HIV-1 immune activation induces Siglec-1 expression and enhances viral trans-infection in blood and tissue myeloid cells.

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State: Public
Version: Final published version
Serval ID
serval:BIB_D6DB30E32E18
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
HIV-1 immune activation induces Siglec-1 expression and enhances viral trans-infection in blood and tissue myeloid cells.
Journal
Retrovirology
Author(s)
Pino M., Erkizia I., Benet S., Erikson E., Fernández-Figueras M.T., Guerrero D., Dalmau J., Ouchi D., Rausell A., Ciuffi A., Keppler O.T., Telenti A., Kräusslich H.G., Martinez-Picado J., Izquierdo-Useros N.
ISSN
1742-4690 (Electronic)
ISSN-L
1742-4690
Publication state
Published
Issued date
2015
Peer-reviewed
Oui
Volume
12
Pages
37
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't Publication Status: epublish
Abstract
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.
Pubmed
Web of science
Open Access
Yes
Create date
22/05/2015 16:40
Last modification date
20/08/2019 15:56
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