Department of Microbiology and Immunology, Eulji University School of Medicine, Daejeon, 34824, Republic of Korea.
Eulji Biomedical Science Research Institute, Eulji University School of Medicine, Daejeon, 34824, Republic of Korea.
J Microbiol. 2021 May;59(5):522-529. doi: 10.1007/s12275-021-1108-6. Epub 2021 Apr 20.
Extracellular vesicles (EVs) play a crucial role in cell-to-cell communication. EVs and viruses share several properties related to their structure and the biogenesis machinery in cells. EVs from virus-infected cells play a key role in virus spread and suppression using various loading molecules, such as viral proteins, host proteins, and microRNAs. However, it remains unclear how and why viruses regulate EV production inside host cells. The purpose of this study is to investigate the molecular mechanisms underlying EV production and their roles in Kaposi's sarcoma-associated herpesvirus (KSHV)-infected cells. Here, we found that KSHV induced EV production in human endothelial cells via Rab-27b upregulation. The suppression of Rab27b expression in KSHV-infected cells enhanced cell death by increasing autophagic flux and autolysosome formation. Our results indicate that Rab27b regulates EV biogenesis to promote cell survival and persistent viral infection during KSHV infection, thereby providing novel insights into the crucial role of Rab-27b in the KSHV life cycle.
细胞外囊泡 (EVs) 在细胞间通讯中发挥着至关重要的作用。EVs 和病毒在结构和细胞内的生物发生机制方面具有一些共同的特性。来自病毒感染细胞的 EVs 通过各种加载分子（如病毒蛋白、宿主蛋白和 microRNAs）在病毒传播和抑制中发挥关键作用。然而，目前尚不清楚病毒如何以及为何在宿主细胞内调节 EV 的产生。本研究旨在探讨 EV 产生的分子机制及其在卡波西肉瘤相关疱疹病毒 (KSHV) 感染细胞中的作用。在这里，我们发现 KSHV 通过上调 Rab-27b 诱导人内皮细胞中 EV 的产生。在 KSHV 感染的细胞中抑制 Rab27b 的表达会通过增加自噬通量和自溶酶体形成来增加细胞死亡。我们的结果表明，Rab27b 通过调节 EV 的生物发生来促进细胞存活和持续性病毒感染，从而为 Rab-27b 在 KSHV 生命周期中的关键作用提供了新的见解。
