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

Retrovirology

Nuria Izquierdo-Useros³  Javier Martinez-Picado¹  Hans-Georg Kräusslich⁸  Amalio Telenti⁹  Oliver T Keppler⁴  Angela Ciuffi⁶  Antonio Rausell⁵  Dan Ouchi³  Judith Dalmau³  Dolores Guerrero²  Maria Teresa Fernández-Figueras⁷  Elina Erikson⁸  Susana Benet³  Itziar Erkizia³  Maria Pino³ 

[1] Institució Catalana de Recerca i Estudis Avançats ICREA, Barcelona, Spain;Otorhinolaryngology Department, HUGTIP, Badalona, Spain;AIDS Research Institute IrsiCaixa, Institut d’Investigació en Ciències de la Salut Germans Trias i Pujol IGTP, Universitat Autònoma de Barcelona, Badalona, Spain;Institute of Medical Virology, National Reference Center for Retroviruses, University of Frankfurt, Frankfurt, Germany;Swiss Institute of Bioinformatics (SIB) - Vital-IT, Lausanne, Switzerland;Institute of Microbiology, University Hospital Center and University of Lausanne, Lausanne, Switzerland;Pathology Department, University Hospital Germans Trias i Pujol (HUGTIP), Badalona, Spain;Department of Infectious Diseases, Virology, Universitätsklinikum Heidelberg, Heidelberg, Germany;Current address: The J. Craig Venter Institute, La Jolla, CA, USA

关键词: Siglec-1;    Trans-infection;    HIV-1;    Dendritic cells;   

Others  :  1210150
DOI  :  10.1186/s12977-015-0160-x

 received in 2015-01-15, accepted in 2015-03-24,  发布年份 2015

【 摘 要 】

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.

【 授权许可】

   
2015 Pino et al.; licensee BioMed Central.

【 图 表 】

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