| Title | Rab27b regulates extracellular vesicle production in cells infected with Kaposi’s sarcoma–associated herpesvirus to promote cell survival and persistent infection |
|---|---|
| Author | Hyungtaek Jeon1, Su-Kyung Kang1, Myung-Ju Lee1, Changhoon Park1, Seung-Min Yoo1,2, Yun Hee Kang1,2, and Myung-Shin Lee1,2 |
| Address | 1Department of Microbiology and Immunology, Eulji University School of Medicine, Daejeon 34824, Republic of Korea, 2Eulji Biomedical Science Research Institute, Eulji University School of Medicine, Daejeon 34824, Republic of Korea |
| Bibliography | Journal of Microbiology, 59(5),522–529, 2021, |
| DOI | 10.1007/s12275-021-1108-6 |
| Key Words | extracellular vesicle, Kaposi’s sarcoma-associated herpesvirus, Rab27b, autophagy, cell death |
| Abstract | 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. |