猿猴免疫缺陷病毒感染会导致肠道中央记忆T细胞严重缺失，这会损害抗逆转录病毒治疗期间CD4+T细胞的恢复。
Simian immunodeficiency virus infection induces severe loss of intestinal central memory T cells which impairs CD4+ T-cell restoration during antiretroviral therapy.
作者信息
Verhoeven D, Sankaran S, Dandekar S
机构信息
Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, CA 95616, USA.
出版信息
J Med Primatol. 2007 Aug;36(4-5):219-27. doi: 10.1111/j.1600-0684.2007.00239.x.
BACKGROUND
Simian immunodeficiency virus (SIV) infection leads to severe loss of intestinal CD4(+) T cells and, as compared to peripheral blood, restoration of these cells is slow during antiretroviral therapy (ART). Mechanisms for this delay have not been examined in context of which specific CD4(+) memory subsets or lost and fail to regenerate during ART.
METHODS
Fifteen rhesus macaques were infected with SIV, five of which received ART (FTC/PMPA) for 30 weeks. Viral loads were measured by real-time PCR. Flow cytometric analysis determined changes in T-cell subsets and their proliferative state.
RESULTS
Changes in proliferative CD4(+) memory subsets during infection accelerated their depletion. This reduced the central memory CD4(+) T-cell pool and contributed to slow CD4(+) T-cell restoration during ART.
CONCLUSION
There was a lack of restoration of the CD4(+) central memory and effector memory T-cell subsets in gut-associated lymphoid tissue during ART, which may contribute to the altered intestinal T-cell homeostasis in SIV infection.
背景
猿猴免疫缺陷病毒（SIV）感染导致肠道CD4(+) T细胞严重损失，与外周血相比，在抗逆转录病毒治疗（ART）期间这些细胞的恢复缓慢。在ART期间，尚未在特定CD4(+)记忆亚群丢失且无法再生的背景下研究这种延迟的机制。
方法
15只恒河猴感染SIV，其中5只接受ART（FTC/PMPA）治疗30周。通过实时PCR测量病毒载量。流式细胞术分析确定T细胞亚群及其增殖状态的变化。
结果
感染期间增殖性CD4(+)记忆亚群的变化加速了它们的耗竭。这减少了中枢记忆CD4(+) T细胞库，并导致ART期间CD4(+) T细胞恢复缓慢。
结论
在ART期间，肠道相关淋巴组织中CD4(+)中枢记忆和效应记忆T细胞亚群缺乏恢复，这可能导致SIV感染中肠道T细胞稳态改变。
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