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From Wasting to Obesity: The Contribution of Nutritional Status to Immune Activation in HIV Infection

机译:从浪费到肥胖:营养状况对HIV感染免疫激活的贡献

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摘要

The impact of human immunodeficiency virus (HIV) infection on innate and adaptive immune activation occurs in the context of host factors, which serve to augment or dampen the physiologic response to the virus. Independent of HIV infection, nutritional status, particularly body composition, affects innate immune activation through a variety of conditions, including reduced mucosal barrier defenses and microbiome dysbiosis in malnutrition and the proinflammatory contribution of adipocytes and stromal vascular cells in obesity. Similarly, T-cell activation, proliferation, and cytokine expression are reduced in the setting of malnutrition and increased in obesity, potentially due to adipokine regulatory mechanisms restraining energy-avid adaptive immunity in times of starvation and exerting a paradoxical effect in overnutrition. The response to HIV infection is situated within these complex interactions between host nutritional health and immunologic function, which contribute to the varied phenotypes of immune activation among HIV-infected patients across a spectrum from malnutrition to obesity.
机译:人类免疫缺陷病毒(HIV)感染对先天性和适应性免疫激活的影响发生在宿主因子的背景下,宿主因子可增强或减弱对该病毒的生理反应。营养状况(尤其是身体成分)不受HIV感染的影响,会通过多种状况影响先天免疫激活,包括营养不良中的粘膜屏障防御作用和微生物组营养不良以及肥胖中脂肪细胞和基质血管细胞的促炎作用。同样,在营养不良的情况下,T细胞的活化,增殖和细胞因子的表达减少,肥胖症的发生也可能增加,这可能是由于在饥饿时限制脂肪能量适应性免疫的脂肪因子调节机制,在营养过剩中发挥了矛盾的作用。对HIV感染的反应位于宿主营养健康与免疫功能之间的这些复杂相互作用中,这些相互作用导致从营养不良到肥胖的整个HIV感染患者的免疫激活表型各异。

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