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内脏利什曼病与HIV-1合并感染患者血清细胞因子的动态变化

Dynamics of serum cytokines in patients with visceral leishmaniasis and HIV-1 co-infection.

作者信息

Medrano F J, Rey C, Leal M, Cañavate C, Rubio A, Sánchez-Quijano A, Alvar J, Lissen E

机构信息

Viral Hepatitis & AIDS Study Group, Department of Internal Medicine, Hospital Universitario Virgen del Rocío, Seville, Spain.

出版信息

Clin Exp Immunol. 1998 Dec;114(3):403-7. doi: 10.1046/j.1365-2249.1998.00733.x.

Abstract

Serum cytokine levels and peripheral T cell subpopulations of HIV-1-infected patients before, during and after active visceral leishmaniasis (VL) were analysed and compared with appropriate controls. At VL diagnosis, co-infected patients showed higher serum levels of interferon-gamma (IFN-gamma) than matched HIV-1 controls without VL, and lower serum concentrations of IL-10 than non-immunocompromised VL controls. High levels of tumour necrosis factor-alpha (TNF-alpha) and IFN-gamma were present in the sera of HIV-1-infected patients with active VL. TNF-alpha remained elevated after VL recovery. A steady decline in the CD4+ cell count, an increase of serum HIV viraemia and a progressive seroconversion for the HIV-1 p24 antigen was observed during the course of VL disease. Thus, an aberrant activation of the TNF system with possible negative immunological and virological consequences is present in HIV-1-infected patients with VL. A more extensive prospective validation of these findings in a bigger cohort of patients will nevertheless be necessary. The results support the hypothesis that different opportunistic infection agents may trigger the production of proinflammatory cytokines during immunodeficiency, and in this way accelerate the course of HIV-1 disease.

摘要

对HIV-1感染患者在活动性内脏利什曼病(VL)之前、期间和之后的血清细胞因子水平及外周血T细胞亚群进行了分析,并与适当的对照组进行比较。在VL诊断时,合并感染的患者血清干扰素-γ(IFN-γ)水平高于未感染VL的匹配HIV-1对照,血清IL-10浓度低于非免疫受损的VL对照。活动性VL的HIV-1感染患者血清中存在高水平的肿瘤坏死因子-α(TNF-α)和IFN-γ。VL恢复后TNF-α仍保持升高。在VL病程中观察到CD4+细胞计数稳步下降、血清HIV病毒血症增加以及HIV-1 p24抗原逐步血清学转换。因此,VL的HIV-1感染患者存在TNF系统的异常激活,可能产生负面的免疫学和病毒学后果。然而,仍需要在更大的患者队列中对这些发现进行更广泛的前瞻性验证。结果支持这样的假设,即不同的机会性感染病原体可能在免疫缺陷期间触发促炎细胞因子的产生,并以此加速HIV-1疾病的进程。

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