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Siglec-1 is a novel dendritic cell receptor that mediates HIV-1 trans-infection through recognition of viral membrane gangliosides.

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Publication date 2012
Author Izquierdo-Useros Nuria, Lorizate Maier, Puertas Maria C, Rodriguez-Plata Maria T, Zangger Nadine, Erikson Elina, Pino Maria, Erkizia Itziar, Glass Bärbel, Clotet Bonaventura, Keppler Oliver T, Telenti Amalio, Kräusslich Hans-Georg, Martinez-Picado Javier,
Project Host evolutionary genomics of HIV-1 and other retroviruses
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Original article (peer-reviewed)

Journal PLoS biology
Volume (Issue) 10(12)
Page(s) 1001448 - 1001448
Title of proceedings PLoS biology
DOI 10.1371/journal.pbio.1001448

Open Access

URL http://www.ncbi.nlm.nih.gov/pubmed/23271952
Type of Open Access Website

Abstract

Dendritic cells (DCs) are essential antigen-presenting cells for the induction of immunity against pathogens. However, HIV-1 spread is strongly enhanced in clusters of DCs and CD4(+) T cells. Uninfected DCs capture HIV-1 and mediate viral transfer to bystander CD4(+) T cells through a process termed trans-infection. Initial studies identified the C-type lectin DC-SIGN as the HIV-1 binding factor on DCs, which interacts with the viral envelope glycoproteins. Upon DC maturation, however, DC-SIGN is down-regulated, while HIV-1 capture and trans-infection is strongly enhanced via a glycoprotein-independent capture pathway that recognizes sialyllactose-containing membrane gangliosides. Here we show that the sialic acid-binding Ig-like lectin 1 (Siglec-1, CD169), which is highly expressed on mature DCs, specifically binds HIV-1 and vesicles carrying sialyllactose. Furthermore, Siglec-1 is essential for trans-infection by mature DCs. These findings identify Siglec-1 as a key factor for HIV-1 spread via infectious DC/T-cell synapses, highlighting a novel mechanism that mediates HIV-1 dissemination in activated tissues.
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