋亡中晚期的形态变化和病毒蛋白的合成。(C)2004 Elsevier Inc.保留所有权利。
Red sea bream iridovirus (RSIV) of the Iridoviridae family is a causative agent of lethal infections in many cultured marine fish species in southwestern Japan. RSIV-induced apoptosis was divided as follows: (1) cell shrinkage and rounding at the early apoptotic stage, (2) cell enlargement at the middle apoptotic stage, (3) formation of apoptotic body-like vesicles at the late apoptotic stage and phagocytosis by neighboring cells, and (4) loss of membrane integrity in apoptotic body-like vesicles without phagocytosis by neighboring cells. By affinity labeling, RSIV-induced apoptosis included caspase-dependent apoptosis. RSIV infection caused cell rounding but not cell enlargement or formation of apoptotic body-like vesicles and further restricted part of the structural protein synthesis in the presence of caspase-3 and -6 inhibitors. These findings showed the involvement of caspase-3 and -6 in the morphological changes at the middle and late apoptotic stages and viral protein synthesis in the late stage of RSIV infection. (C) 2004 Elsevier Inc. All rights reserved.