TY - JOUR
T1 - HIV-1 immune activation induces Siglec-1 expression and enhances viral trans-infection in blood and tissue myeloid cells
AU - Pino, Maria
AU - Erkizia, Itziar
AU - Benet, Susana
AU - Erikson, Elina
AU - Fernández-Figueras, Maria Teresa
AU - Guerrero, Dolores
AU - Dalmau, Judith
AU - Ouchi, Dan
AU - Rausell, Antonio
AU - Ciuffi, Angela
AU - Keppler, Oliver T.
AU - Telenti, Amalio
AU - Kräusslich, Hans Georg
AU - Martinez-Picado, Javier
AU - Izquierdo-Useros, Nuria
PY - 2015/5/7
Y1 - 2015/5/7
N2 - © 2015 Pino et al. 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.
AB - © 2015 Pino et al. 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.
KW - Dendritic cells
KW - HIV-1
KW - Siglec-1
KW - Trans-infection
U2 - 10.1186/s12977-015-0160-x.
DO - 10.1186/s12977-015-0160-x.
M3 - Article
SN - 1742-4690
VL - 12
JO - Retrovirology
JF - Retrovirology
IS - 1
M1 - 37
ER -
