TY  - JOUR
EP  - 15
A1  - Pino, Maria
A1  - Erkizia, Itziar
A1  - Benet, Susana
A1  - Erikson, Elina
A1  - Fernández-Figueras, Maria Teresa
A1  - Guerrero, Dolores
A1  - Dalmau, Judith
A1  - Ouchi, Dan
A1  - Rausell, Antonio
A1  - Ciuffi, Angela
A1  - Keppler, Oliver T.
A1  - Telenti, Amalio
A1  - Kräusslich, Hans-Georg
A1  - Martinez-Picado, Javier
A1  - Izquierdo-Useros, Nuria
IS  - 37
UR  - https://archiv.ub.uni-heidelberg.de/volltextserver/19378/
SN  - 1742-4690
PB  - BioMed Central
N2  - Background: Myeloid cells are key players in the recognition and response of the host against invading viruses. Paradoxically, upon HIV-1 infection, myeloid cells might also promote viral pathogenesis through trans-infection, a mechanism that promotes HIV-1 transmission to target cells via viral capture and storage. The receptor Siglec-1 (CD169) potently enhances HIV-1 trans-infection and is regulated by immune activating signals present throughout the course of HIV-1 infection, such as interferon ? (IFN?).   Results: Here we show that IFN?-activated dendritic cells, monocytes and macrophages have an enhanced ability to capture and trans-infect HIV-1 via Siglec-1 recognition of viral membrane gangliosides. Monocytes from untreated HIV-1-infected individuals trans-infect HIV-1 via Siglec-1, but this capacity diminishes after effective antiretroviral treatment. Furthermore, Siglec-1 is expressed on myeloid cells residing in lymphoid tissues, where it can mediate viral trans-infection.   Conclusions: Siglec-1 on myeloid cells could fuel novel CD4+ T-cell infections and contribute to HIV-1 dissemination in vivo.  
CY  - London
AV  - public
Y1  - 2015///
TI  - HIV-1 immune activation induces Siglec-1 expression and enhances viral trans-infection in blood and tissue myeloid cells
VL  - 12
SP  - 1
ID  - heidok19378
JF  - Retrovirology
ER  -