Mechanisms of Accelerated Liver Fibrosis Progression during HIV Infection

被引:43
作者
Debes, Jose D. [1 ]
Bohjanen, Paul R. [1 ]
Boonstra, Andre [2 ]
机构
[1] Univ Minnesota, Dept Med, Div Infect Dis & Int Med, 2001 6th St SE, Minneapolis, MN 55455 USA
[2] Erasmus MC, Dept Gastroenterol & Hepatol, Rotterdam, Netherlands
基金
美国国家卫生研究院;
关键词
HIV; Liver fibrosis; Mitochondrial toxicity; Bacterial translocation;
D O I
10.14218/JCTH.2016.00034
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
With the introduction of antiretroviral therapy (ART), a dramatic reduction in HIV-related morbidity and mortality has been observed. However, it is now becoming increasingly clear that liver-related complications, particularly rapid fibrosis development from ART as well as from the chronic HIV infection itself, are of serious concern to HIV patients. The pathophysiology of liver fibrosis in patients with HIV is a multifactorial process whereby persistent viral replication, and bacterial translocation lead to chronic immune activation and inflammation, which ART is unable to fully suppress, promoting production of fibrinogenic mediators and fibrosis. In addition, mitochondrial toxicity, triggered by both ART and HIV, contributes to intrahepatic damage, which is even more severe in patients co-infected with viral hepatitis. In recent years, new insights into the mechanisms of accelerated fibrosis and liver disease progression in HIV has been obtained, and these are detailed and discussed in this review. (c) 2016 The Second Affiliated Hospital of Chongqing Medical University. Published by XIA & HE Publishing Inc. All rights reserved.
引用
收藏
页码:328 / 335
页数:8
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