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.

青蛙病毒 3 (FV3) 导致一系列两栖动物物种死亡。尽管皮肤上皮细胞作为抵御 FV3 的第一道防线很重要，但两栖动物皮肤上皮细胞和 FV3 之间的相互作用在很大程度上仍未得到表征。在这里，我们使用了新建立的非洲爪蟾皮肤上皮样细胞系 Xela DS2 和 Xela VS2，研究青蛙皮肤上皮细胞对 FV3 的敏感性和许可性，以及这些细胞对 FV3 的先天免疫抗病毒和促炎基因调控反应。两种细胞系都对 FV3 敏感和允许，但没有表现出被认为被 FV3 用于细胞进入的清道夫受体的明显转录水平。Xela DS2 和 Xela VS2 上调抗病毒和促炎细胞因子转录物，以响应 poly(I:C) 而不是 FV3 或紫外线灭活的 FV3。Poly(I:C) 预处理限制了两种细胞系中的 FV3 复制和 FV3 诱导的细胞病变效应。因此，Xela DS2 和 Xela VS2 可以支持 FV3 复制，代表体外研究青蛙皮肤上皮细胞抗病毒反应的系统，并可作为筛选化合物的新工具，这些化合物启动有效的抗病毒程序以限制 FV3 复制。