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丙型肝炎病毒与1型人类免疫缺陷病毒合并感染且接受高效抗逆转录病毒治疗的患者,其T细胞区室中高水平的慢性免疫激活可通过α干扰素和利巴韦林治疗得到逆转。

High levels of chronic immune activation in the T-cell compartments of patients coinfected with hepatitis C virus and human immunodeficiency virus type 1 and on highly active antiretroviral therapy are reverted by alpha interferon and ribavirin treatment.

作者信息

Gonzalez Veronica D, Falconer Karolin, Blom Kim G, Reichard Olle, Mørn Birgitte, Laursen Alex Lund, Weis Nina, Alaeus Annette, Sandberg Johan K

机构信息

Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, 14186 Stockholm, Sweden.

出版信息

J Virol. 2009 Nov;83(21):11407-11. doi: 10.1128/JVI.01211-09. Epub 2009 Aug 26.

DOI:10.1128/JVI.01211-09
PMID:19710147
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2772767/
Abstract

Chronic immune activation is a driver of human immunodeficiency virus type 1 (HIV-1) disease progression. Here, we describe that subjects with chronic hepatitis C virus (HCV)/HIV-1 coinfection display sharply elevated immune activation as determined by CD38 expression in T cells. This occurs, despite effective antiretroviral therapy, in both CD8 and CD4 T cells and is more pronounced than in the appropriate monoinfected control groups. Interestingly, the suppression of HCV by pegylated alpha interferon and ribavirin treatment reduces activation. High HCV loads and elevated levels of chronic immune activation may contribute to the high rates of viral disease progression observed in HCV/HIV-1-coinfected patients.

摘要

慢性免疫激活是人类免疫缺陷病毒1型(HIV-1)疾病进展的驱动因素。在此,我们描述了慢性丙型肝炎病毒(HCV)/HIV-1合并感染的受试者表现出免疫激活急剧升高,这通过T细胞中CD38的表达来确定。尽管进行了有效的抗逆转录病毒治疗,但在CD8和CD4 T细胞中均出现这种情况,并且比相应的单一感染对照组更为明显。有趣的是,聚乙二醇化α干扰素和利巴韦林治疗对HCV的抑制作用可降低激活水平。高HCV载量和慢性免疫激活水平升高可能导致HCV/HIV-1合并感染患者中观察到的高病毒疾病进展率。

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Emerging concepts in the immunopathogenesis of AIDS.艾滋病免疫发病机制的新观念
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