IFN-γ促进中华鳖虹彩病毒（STIV）感染细胞凋亡的抗病毒机理研究

蛙虹彩病毒属是一类严重危害鱼类、两栖类和爬行类的双链DNA病毒，不仅造成重要经济损失制约着养殖业的发展，而且对自然界中的低等脊椎动物尤其是两栖和爬行类的一些珍稀物种造成重大威胁。中华鳖虹彩病毒（Soft-shelled turtle iridovirus，STIV），隶属蛙病毒属，是从患“红脖子”幼鳖中分离得到的，是中华鳖常见的病毒性病原之一。我们前期研究结果发现，过表达IFN-γ能促进STIV感染细胞的凋亡，从而抑制病毒增殖；但是，不能诱导未感染细胞凋亡。然而，对其机理尚不明了。本研究拟通过过表达及RNA干扰技术，研究死亡受体、线粒体和内质网途径介导细胞凋亡通路中相关基因在STIV诱导细胞凋亡过程中的作用以及在IFN-γ促进STIV感染细胞凋亡过程中的协同作用，阐明IFN-γ促进病毒感染细胞凋亡而发挥抗病毒作用的机制，从而在IFN-γ的作用以及抗蛙虹彩病毒病感染方面具有重要意义。

Ranaviruses are large icosahedral, double-strand DNA viruses, and can infect fish, amphibian and reptile, being a threat to aquaculture and global biodiversity. Soft-shelled turtle iridovirus (STIV), belonging to the Ranavirus, isolated from ‘red neck disease’ of the turtle, was one of the important viral pathogens of the turtle in aquaculture. Previous study showed that STIV could replicate and induce apoptosis in host cells, i.e. the soft-shelled turtle artery (STA) cell line, and that IFN-γ overexpression in STA cells could sensitize STIV infected cells to death with decreased virus gene synthesis and viral loads. However, the mechanism involved in the cell death was unknown. This proposed research is thus designed to illustrate the role of apoptosis related genes, that is to understand the death receptor-, mitochondrial-, and endoplasmic reticulum stress- mediated apoptosis pathways by using overexpression and RNA interferring technologies in STIV-infected cells. It is believed that this proposed research will provide novel insights into antiviral activity of IFN-γ through promoting apoptosis in virus-infected cells, and also provide a leading effect on ranavirus disease control.