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
Laboratory of AIDS Immunopathogenesis, Division of Immunology and Allergy, Department of Medicine, Centre Hospitalier Universitaire Vaudois, University of Lausanne, Switzerland.
Blood. 2002 Aug 15;100(4):1381-7. 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-gamma-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.
在16例有记录的原发性人类免疫缺陷病毒1型（HIV-1）感染患者（16名受试者中有4名也有原发性巨细胞病毒（CMV）感染）中，研究了CD4 T细胞对HIV-1和CMV的特异性记忆抗病毒反应，并与慢性HIV-1和CMV合并感染患者中观察到的反应进行比较。基于趋化因子受体CCR7的表达对病毒特异性记忆CD4 T细胞进行了表征。在原发性和慢性HIV-1和CMV合并感染患者中均检测到HIV-1和CMV特异性分泌干扰素-γ的CD4 T细胞，且大多存在于缺乏CCR7表达的细胞群体中。原发性CMV特异性CD4 T细胞反应的强度显著大于慢性CMV感染，而原发性和慢性HIV-1特异性CD4 T细胞反应之间没有差异。相当一部分CD4(+)CCR7(-) T细胞感染了HIV-1。这些结果推进了对抗病毒记忆CD4 T细胞反应的表征以及对可能在原发性感染期间阻止强大的CD4 T细胞免疫反应产生的潜在机制的描述。
