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Retrovirology. 2015 May 7;12:37. doi: 10.1186/s12977-015-0160-x.

HIV-1 immune activation induces Siglec-1 expression and enhances viral trans-infection in blood and tissue myeloid cells.

Author information

1
AIDS Research Institute IrsiCaixa, Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol IGTP, Universitat Autònoma de Barcelona, Badalona, Spain. mpino@irsicaixa.es.
2
AIDS Research Institute IrsiCaixa, Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol IGTP, Universitat Autònoma de Barcelona, Badalona, Spain. ierkizia@irsicaixa.es.
3
AIDS Research Institute IrsiCaixa, Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol IGTP, Universitat Autònoma de Barcelona, Badalona, Spain. sbenet@irsicaixa.es.
4
Institute of Medical Virology, National Reference Center for Retroviruses, University of Frankfurt, Frankfurt, Germany. Elina.Erikson@kgu.de.
5
Department of Infectious Diseases, Virology, Universitätsklinikum Heidelberg, Heidelberg, Germany. Elina.Erikson@kgu.de.
6
Pathology Department, University Hospital Germans Trias i Pujol (HUGTIP), Badalona, Spain. maiteffig@gmail.com.
7
Otorhinolaryngology Department, HUGTIP, Badalona, Spain. lolagg1969@gmail.com.
8
AIDS Research Institute IrsiCaixa, Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol IGTP, Universitat Autònoma de Barcelona, Badalona, Spain. jdalmau@irsicaixa.es.
9
AIDS Research Institute IrsiCaixa, Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol IGTP, Universitat Autònoma de Barcelona, Badalona, Spain. douchi@irsicaixa.es.
10
Institute of Microbiology, University Hospital Center and University of Lausanne, Lausanne, Switzerland. rausell.biocomp@gmail.com.
11
Swiss Institute of Bioinformatics (SIB) - Vital-IT, Lausanne, Switzerland. rausell.biocomp@gmail.com.
12
Institute of Microbiology, University Hospital Center and University of Lausanne, Lausanne, Switzerland. Angela.Ciuffi@chuv.ch.
13
Institute of Medical Virology, National Reference Center for Retroviruses, University of Frankfurt, Frankfurt, Germany. Oliver.Keppler@kgu.de.
14
Institute of Microbiology, University Hospital Center and University of Lausanne, Lausanne, Switzerland. atelenti@jcvi.org.
15
Current address: The J. Craig Venter Institute, La Jolla, CA, USA. atelenti@jcvi.org.
16
Department of Infectious Diseases, Virology, Universitätsklinikum Heidelberg, Heidelberg, Germany. hans-georg.kraeusslich@med.uni-heidelberg.de.
17
AIDS Research Institute IrsiCaixa, Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol IGTP, Universitat Autònoma de Barcelona, Badalona, Spain. jmpicado@irsicaixa.es.
18
Institució Catalana de Recerca i Estudis Avançats ICREA, Barcelona, Spain. jmpicado@irsicaixa.es.
19
University of Vic-Central University of Catalonia (UVic-UCC), Vic, Spain. jmpicado@irsicaixa.es.
20
AIDS Research Institute IrsiCaixa, Institut d'Investigació en Ciències de la Salut Germans Trias i Pujol IGTP, Universitat Autònoma de Barcelona, Badalona, Spain. nizquierdo@irsicaixa.es.

Abstract

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.

PMID:
25947229
PMCID:
PMC4423124
DOI:
10.1186/s12977-015-0160-x
[Indexed for MEDLINE]
Free PMC Article

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