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Prepublished online as a Blood First Edition Paper on January 16, 2003; DOI 10.1182/blood-2002-11-3353.

Submitted November 6, 2002
Accepted December 24, 2002
The heat shock protein receptor CD91 is upregulated in monocytes of HIV-1-infected "true" long-term non-progressors
Justin Stebbing*, Brian Gazzard, Louise Kim, Simon Portsmouth, Adrian Wildfire, Ian Teo, Mark Nelson, Mark Bower, Frances Gotch, Sunil Shaunak, Pramod Srivastava, and Steve Patterson
Division of Investigative Science, Department of Immunology, Chelsea and Westminster Hospital, London, United Kingdom
Division of Investigative Science, Department of Infectious Diseases, Hammersmith Hospital, London, United Kingdom
Center for Immunotherapy of Cancer and Infectious Diseases, University of Conneticut, Farmington, CT, USA
* Corresponding author; email: j.stebbing{at}ic.ac.uk.
A small proportion of human immunodeficiency virus type 1 (HIV-1) infected individuals remain asymptomatic for a long period post infection. It is thought that a vigorous immune response may contribute to long term non progression although studies are confounded by heterogeneity among patients. We studied the levels of HIV-1 receptors, co-stimulatory T cell molecules and dendritic cell (DC) numbers in 18 individuals with long term infection, a CD4 count > 400 cells/mm3 and an HIV-1 viral load < 50 copies/mL. These patients were further differentiated by the presence or absence of 2-LTR DNA circles, a possible marker for residual ongoing HIV-1 replication. A statistically significant increase in levels of CD91, the heat shock protein (HSP) receptor, was observed in therapy naive individuals who had no evidence of ongoing viral replication (p = 0.01). This difference was most notable on their monocytes. High levels of CD91 may be a host factor that contributes to maintenance of long term non progression. Its ability to internalise -defensins and cross present exogenous antigen to cytotoxic T lymphocytes via MHC class I may maintain CD8+ responses in these individuals.

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