由于长期抗逆转录病毒疗法(ART)而达到无法检测到的病毒载量和改善的CD4T细胞计数的HIV感染(HIV)老年成年个体可能会继续经历炎症和免疫衰老。因此,我们评估了173名年龄在22~81岁之间的HIV+老年成人个体的血浆促炎和抗炎细胞因子水平,这些个体接受长期ART治疗,病毒载量大多<20HIVRNA拷贝/mL,并与92名未感染HIV(HIV-或健康对照)老年个体进行了比较.我们发现TNF-α的中位数水平,IFN-γ,IL-1β,与健康对照相比,IL-6和IL-10在HIV+个体中更高(p<0.001至<0.0001),IL-17倾向于更低。HIV+队列中CD4T细胞计数的增加并没有显著改变循环细胞因子水平,虽然IL-1β水平升高。然而,在健康对照中,IL-17水平随着CD4计数的增加而显著降低,但在HIV+队列中没有改变。值得注意的是,在CD4计数低于500的健康对照组中,循环IL-17水平显著降低,但一旦高于500,则CD4,IL-17水平与HIV+队列相当.随着CD8T细胞计数的增加,这些细胞因子的水平没有显著改变,虽然TNF-α的水平,IFN-γ,IL-6下降了,而IL-1β和IL-17略有升高。此外,尽管TNF-α略有增加,但HIV+队列的年龄增加并未显着影响细胞因子水平,观察到IL-6、IL-10和IL-17。同样,这些细胞因子并没有随着检测不到的病毒载量水平的增加而显著调节,而一些HIV+个体的TNF-α水平较高,IFN-γ,和IL-1β。总之,我们的研究结果表明,与健康对照相比,由于长期ART而无法检测到病毒载量和恢复的CD4T细胞计数的HIV+衰老成人个体仍然产生更高水平的促炎和抗炎细胞因子,提示一定程度的炎症.
HIV-infected (HIV+) aging adult individuals who have achieved undetectable viral load and improved CD4 T cell counts due to long-term antiretroviral therapy (ART) may continue to experience inflammation and immunosenescence. Therefore, we evaluated the plasma levels of proinflammatory and anti-inflammatory cytokines in 173 HIV+ aging adult individuals with age ranging from 22 to 81 years on long-term ART with viral load mostly <20 HIV RNA copies/mL and compared with 92 HIV-uninfected (HIV- or healthy controls) aging individuals. We found that the median levels of TNF-α, IFN-γ, IL-1β, IL-6, and IL-10 were higher (p < 0.001 to <0.0001) and IL-17 trended lower in HIV+ individuals than healthy controls. Increasing CD4 T cell counts in the HIV+ cohort did not significantly change the circulating cytokine levels, although levels of IL-1β increased. However, IL-17 levels significantly decreased with increasing CD4 counts in the healthy controls and yet unchanged in the HIV+ cohort. Of note, the levels of circulating IL-17 were significantly reduced comparatively in the healthy controls where the CD4 count was below 500, yet once above 500 the levels of CD4, IL-17 levels were comparable with the HIV+ cohort. With increasing CD8 T cell counts, the levels of these cytokines were not significantly altered, although levels of TNF-α, IFN-γ, and IL-6 declined, whereas IL-1β and IL-17 were slightly elevated. Furthermore, increasing age of the HIV+ cohort did not significantly impact the cytokine levels although a slight increase in TNF-α, IL-6, IL-10, and IL-17 was observed. Similarly, these cytokines were not significantly modulated with increasing levels of undetectable viral loads, whereas some of the HIV+ individuals had higher levels of TNF-α, IFN-γ, and IL-1β. In summary, our findings show that HIV+ aging adult individuals with undetectable viral load and restored CD4 T cell counts due to long-term ART still produce higher levels of both proinflammatory and anti-inflammatory cytokines compared with healthy controls, suggesting some level of inflammation.