Department of Infectious Diseases, L'Archet Hospital, University of Nice, France.
J Neurovirol. 2013 Aug;19(4):376-82. doi: 10.1007/s13365-013-0181-y. Epub 2013 Jul 12.
Contributory factors to HIV-associated neurocognitive disorders (HAND) have been shown to include age, co-morbid infections, medication toxicity, virological, genetic and vascular mechanisms, as well as microbial translocation of lipopolysaccharide (LPS), which is suspected to trigger monocyte activation and increase trafficking of infected cells into the brain. In this study, our aim was to assess the degree of neurocognitive impairment in a group of randomly selected HIV-infected patients and investigate potential risk factors, including LPS plasma levels. Furthermore, we evaluated the relevance of LPS as a potential marker for screening patients with mild neurocognitive impairment. LPS plasma levels were compared among patients with HAND and those with no HAND. As LPS has also been shown to be elevated in hepatitis C co-infection, the analysis was stratified according to the presence or not of hepatitis C virus (HCV) co-infection. Differences between groups were evaluated using chi-square tests and Kruskal-Wallis non-parametric tests. Stepwise logistic regression was performed to identify independent risk factors for HAND in the subgroups of HCV-positive and negative patients. A p value <0.05 was considered significant. Analyses were conducted using SPSS® software. From December 2007 to July 2009, 179 patients were tested (mean age 44, 73 % male, 87 % on treatment, 30 % HCV co-infected, median CD4 504/ml and 67 % with viral load below 40 copies/ml). HAND was identified in 40/179 patients (22 %), the majority displaying asymptomatic neurocognitive impairment or mild neurocognitive disorder. Univariate analysis showed that age, illicit drug use, hepatitis C co-infection, prior AIDS-defining events, CD4/CD8 ratio and LPS plasma levels were significantly associated with HAND. The median LPS level was 98.2 pg/ml in the non-HAND group versus 116.1 pg/ml in the HAND group (p < 0.014). No differences were found in LPS values between subgroups of impairment. There was a clear association between LPS levels and HAND in the HCV-positive group (p = 0.036), while there was none in the HCV-negative group (p = 0.502). No difference in degree of hepatic fibrosis was found between the HAND and non-HAND groups. In conclusion, LPS levels were associated with HAND in the HCV-positive group, while, in the HCV-negative group, age and pro-viral DNA were the only variables independently associated with HAND. There was no difference in degree of liver disease as predicted by score of fibrosis between HAND and non-HAND groups. The role of HCV co-infection and higher LPS levels in the pathogenesis of HAND in patients with viral suppression on treatment requires further investigation.
与 HIV 相关的神经认知障碍(HAND)的促成因素已被证明包括年龄、合并感染、药物毒性、病毒学、遗传和血管机制,以及脂多糖(LPS)的微生物易位,这被怀疑会触发单核细胞激活并增加感染细胞向大脑的迁移。在这项研究中,我们的目的是评估一组随机选择的 HIV 感染患者的神经认知障碍程度,并调查潜在的危险因素,包括 LPS 血浆水平。此外,我们评估了 LPS 作为筛选轻度神经认知障碍患者的潜在标志物的相关性。比较了 HAND 患者和无 HAND 患者的 LPS 血浆水平。由于 LPS 也被证明在丙型肝炎合并感染中升高,因此根据是否存在丙型肝炎病毒(HCV)合并感染对分析进行了分层。使用卡方检验和 Kruskal-Wallis 非参数检验评估组间差异。使用逐步逻辑回归识别 HCV 阳性和阴性患者亚组中 HAND 的独立危险因素。p 值<0.05 被认为具有统计学意义。使用 SPSS®软件进行分析。从 2007 年 12 月至 2009 年 7 月,共检测了 179 名患者(平均年龄 44 岁,73%为男性,87%接受治疗,30%合并丙型肝炎感染,中位 CD4 504/ml,67%病毒载量低于 40 拷贝/ml)。在 179 名患者中发现 40 名(22%)患有 HAND,大多数表现为无症状性神经认知障碍或轻度神经认知障碍。单因素分析显示,年龄、非法药物使用、丙型肝炎合并感染、既往艾滋病定义事件、CD4/CD8 比值和 LPS 血浆水平与 HAND 显著相关。非 HAND 组的 LPS 中位数为 98.2 pg/ml,HAND 组为 116.1 pg/ml(p<0.014)。在损伤亚组中,LPS 值没有差异。在 HCV 阳性组中,LPS 水平与 HAND 之间存在明显关联(p=0.036),而在 HCV 阴性组中则没有(p=0.502)。HAND 组和非 HAND 组之间的肝纤维化程度无差异。结论:LPS 水平与 HCV 阳性组的 HAND 相关,而在 HCV 阴性组中,年龄和前病毒 DNA 是唯一与 HAND 独立相关的变量。HAND 组和非 HAND 组的纤维化评分预测的肝脏疾病程度无差异。在接受治疗且病毒抑制的患者中,HCV 合并感染和 LPS 水平升高在 HAND 发病机制中的作用需要进一步研究。