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 ...»»»»
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.^^^^