Mechanisms of accelerated liver fibrosis progression during HIV infection

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43 Scopus citations


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 fib-rosis 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.

Original languageEnglish (US)
Pages (from-to)328-335
Number of pages8
JournalJournal of Clinical and Translational Hepatology
Issue number4
StatePublished - 2016

Bibliographical note

Publisher Copyright:
© 2016 The Second Affiliated Hospital of Chongqing Medical University. Published by XIA & HE Publishing Inc. All rights reserved.


  • Bacterial translocation
  • HIV
  • Liver fibrosis
  • Mitochondrial toxicity


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