Monocytes in HIV and SIV Infection and Aging: Implications for Inflamm-Aging and Accelerated Aging.
Monocytes in HIV and SIV Infection and Aging: Implications for Inflamm-Aging and Accelerated Aging.
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DOI：
10.3390/v14020409
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发表时间：
2022-02-17
期刊：
影响因子：
--
通讯作者：
Williams KC
中科院分区：
文献类型：
--
作者：
Wallis ZK;Williams KC
在抗逆转录病毒治疗（ART）时代之前，艾滋病毒感染者（PLWH）经历的艾滋病并发症比衰老更多。随着ART和PLWH寿命的延长，HIV合并症还包括衰老-最有可能是由于加速衰老-以及心血管、神经认知障碍、肺和肾脏疾病和恶性肿瘤。广泛的证据表明，艾滋病毒与抗逆转录病毒治疗与衰老加剧有关，年龄相关的合并症发生更早，部分原因是慢性免疫激活，合并感染，以及可能的抗逆转录病毒治疗的影响。正常情况下，免疫系统会随着年龄的增长而发生淋巴细胞和单核细胞群的变化，包括幼稚T淋巴细胞和B淋巴细胞数量减少，对记忆淋巴细胞的依赖，以及骨髓细胞的偏斜产生，导致年龄相关的炎症，称为“炎症老化”。具体而言，单核细胞和单核细胞亚群的绝对数量和相对比例随着年龄沿着骨髓线粒体功能障碍而偏斜，导致活性氧（ROS）的积累增加。此外，髓系活化的生物标志物（IL-6、sCD 14和sCD 163）随着慢性HIV感染和年龄的增长而增加，可能有助于免疫衰老。慢性HIV感染加速衰老;同时，ART治疗可能减缓与年龄相关的加速，但不足以阻止衰老或与年龄相关的合并症。总的来说，未来的治疗需要更好地了解艾滋病毒加速衰老背后的机制以及骨髓激活和周转的影响。
Before the antiretroviral therapy (ART) era, people living with HIV (PLWH) experienced complications due to AIDS more so than aging. With ART and the extended lifespan of PLWH, HIV comorbidities also include aging—most likely due to accelerated aging—as well as a cardiovascular, neurocognitive disorders, lung and kidney disease, and malignancies. The broad evidence suggests that HIV with ART is associated with accentuated aging, and that the age-related comorbidities occur earlier, due in part to chronic immune activation, co-infections, and possibly the effects of ART alone. Normally the immune system undergoes alterations of lymphocyte and monocyte populations with aging, that include diminished naïve T- and B-lymphocyte numbers, a reliance on memory lymphocytes, and a skewed production of myeloid cells leading to age-related inflammation, termed “inflamm-aging”. Specifically, absolute numbers and relative proportions of monocytes and monocyte subpopulations are skewed with age along with myeloid mitochondrial dysfunction, resulting in increased accumulation of reactive oxygen species (ROS). Additionally, an increase in biomarkers of myeloid activation (IL-6, sCD14, and sCD163) occurs with chronic HIV infection and with age, and may contribute to immunosenescence. Chronic HIV infection accelerates aging; meanwhile, ART treatment may slow age-related acceleration, but is not sufficient to stop aging or age-related comorbidities. Overall, a better understanding of the mechanisms behind accentuated aging with HIV and the effects of myeloid activation and turnover is needed for future therapies.
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影响因子：
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作者：
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通讯作者：
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发表时间：
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