serval:BIB_D6DB30E32E18
HIV-1 immune activation induces Siglec-1 expression and enhances viral trans-infection in blood and tissue myeloid cells.
10.1186/s12977-015-0160-x
000353994000001
25947229
Pino
M.
author
Erkizia
I.
author
Benet
S.
author
Erikson
E.
author
Fernández-Figueras
M.T.
author
Guerrero
D.
author
Dalmau
J.
author
Ouchi
D.
author
Rausell
A.
author
Ciuffi
A.
author
Keppler
O.T.
author
Telenti
A.
author
Kräusslich
H.G.
author
Martinez-Picado
J.
author
Izquierdo-Useros
N.
author
article
2015
Retrovirology
1742-4690
1742-4690
journal
12
37
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 α (IFNα).
RESULTS: Here we show that IFNα-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.
eng
60_published
true
peer-reviewed
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: epublish
University of Lausanne
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