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

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Blood, 15 May 2003, Vol. 101, No. 10, pp. 4000-4004

IMMUNOBIOLOGY

The heat-shock protein receptor CD91 is up-regulated in monocytes of HIV-1-infected "true" long-term nonprogressors

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

From the Department of Immunology, Division of Investigative Science, Faculty of Medicine, Imperial College of Science, Technology and Medicine, The Chelsea and Westminster Hospital, London; the Department of Infectious Diseases, Division of Investigative Science, Faculty of Medicine, Imperial College at Hammersmith Hospital, London, United Kingdom; and the Center for Immunotherapy of Cancer and Infectious Diseases, University of Connecticut School of Medicine, Farmington.

A small proportion of patients with human immunodeficiency virus type 1 (HIV-1) remains asymptomatic for a long period after infection. It is thought that a vigorous immune response may contribute to long-term nonprogression, though studies are confounded by heterogeneity among patients. We studied the levels of HIV-1 receptors, costimulatory T-cell molecules, and dendritic cell (DC) numbers in 18 patients with long-term infection, CD4 counts greater than 400 cells/mm3, and HIV-1 viral loads lower than 50 copies/mL. These patients were further differentiated through 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 patients who had no evidence of ongoing viral replication (P = .01). This difference was most notable on their monocytes. High levels of CD91 may be a host factor that contributes to the maintenance of long-term nonprogression. The ability of CD91 to internalize alpha -defensins and to cross-present exogenous antigen to cytotoxic T lymphocytes through major histocompatibility complex (MHC) class 1 may maintain CD8+ responses in these patients.

© 2003 by The American Society of Hematology.
 

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