2020年12月
M-Sec facilitates intercellular transmission of HIV-1 through multiple mechanisms
Retrovirology
- ,
- ,
- ,
- ,
- ,
- ,
- 巻
- 17
- 号
- 1
- 開始ページ
- 20
- 終了ページ
- 20
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1186/s12977-020-00528-y
- 出版者・発行元
- Springer Science and Business Media LLC
BACKGROUND: HIV-1 promotes the formation of tunneling nanotubes (TNTs) that connect distant cells, aiding cell-to-cell viral transmission between macrophages. Our recent study suggests that the cellular protein M-Sec plays a role in these processes. However, the timing, mechanism, and to what extent M-Sec contributes to HIV-1 transmission is not fully understood, and the lack of a cell line model that mimics macrophages has hindered in-depth analysis. RESULTS: We found that HIV-1 increased the number, length and thickness of TNTs in a manner dependent on its pathogenic protein Nef and M-Sec in U87 cells, as observed in macrophages. In addition, we found that M-Sec was required not only for TNT formation but also motility of U87 cells, both of which are beneficial for viral transmission. In fact, M-Sec knockdown in U87 cells led to a significantly delayed viral production in both cellular and extracellular fractions. This inhibition was observed for wild-type virus, but not for a mutant virus lacking Nef, which is known to promote not only TNT formation but also migration of infected macrophages. CONCLUSIONS: By taking advantage of useful features of U87 cells, we provided evidence that M-Sec mediates a rapid and efficient cell-cell transmission of HIV-1 at an early phase of infection by enhancing both TNT formation and cell motility.
- リンク情報
-
- DOI
- https://doi.org/10.1186/s12977-020-00528-y
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/32650782
- PubMed Central
- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7350586
- URL
- http://link.springer.com/content/pdf/10.1186/s12977-020-00528-y.pdf
- URL
- http://link.springer.com/article/10.1186/s12977-020-00528-y/fulltext.html
- ID情報
-
- DOI : 10.1186/s12977-020-00528-y
- eISSN : 1742-4690
- PubMed ID : 32650782
- PubMed Central 記事ID : PMC7350586