Medical Microbiology Interdisciplinary Program, Graduate School, Chulalongkorn University, Bangkok, 10330, Thailand.
Applied Medical Virology Research Unit, Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.
Curr Microbiol. 2021 Dec 14;79(1):23. doi: 10.1007/s00284-021-02716-1.
Enhanced HSV-1 production is found in activated T-lymphocytes, but the mechanism is still unknown. In this paper, the HSV-1 entry step in CD3CD4CD8Jurkat T lymphocytes was investigated. Observation under electron microscopy revealed the level of filopodia formation on the surface of activated Jurkat cells was significantly higher than that of non-activated Jurkat cells especially after adding HSV-1 for 15 min. A significant increase of actin protein was demonstrated in HSV-1 infected, activated Jurkat cells compared to HSV-1 infected, non-activated Jurkat cells. After the cells were treated with 2.5 and 5 µg/mL cytochalasin D, an inhibitor of actin polymerization that causes depolymerization of actin's filamentous form, the actin protein was decreased significantly, resulting in an absence of filopodia formation. In summary, this is the first study revealing that HSV-1 induced filopodia formation through actin polymerization in activated T cells similar to epithelial, mucosal and neuronal cells. This phenomenon supported the virus entry resulting to increased yield of HSV-1 production.
单纯疱疹病毒 1 （HSV-1）产量增强存在于活化的 T 淋巴细胞中，但具体机制仍不清楚。本文研究了 HSV-1 在 CD3+CD4+CD8+Jurkat T 淋巴细胞中的进入步骤。电子显微镜观察发现，与非活化的 Jurkat 细胞相比，活化的 Jurkat 细胞表面丝状伪足的形成水平明显更高，尤其是在加入 HSV-1 15 分钟后。与 HSV-1 感染的非活化 Jurkat 细胞相比，HSV-1 感染的活化 Jurkat 细胞中肌动蛋白蛋白明显增加。用 2.5 和 5µg/mL 细胞松弛素 D 处理细胞后，肌动蛋白聚合抑制剂导致肌动蛋白丝状形式解聚，肌动蛋白蛋白显著减少，导致丝状伪足形成缺失。总之，这是第一项表明 HSV-1 通过激活的 T 细胞中的肌动蛋白聚合诱导丝状伪足形成的研究，类似于上皮、黏膜和神经元细胞。这种现象支持病毒进入导致 HSV-1 产量增加。
