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Antigen presenting cells from the cervical mucosa are thought to amplify incoming HIV-1 and spread infection systemically without being productively infected. Yet, the molecular mechanism at the cervical mucosa underlying this viral transmission pathway remains unknown. Here we identified a subset of HLA-DR +  CD14 +  CD11c +  cervical DCs at the lamina propria of the ectocervix and the endocervix that expressed the type-I interferon inducible lectin Siglec-1 (CD169), which promoted viral uptake. In the cervical biopsy of a viremic HIV-1 +  patient, Siglec-1 +  cells harbored HIV-1-containing compartments, demonstrating that  in vivo , these cells trap viruses . Ex vivo , a type-I interferon antiviral environment enhanced viral capture and  trans -infection via Siglec-1. Nonetheless, HIV-1 transfer via cervical DCs was effectively prevented with antibodies against Siglec-1. Our findings contribute to decipher how cervical DCs may boost HIV-1 replication and promote systemic viral spread from the cervical mucosa, and highlight the importance of including inhibitors against Siglec-1 in microbicidal strategies.

Dendritic Cells From the Cervical Mucosa Capture and Transfer HIV-1 via Siglec-1