2024-03-29T10:02:55Z
https://u-ryukyu.repo.nii.ac.jp/oai
oai:u-ryukyu.repo.nii.ac.jp:02012192
2023-08-03T05:36:14Z
1642838163960:1642838338003
1642838403551:1642838407795
Dendritic cell maturation, but not type I interferon exposure, restricts infection by HTLV-1, and viral transmission to T-cells.
Rizkallah, Gergès
Alais, Sandrine
Nicolas, Futsch
Tanaka, Yuetsu
Journo, Chloè
Mahieux, Renaud
Dutartre, Hélène
open access
Human T lymphotropic Virus type 1 (HTLV-1) is the etiological agent of Adult T cell Leukemia/ Lymphoma (ATLL) and HTLV-1-Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP). Both CD4^+ T-cells and dendritic cells (DCs) infected with HTLV-1 are found in peripheral blood from HTLV-1 carriers. We previously demonstrated that monocyte-derived IL-4 DCs are more susceptible to HTLV-1 infection than autologous primary T-cells, suggesting that DC infection precedes T-cell infection. However, during blood transmission, breast-feeding or sexual transmission, HTLV-1 may encounter different DC subsets present in the blood, the intestinal or genital mucosa respectively. These different contacts may impact HTLV-1 ability to infect DCs and its subsequent transfer to T-cells. Using in vitro monocyte-derived IL-4 DCs, TGF-β DCs and IFN-α DCs that mimic DCs contacting HTLV-1 in vivo, we show here that despite their increased ability to capture HTLV-1 virions, IFN-α DCs restrict HTLV-1 productive infection. Surprisingly, we then demonstrate that it is not due to the antiviral activity of type-I interferon produced by IFN-α DCs, but that it is likely to be linked to a distinct trafficking route of HTLV-1 in IL-4 DCs vs. IFN-α DCs. Finally, we demonstrate that, in contrast to IL-4 DCs, IFN-α DCs are impaired in their capacity to transfer HTLV-1 to CD4 T-cells, both after viral capture and trans-infection and after their productive infection. In conclusion, the nature of the DCs encountered by HTLV-1 upon primo-infection and the viral trafficking route through the vesicular pathway of these cells determine the efficiency of viral transmission to T-cells, which may condition the fate of infection.
論文
Public Library of Science
2017-04-20
eng
journal article
VoR
http://hdl.handle.net/20.500.12000/45206
http://hdl.handle.net/20.500.12000/45206
https://u-ryukyu.repo.nii.ac.jp/records/2012192
https://doi.org/10.1371/journal.ppat.1006353
10.1371/journal.ppat.1006353
1553-7366
1553-7374
AA12072310
PLOS pathogens
13
4
https://u-ryukyu.repo.nii.ac.jp/record/2012192/files/No13p1.pdf