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Volume 9 Supplement 2

AIDS Vaccine 2012

  • Poster presentation
  • Open Access

Frequent and strong antibody-mediated NK cell activation to HIV-1 Env in individuals with chronic HIV-1 infection

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  • 2,
  • 2,
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Retrovirology20129 (Suppl 2) :P171

https://doi.org/10.1186/1742-4690-9-S2-P171

  • Published:

Keywords

  • Natural Killer Cell
  • Natural Killer Cell Activation
  • Peptide Pool
  • Uninfected Individual
  • High CD57 Expression

Background

Natural killer (NK) cells are critical in viral control and NK cells that respond to HIV-1 peptides have been described. However, it is unclear how NK cells recognize HIV-1 antigen. We investigated NK cell responses to HIV-1 peptides during early and chronic HIV-1 clade B infection.

Methods

NK cells responding to HIV-1 peptides were assessed by multiparameter flow cytometry using whole blood from 74 individuals with treated or untreated early or chronic HIV-1 infection. In addition, 15 HIV uninfected individuals were also studied.

Results

No NK cell responses to HIV-1 peptides were detected in HIV-1 uninfected individuals. The HIV-1 NK cell specific responses to peptide were less frequent during the first year of infection but were of high magnitude and frequent in individuals with controlled or progressive infection (22% vs 79%; P<0.00001). The activation of NK cells to peptide pools required the presence of plasma IgG and the responding NK cells had a low CD16 expression and high CD57 expression. Furthermore, plasma derived from HIV-1 infected individuals was sufficient to trigger a response to HIV-1 Env peptide pool by NK cells from healthy donors suggesting the role of antibodies in mediating this activity.

Conclusion

NK cell responses to specific antigens can be induced in HIV-1 infection. Large cohorts are needed to assess the consequences of these NK cells against HIV-1 control or protection from infection.

Authors’ Affiliations

(1)
University of KwaZulu-Natal, Durban, South Africa
(2)
Ragon Institute of MIT, MGH and Harvard, Boston, MA, USA
(3)
Cancer and Inflammation Program, Laboratory of Experimental Immunology, Frederick, MD, USA

Copyright

© Thobakgale et al; licensee BioMed Central Ltd. 2012

This article is published under license to 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.

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