Bui-Marinos Maxwell P, Todd Lauren A, Wasson Marie-Claire D, Morningstar Brandon E E, Katzenback Barbara A
Department of Biology, University of Waterloo, Waterloo, Ontario, N2L 3G1, Canada.
Department of Biology, University of Waterloo, Waterloo, Ontario, N2L 3G1, Canada.
Dev Comp Immunol. 2021 Nov;124:104200. doi: 10.1016/j.dci.2021.104200. Epub 2021 Jul 5.
Frog virus 3 (FV3) causes mortality in a range of amphibian species. Despite the importance of the skin epithelium as a first line of defence against FV3, the interaction between amphibian skin epithelial cells and FV3 remains largely uncharacterized. Here, we used newly established Xenopus laevis skin epithelial-like cell lines, Xela DS2 and Xela VS2, to study the susceptibility and permissiveness of frog skin epithelial cells to FV3, and the innate immune antiviral and proinflammatory gene regulatory responses of these cells to FV3. Both cell lines are susceptible and permissive to FV3, yet do not exhibit appreciable transcript levels of scavenger receptors thought to be used by FV3 for cellular entry. Xela DS2 and Xela VS2 upregulate antiviral and proinflammatory cytokine transcripts in response to poly(I:C) but not to FV3 or UV-inactivated FV3. Poly(I:C) pretreatment limits FV3 replication and FV3-induced cytopathic effects in both cell lines. Thus, Xela DS2 and Xela VS2 can support FV3 replication, represent in vitro systems to investigate antiviral responses of frog skin epithelial cells, and can serve as novel tools for screening compounds that initiate effective antiviral programs to limit FV3 replication.
蛙病毒3（FV3）可导致多种两栖动物死亡。尽管皮肤上皮作为抵御FV3的第一道防线至关重要，但两栖动物皮肤上皮细胞与FV3之间的相互作用在很大程度上仍未得到充分研究。在此，我们利用新建立的非洲爪蟾皮肤上皮样细胞系Xela DS2和Xela VS2，来研究蛙皮肤上皮细胞对FV3的易感性和允许性，以及这些细胞对FV3的先天性免疫抗病毒和促炎基因调控反应。这两种细胞系对FV3均易感且允许其感染，但未表现出FV3用于进入细胞的清道夫受体的明显转录水平。Xela DS2和Xela VS2对聚肌胞苷酸（poly(I:C)）有反应，会上调抗病毒和促炎细胞因子转录本，但对FV3或紫外线灭活的FV3无反应。聚肌胞苷酸预处理可限制两种细胞系中FV3的复制以及FV3诱导的细胞病变效应。因此，Xela DS2和Xela VS2可支持FV3复制，是研究蛙皮肤上皮细胞抗病毒反应的体外系统，并且可作为筛选启动有效抗病毒程序以限制FV3复制的化合物用的新型工具。
