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Prepublished online as a Blood First Edition Paper on June 28, 2002; DOI 10.1182/blood-2001-11-0080.
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Blood, 15 August 2002, Vol. 100, No. 4, pp. 1381-1387
IMMUNOBIOLOGY
Analysis of HIV-1- and CMV-specific memory CD4 T-cell
responses during primary and chronic infection
Alexandre Harari,
G. Paolo Rizzardi,
Kim Ellefsen,
Donatella Ciuffreda,
Patrick Champagne,
Pierre-Alexandre Bart,
Daniel Kaufmann,
Amalio Telenti,
Roland Sahli,
Giuseppe Tambussi,
Laurent Kaiser,
Adriano Lazzarin,
Luc Perrin, and
Giuseppe Pantaleo
From the Laboratory of AIDS Immunopathogenesis,
Divisions of Immunology and Allergy and Infectious Diseases, Department
of Medicine, and Institute of Microbiology, Centre Hospitalier
Universitaire Vaudois, University of Lausanne, Switzerland; the
Division of Infectious Diseases, San Raffaele Institute, Milan, Italy;
and the Laboratory of Virology, University of Geneva, Switzerland.
CD4 T-cell-specific memory antiviral responses to human
immunodeficiency virus type 1 (HIV-1) and cytomegalovirus (CMV) were investigated in 16 patients with documented primary HIV-1 infection (4 of the 16 subjects also had primary CMV infection) and compared with
those observed in patients with chronic HIV-1 and CMV coinfection. Virus-specific memory CD4 T cells were characterized on the basis of
the expression of the chemokine receptor CCR7. HIV-1- and CMV-specific interferon- -secreting CD4 T cells were detected in patients
with primary and chronic HIV-1 and CMV coinfection and were mostly contained in the cell population lacking expression of CCR7. The magnitude of the primary CMV-specific CD4 T-cell response was significantly greater than that of chronic CMV infection, whereas there
were no differences between primary and chronic HIV-1-specific CD4
T-cell responses. A substantial proportion of
CD4+CCR7 T cells were infected with HIV-1.
These results advance the characterization of antiviral memory
CD4 T-cell response and the delineation of the potential mechanisms
that likely prevent the generation of a robust CD4 T-cell immune
response during primary infection.

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