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Title :Dendritic cell maturation, but not type I interferon exposure, restricts infection by HTLV-1, and viral transmission to T-cells.
Authors :Rizkallah, Gergès
Alais, Sandrine
Nicolas, Futsch
Tanaka, Yuetsu
Journo, Chloè
Mahieux, Renaud
Dutartre, Hélène
Issue Date :20-Apr-2017
Abstract :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.
URL :https://doi.org/10.1371/journal.ppat.1006353
Type Local :雑誌掲載論文
ISSN :1553-7366
1553-7374
Publisher :Public Library of Science
URI :http://hdl.handle.net/20.500.12000/45206
Citation :PLOS pathogens Vol.13 no.4
Appears in Collections:Peer-reviewed Journal Articles (Faculty of Medicine)

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