Early immune senescence in HIV disease.
Early immune senescence in HIV disease.
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DOI：
10.1007/s11904-009-0038-4
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发表时间：
2010-02
影响因子：
4.6
通讯作者：
Landay, Alan
中科院分区：
文献类型：
--
作者：
Desai, Seema;Landay, Alan
尽管使用抗逆转录病毒治疗进行病毒抑制和免疫重建，但非艾滋病定义的合并症描述了艾滋病毒感染者的早期衰老过程。在衰老过程中，T细胞更新的减少，以及终末分化的T细胞的逐渐丰富，转化为免疫系统的普遍下降，逐渐导致免疫衰老。炎症是年龄相关性合并症的标志，免疫激活是艾滋病毒疾病的标志。艾滋病毒或混合感染对免疫系统的持续刺激会激活先天免疫系统和获得性免疫系统，导致炎症介质的释放。免疫激活加上缺乏抗炎反应可能会导致艾滋病毒疾病加速衰老。胸腺输出功能障碍，以及艾滋病毒介导的胃肠道屏障破坏导致微生物易位，导致循环抗原负荷，推动艾滋病毒疾病的早期衰老。
Non-AIDS–defining comorbidities that occur despite viral suppression and immune reconstitution using antiretroviral therapy depict early aging process in HIV-infected individuals. During aging, a reduction in T-cell renewal, together with a progressive enrichment of terminally differentiated T cells, translates into a general decline of the immune system, gradually leading to immunosenescence. Inflammation is a hallmark of age-associated comorbidities, and immune activation is a hallmark of HIV disease. Constant stimulation of the immune system by HIV or due to co-infections activates the innate and adaptive immune system, resulting in release of mediators of inflammation. Immune activation coupled with lack of anti-inflammatory responses likely results in accelerated aging in HIV disease. Dysfunctional thymic output, along with HIV-mediated disruption of the gastrointestinal barrier leading to microbial translocation, contributes to the circulating antigenic load driving early senescence in HIV disease.