کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3425133 | 1227271 | 2010 | 7 صفحه PDF | دانلود رایگان |

A central, yet unresolved issue in the pathogenesis of HIV disease is the mechanism of antibody perturbation. In this study, HIV-specific memory B-cells were quantified in groups of infected subjects and compared with memory responses to other antigens and antibody titers. HIV-specific memory B-cell responses were vigorous in individuals with CD4+ T-cell counts > 350/μl and weak or undetectable in subjects with CD4+ T-cell numbers < 200/μl. Memory B-cell loss was permanent, because antiretroviral therapy failed to restore HIV-specific memory responses while influenza- and tetanus toxoid-specific memory B-cells remained unaffected or recovered. Antibody titers to Gag strongly correlated with memory B-cell frequencies. In contrast, Env-specific antibodies were maintained in advanced disease despite low or undetectable levels of memory B-cells. These results provide a potential mechanism by which destruction of HIV-specific CD4+ T-cells affects the humoral immune response against HIV and compromises the ability to maintain an effective antibody response.
Journal: Virology - Volume 397, Issue 1, 5 February 2010, Pages 7–13