Ho Emily L, Maxwell Clare L, Dunaway Shelia B, Sahi Sharon K, Tantalo Lauren C, Lukehart Sheila A, Marra Christina M
Department of Neurology, Swedish Neuroscience Institute, Seattle.
Neurology.
Clin Infect Dis. 2017 Sep 15;65(6):943-948. doi: 10.1093/cid/cix473.
Individuals infected with human immunodeficiency virus (HIV) who have previously had syphilis may have cognitive impairment. We tested the hypothesis that neurosyphilis causes cognitive impairment in HIV by amplifying HIV-related central nervous system (CNS) inflammation.
HIV-infected participants enrolled in a study of cerebrospinal fluid (CSF) abnormalities in syphilis underwent the mental alternation test (MAT), venipuncture, and lumbar puncture. CSF concentrations of chemokine (C-X-C motif) ligand 10 (CXCL10), chemokine (C-C motif) ligand 2 (CCL2), and neurofilament light (NFL) were determined by commercial assays. The proportion of peripheral blood mononuclear cells (PBMCs) and of CSF white blood cells (WBCs) that were activated monocytes (CD14+CD16+) was determined by flow cytometry. Neurosyphilis was defined as detection of Treponema pallidum 16S RNA in CSF or CSF white blood cells (WBCs) >20/uL or a reactive CSF-Venereal Disease Research Laboratory (VDRL) test; uncomplicated syphilis was defined as undetectable CSF T. pallidum, CSF WBCs ≤5/uL and nonreactive CSF-VDRL. MAT <18 was considered low.
Median proportion of PBMCs that were activated monocytes (16.6 vs. 5.3), and median CSF CXCL10 (10658 vs. 2530 units), CCL2 (519 vs. 337 units) and HIV RNA (727 vs. 50 c/mL) were higher in neurosyphilis than in uncomplicated syphilis (P ≤ .001 for all comparisons). Neurosyphilis was not related to low MAT scores. Participants with low MAT scores had higher median CSF CXCL10 (10299 vs. 3650 units, P = .008) and CCL2 (519 vs. 365 units, P = .04) concentrations than those with high MAT scores.
Neurosyphilis may augment HIV-associated CNS inflammation, but it does not explain cognitive impairment in HIV-infected individuals with syphilis.
既往感染梅毒的人类免疫缺陷病毒(HIV)感染者可能存在认知障碍。我们通过放大与HIV相关的中枢神经系统(CNS)炎症来检验神经梅毒导致HIV感染者认知障碍这一假说。
参与梅毒脑脊液(CSF)异常研究的HIV感染者接受了精神交替试验(MAT)、静脉穿刺和腰椎穿刺。通过商业检测法测定CSF中趋化因子(C-X-C基序)配体10(CXCL10)、趋化因子(C-C基序)配体2(CCL2)和神经丝轻链(NFL)的浓度。通过流式细胞术测定外周血单核细胞(PBMC)和CSF白细胞(WBC)中被激活的单核细胞(CD14+CD16+)的比例。神经梅毒定义为在CSF中检测到梅毒螺旋体16S RNA或CSF白细胞(WBC)>20/μL或CSF性病研究实验室(VDRL)试验呈反应性;单纯性梅毒定义为CSF中未检测到梅毒螺旋体、CSF白细胞≤5/μL且CSF-VDRL无反应。MAT<18被认为较低。
神经梅毒患者中被激活的单核细胞在PBMC中的中位比例(16.6对5.3)以及CSF中CXCL10(10658对2530单位)、CCL2(519对337单位)和HIV RNA(727对50拷贝/mL)的中位浓度均高于单纯性梅毒患者(所有比较P≤0.001)。神经梅毒与MAT低评分无关。MAT低评分的参与者CSF中CXCL10(10299对3650单位,P = 0.008)和CCL2(519对365单位,P = 0.04)的中位浓度高于MAT高评分的参与者。
神经梅毒可能会加剧与HIV相关的CNS炎症,但它并不能解释合并梅毒的HIV感染者的认知障碍。