The mechanisms of lymphocystis cell formation in Japanese flounder Paralichthys olivaceus experimentally infected with lymphocystis disease virus

淋巴囊肿病病毒（LCDV）是引起淋巴囊肿病（LCD）的病原体。在本研究中，我们通过芯片实验研究了感染LCDV的鱼鳍中淋巴囊肿细胞（LCC）的形成机制。lcc首次出现于感染后21天（dpi）。微阵列检测到少量基因表达变化，直到28 dpi。然而，在lcc形成活跃的28和42 dpi之间，表达改变基因的数量急剧增加。从微阵列数据分析来看，凋亡相关基因和细胞周期蛋白依赖性激酶（CDK） 1基因在42 dpi时下调，而细胞融合和胶原相关基因则上调。结合以往报道中对LCC形态学变化的观察，我们认为LCC的形成涉及以下几个步骤：病毒感染的细胞(1)在扩大前经历了被抑制的凋亡死亡，(2)G2/M细胞周期阻滞抑制了细胞分裂，(3)细胞融合导致肥大，(4)被与胶原纤维改变相关的透明囊包围。

Lymphocystis disease virus (LCDV) is the causative agent of lymphocystis disease (LCD). In this study, we investigated the mechanisms of lymphocystis cell (LCC) formation in the fin of the fish infected with LCDV by microarray experiments. LCCs firstly appeared in the fish at 21 days post infection (dpi). The microarray detected a few gene expression changes until 28 dpi. However, the number of expression changed genes dramatically increased between 28 and 42 dpi in which LCCs formation was active. From the microarray data analyses, apoptosis-related genes and cyclin-dependent kinase (CDK) 1 gene were down-regulated, whereas cell fusion and collagen related genes were up-regulated at 42 dpi. Together with the observation of morphological changes of LCCs in previous reports, it is suggested that the following steps are involved in LCC formation: the virus infected cells(1) experienced inhibited apoptotic death before enlargement,(2) experienced inhibited cell division by G2/M cell cycle arrest,(3) were hypertrophied by cell fusion, and(4) were surrounded by a hyaline capsule associated with the alteration of collagen fibers.