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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  -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.
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