M-Sec induced by HTLV-1 mediates an efficient viral transmission.
| Autor: | Masateru Hiyoshi, Naofumi Takahashi, Youssef M Eltalkhawy, Osamu Noyori, Sameh Lotfi, Jutatip Panaampon, Seiji Okada, Yuetsu Tanaka, Takaharu Ueno, Jun-Ichi Fujisawa, Yuko Sato, Tadaki Suzuki, Hideki Hasegawa, Masahito Tokunaga, Yorifumi Satou, Jun-Ichirou Yasunaga, Masao Matsuoka, Atae Utsunomiya, Shinya Suzu |
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| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: | |
| Zdroj: | PLoS Pathogens, Vol 17, Iss 11, p e1010126 (2021) |
| Druh dokumentu: | article |
| ISSN: | 1553-7366 1553-7374 |
| DOI: | 10.1371/journal.ppat.1010126 |
| Popis: | Human T-cell leukemia virus type 1 (HTLV-1) infects target cells primarily through cell-to-cell routes. Here, we provide evidence that cellular protein M-Sec plays a critical role in this process. When purified and briefly cultured, CD4+ T cells of HTLV-1 carriers, but not of HTLV-1- individuals, expressed M-Sec. The viral protein Tax was revealed to mediate M-Sec induction. Knockdown or pharmacological inhibition of M-Sec reduced viral infection in multiple co-culture conditions. Furthermore, M-Sec knockdown reduced the number of proviral copies in the tissues of a mouse model of HTLV-1 infection. Phenotypically, M-Sec knockdown or inhibition reduced not only plasma membrane protrusions and migratory activity of cells, but also large clusters of Gag, a viral structural protein required for the formation of viral particles. Taken together, these results suggest that M-Sec induced by Tax mediates an efficient cell-to-cell viral infection, which is likely due to enhanced membrane protrusions, cell migration, and the clustering of Gag. |
| Databáze: | Directory of Open Access Journals |
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