Elevated sCD163 in plasma but not cerebrospinal fluid is a marker of neurocognitive impairment in HIV infection.
Elevated sCD163 in plasma but not cerebrospinal fluid is a marker of neurocognitive impairment in HIV infection.
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DOI：
10.1097/qad.0b013e32836010bd
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发表时间：
2013-06-01
期刊：
影响因子：
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通讯作者：
Williams KC
中科院分区：
文献类型：
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作者：
Burdo TH;Weiffenbach A;Woods SP;Letendre S;Ellis RJ;Williams KC
在这里，我们评估了接受有效抗逆转录病毒治疗 (ART) 的 HIV 感染者的神经认知障碍是否与持续单核细胞激活有关，以单核细胞/巨噬细胞脱落的可溶性 CD163 (sCD163) 水平为指标。长期以来，HIV 感染者在连续两次就诊时接受检查，中位值[四分位距 (IQR)] 相隔 16 (7-32) 个月。所有患者均接受 ART 治疗，并在每次就诊时均得到持久的病毒学抑制（血浆 HIV RNA <50 拷贝/ml）。 34 名年龄匹配的 HIV 血清阴性患者被用作对照。根据标准方法，基于综合神经心理学评估计算总体赤字评分（GDS）。根据已发布的 HIV 相关神经认知障碍 (HAND) 指南，使用神经心理学和医学数据来分配神经认知状态，如下：神经心理学正常 (NP-nml)、无症状神经心理障碍 (ANI) 和轻微神经认知障碍 (MND)。使用ELISA测定血浆和脑脊液中的sCD163。 GDS 受损患者的血浆 sCD163 水平高于未受损患者[中位 (IQR) 1401 ng/ml (1057–2258) vs 955 ng/ml (586–1313)；威尔科克森 P = 0.028]。 MND 患者 (N = 6) 的血浆 sCD163 显着高于 ANI (P = 0.04) 或 NP-nml (P = 0.02)。尽管首次就诊后 GDS 稳定未受损的患者血浆 sCD163 水平下降（P < 0.032），但 GDS 仍受损的患者血浆 sCD163 水平仍然升高（P = 0.50）。这些发现与神经生理学受损的 HIV 感染者中单核细胞/巨噬细胞持续激活一致，尽管进行了病毒抑制性 ART。总体而言，这些观察结果强调了 HIV 中单核细胞/巨噬细胞免疫反应的重要性、HAND 中持续单核细胞激活以及 sCD163 作为神经认知障碍血浆标志物的价值。
Here we evaluated whether neurocognitive disorders in HIV-infected individuals on effective antiretroviral therapy (ART) are associated with persistent monocyte activation as indexed by levels of soluble CD163 (sCD163), shed by monocyte/macrophages. Chronically, HIV-infected individuals were examined at two consecutive visits median [interquartile range (IQR)] 16 (7–32) months apart. All patients were on ART and durably virologically suppressed (plasma HIV RNA <50 copies/ml) at all visits. Thirty-four age-matched HIV-seronegative patients were used as controls. A global deficit score (GDS) was calculated based on comprehensive neuropsychological assessment according to standard methods. Neuropsychological and medical data were used to assign neurocognitive status according to published guidelines for HIV-associated neurocognitive disorders (HAND) as follows: neuropsychologically normal (NP-nml), asymptomatic neuropsychological impairment (ANI) and minor neurocognitive disorder (MND). sCD163 in plasma and cerebrospinal fluid was measured using ELISA. GDS-impaired patients had higher plasma sCD163 than those who were not impaired [median (IQR) 1401 ng/ml (1057–2258) versus 955 ng/ml (586–1313); Wilcoxon P = 0.028]. Patients with MND (N = 6) had significantly higher plasma sCD163 than ANI (P = 0.04) or NP-nml (P = 0.02). Whereas plasma sCD163 levels dropped in patients who were stably GDS-unimpaired after the first visit (P < 0.032), levels remained elevated in those who remained GDS-impaired (P = 0.50). These findings are consistent with persistent monocyte/macrophage activation in neurophysiologically impaired HIV-infected individuals despite virally suppressive ART. Overall, these observations underscore the significance of monocyte/macrophage immune responses in HIV, persistent monocyte activation in HAND and the value of sCD163, as a plasma marker of neurocognitive impairment.