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

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 o...

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Detalles Bibliográficos
Autores: Perez-Zsolt, Daniel|||0000-0003-4192-7622, Cantero, Jon|||0000-0003-4844-6143, Erkizia, Itziar|||0000-0003-1244-8972, Benet, Susana|||0000-0002-2219-8826, Pino, M., Serra-Peinado, Carla|||0000-0003-1413-3990, Hernández Gallego, Alba|||0000-0002-4595-468X, Castellvi, Josep|||0000-0001-5745-9996, Tapia, G., Arnau-Saz, V., Garrido, Joseba M., Tarrats, Antoni|||0000-0002-1276-8522, Buzón, Maria José|||0000-0003-4427-9413, Martinez-Picado, J., Izquierdo Useros, Nuria|||0000-0002-1039-1821, Genescà Ferrer, Meritxell|||0000-0001-6413-3812
Tipo de recurso: artículo
Fecha de publicación:2019
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:ddd.uab.cat:223637
Acceso en línea:https://ddd.uab.cat/record/223637
https://dx.doi.org/urn:doi:10.3389/fimmu.2019.00825
Access Level:acceso abierto
Palabra clave:Cervix
Siglec-1
HIV-1
Trans-infection
Myeloid cells
Descripción
Sumario: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.

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