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Internalization of Swine Vesicular Disease Virus into Cultured Cells: a Comparative Study with Foot-and-Mouth Disease Virus

机译:猪水泡病病毒在培养细胞中的内在化:与口蹄疫病毒的比较研究

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摘要

We performed a comparative analysis of the internalization mechanisms used by three viruses causing important vesicular diseases in animals. Swine vesicular disease virus (SVDV) internalization was inhibited by treatments that affected clathrin-mediated endocytosis and required traffic through an endosomal compartment. SVDV particles were found in clathrin-coated pits by electron microscopy and colocalized with markers of early endosomes by confocal microscopy. SVDV infectivity was significantly inhibited by drugs that raised endosomal pH. When compared to foot-and-mouth disease virus (FMDV), which uses clathrin-mediated endocytosis, the early step of SVDV was dependent on the integrity of microtubules. SVDV-productive endocytosis was more sensitive to plasma membrane cholesterol extraction than that of FMDV, and differential cell signaling requirements for virus infection were also found. Vesicular stomatitis virus, a model virus internalized by clathrin-mediated endocytosis, was included as a control of drug treatments. These results suggest that different clathrin-mediated routes are responsible for the internalization of these viruses.
机译:我们对引起动物重要水泡疾病的三种病毒使用的内在化机制进行了比较分析。猪水泡病病毒(SVDV)的内在化受到影响网格蛋白介导的内吞作用和需要通过内体区室运输的治疗的抑制。 SVDV颗粒通过电子显微镜在网格蛋白包被的凹坑中发现,并通过共聚焦显微镜与早期内体标记物共定位。升高内体pH的药物显着抑制了SVDV的感染性。与使用网格蛋白介导的内吞作用的口蹄疫病毒(FMDV)相比,SVDV的早期依赖于微管的完整性。 SVDV产生的内吞作用比FMDV对质膜胆固醇提取更敏感,并且还发现了病毒感染的差异细胞信号传导要求。水泡性口炎病毒是通过网格蛋白介导的内吞作用而内在化的模型病毒,作为药物治疗的对照。这些结果表明,不同的网格蛋白介导的途径负责这些病毒的内在化。

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