Analysis of HIV-1– and CMV-specific memory CD4 T-cell responses during primary and chronic infection

• Published in: Blood 2002-08, Vol.100 (4), p.1381-1387
• Main Authors: Harari, Alexandre, Rizzardi, G. Paolo, Ellefsen, Kim, Ciuffreda, Donatella, Champagne, Patrick, Bart, Pierre-Alexandre, Kaufmann, Daniel, Telenti, Amalio, Sahli, Roland, Tambussi, Giuseppe, Kaiser, Laurent, Lazzarin, Adriano, Perrin, Luc, Pantaleo, Giuseppe
• Format: Article
• Language: English
• Subjects: Acquired Immunodeficiency Syndrome - complications; Acquired Immunodeficiency Syndrome - immunology; Adult; Antibodies, Viral - blood; CD4-Positive T-Lymphocytes - immunology; Chronic Disease; Cytomegalovirus - immunology; Cytomegalovirus Infections - complications; Cytomegalovirus Infections - immunology; Female; HIV-1 - immunology; Humans; Immunologic Memory; Male; Phenotype; Receptors, CCR7; Receptors, Chemokine - analysis; Viral Load; Viremia
• ISSN: 0006-4971; 1528-0020
• DOI: 10.1182/blood-2001-11-0080

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-γ–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.