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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 .    Electronic supplementary material  The online version of this article (doi:10.1186/s12977-015-0160-x) contains supplementary material, which is available to authorized users.

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