减少胸腺输出是艾滋病毒感染者长期抗逆转录病毒治疗之后免疫功能重建失败的主要机制

2011-12-08 17:02 来源:丁香园 作者:北京协和医院传染病室
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Clin Infect Dis 2011 Nov;53(9):944-51. [IF:8.186]

Reduced thymic output is a major mechanism of immune reconstitution failure in HIV-infected patients after long-term antiretroviral therapy.


Li T , Wu N , Dai Y , Qiu Z , Han Y , Xie J , Zhu T , Li Y .

Department of Infectious Disease, Peking Union Medical College Hospital, and Chinese Academy of Medical Sciences, Beijing, China. litsh@263.net

北京协和医院传染病室,北京中国医学科学院

Abstract

Approximately 20% of human immunodeficiency virus type 1 (HIV-1)--infected adults do not normalize their CD4(+) T lymphocytes after long-term effective highly active antiretroviral therapy (HAART). The mechanistic basis for this failure is unclear. Seventy-four patients were followed up regularly for 3-7 years. Patients with undetectable plasma viral load (<50 copies/mL) for over 12 months were further classified into 2 groups: (1) immunological nonresponders, whose CD4(+) T-cell count was < 200/μL or <20% compared with baseline; and (2) immunological responders, whose CD4(+) T-cell count was > 300/μL or >30% compared with baseline. Compared with 17 immunological responders, 13 immunological nonresponders had a lower magnitude of naive CD4(+) T-cell increase, a lower percentage of recent thymic immigrants (CD31(+)%), and a higher percentage of activated CD8(+) T cells. Furthermore, unlike CD4(+) T cells, which increased along with the decrease of viral load, the percentage of recent thymic immigrants (CD31(+)%) had little change in the majority of patients. These data were fit into a mathematical model, , from which we deduced that the initial rate of CD4(+) T-cell restoration is associated significantly with the percentage of recent thymic immigrants (CD31(+)%). Our data indicate that the failure to restore CD4(+) T-cell count following HAART was associated primarily with a defect in recent thymic immigrants, which suggests the existence of thymus exhaustion.

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