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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, María Teresa; Guerrero, Dolores; Dalmau, Judith; Ouchi, Dan; Rausell, Antonio; Ciuffi, Angela; Keppler, Oliver T.; Telenti, Amalio; Kräusslich, H.G.; Martinez Picado, Francisco Javier; Izquierdo Useros, Nuria
Universitat de Vic - Universitat Central de Catalunya. Càtedra de la Sida i Malalties Relacionades
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.
-Sida -- Tractament
-VIH (Virus)
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BioMed Central
         

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