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慢性免疫激活在 HCV/HIV-1 共感染患者的 T 细胞区室中。

Chronic immune activation in the T cell compartment of HCV/HIV-1 co-infected patients.

机构信息

Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.

出版信息

Virulence. 2010 May-Jun;1(3):177-9. doi: 10.4161/viru.1.3.11206.

Abstract

Activation of innate and adaptive immune mechanisms in response to infection is necessary to control and clear infections. However, chronic immune activation in human immunodeficiency virus 1 (HIV-1) infection has a series of detrimental effects and is a major driving force in HIV-1 disease progression. We recently found that patients with chronic hepatitis C virus (HCV)/HIV-1 co-infection display sharply elevated immune activation as determined by expression of CD38 in T cells. High immune activation was observed despite that these patients were on effective antiretroviral therapy (ART), which usually brings down activation levels in HIV-infected people. HCV treatment with pegylated interferon-α (IFNα) and ribavirin reduced activation, and this was at first glance unexpected as IFNα is believed to be involved in driving activation. Here, we briefly summarize these findings and discuss them in context of the emerging roles of the gut barrier and the liver in chronic immune activation and viral disease progression.

摘要

针对感染,固有免疫和适应性免疫机制的激活对于控制和清除感染是必需的。然而,人类免疫缺陷病毒 1(HIV-1)感染中的慢性免疫激活具有一系列有害影响,是 HIV-1 疾病进展的主要驱动力。我们最近发现,慢性丙型肝炎病毒(HCV)/HIV-1 合并感染的患者表现出明显升高的免疫激活,这是通过 T 细胞中 CD38 的表达来确定的。尽管这些患者正在接受有效的抗逆转录病毒治疗(ART),通常会降低 HIV 感染者的激活水平,但仍观察到高免疫激活。聚乙二醇干扰素-α(IFNα)和利巴韦林治疗 HCV 可降低激活水平,这起初是出乎意料的,因为 IFNα 被认为参与驱动激活。在这里,我们简要总结了这些发现,并结合肠道屏障和肝脏在慢性免疫激活和病毒疾病进展中的新作用对其进行了讨论。

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