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This article is part of the supplement: Frontiers of Retrovirology 2011

Open Access Oral presentation

Variant cell types and host glycoproteins influencing HIV-1 infection

William A Paxton

  • Correspondence: William A Paxton

Author Affiliations

University of Amsterdam, the Netherlands

Retrovirology 2011, 8(Suppl 2):O28  doi:10.1186/1742-4690-8-S2-O28


The electronic version of this article is the complete one and can be found online at: http://www.retrovirology.com/content/8/S2/O28


Published:3 October 2011

© 2011 Paxton; licensee BioMed Central Ltd.

This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Oral presentation

A number of variant cell types are associated with HIV-1 transmission and disease progression, including dendritic cells (DCs), macrophages and CD4 lymphocytes. The cell types and their phenotypes associated with infection are still poorly defined and will greatly influence HIV-1 transmission as well as disease progression. The types of immune responses mounted against infectious pathogens will also influence the pool of cells to be infected and thereby influence disease course. We have described CD4 lymphocyte cellular phenotypes induced within the same HIV-1 infected individuals against variant pathogens (namely CMV and TB antigens) and shown that these responses are highly variable. We further demonstrate that their distinctive cytokine and chemokine expression patterns correlate to their HIV-1 infectivity profile both in vitro and in vivo. We have additionally addressed whether viruses produced from variant cellular populations have similar or distinctive phenotypes. Here we show that viruses produced from macrophages opposed to Th1 or Th2 CD4 lymphocytes vary for their interaction with DC-SIGN expressed on DCs and have variant neutralization profiles for 2G12. Furthermore, we have identified a number of host glycopoteins (BSSL and MUC6) that can inhibit HIV-1 from interacting with DCs through binding DC-SIGN. We show that genetic polymorphisms within the BSSL gene can associate with strength of binding to DC-SIGN and that these variants can also be associated with markers of disease progression as well as time to coreceptor switch. In conclusion, the interactions between the adaptive and innate immune response can influence HIV-1 transmission and modulate disease course.