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

淋巴囊病病毒(LCDV)是淋巴囊病(LCD)的病原体。在本研究中，我们通过基因芯片实验研究了感染LCDV的鱼鳍中淋巴囊细胞(LCC)的形成机制。LCC最早出现在感染后21d(Dpi)。微阵列检测到了一些基因表达的变化，直到28dpi。然而，在28-42dpi之间，表达变化的基因数量急剧增加，其中LCC形成活跃。从芯片数据分析，在42dpi时，细胞凋亡相关基因和细胞周期蛋白依赖性激酶(CDK)1基因下调，而细胞融合和胶原相关基因上调。结合前人对LCC形态变化的观察，认为LCC的形成涉及以下几个步骤：(1)病毒感染的细胞在扩大前经历了抑制凋亡的死亡；(2)经历了G2/M期细胞周期停滞而抑制了细胞分裂；(3)由于细胞融合而肥大；(4)被透明的囊膜包裹，伴随着胶原纤维的改变。

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.