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

Pino, Maria; Erkizia, Itziar; Benet, Susana; Erikson, Elina; Fernández-Figueras, Maria Teresa; Guerrero, Dolores; Dalmau, Judith; Ouchi, Dan; Rausell, Antonio; Ciuffi, Angela; Keppler, Oliver T; Telenti, Amalio; Kräusslich, Hans-Georg; Martinez-Picado, Javier; Izquierdo-Useros, Nuria.
Retrovirology; 12: 37, 2015 May 07.
Artigo em Inglês | MEDLINE | ID: mdl-25947229


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).


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.


Siglec-1 on myeloid cells could fuel novel CD4(+) T-cell infections and contribute to HIV-1 dissemination in vivo.
Selo DaSilva