Immunopathogenesis of Hepatic Flare in HIV/Hepatitis B Virus (HBV)-Coinfected Individuals after the Initiation of HBV-Active Antiretroviral Therapy

M. Crane, B. Oliver, G. Matthews, A. Avihingsanon, S. Ubolyam, V. Markovska, J.J. Chang, G.J. Dore, Patricia Price, K. Visvanathan, Martyn French, K. Ruxrungtham, S.R. Lewin

    Research output: Contribution to journalArticle

    56 Citations (Scopus)

    Abstract

    Background: The pathogenesis of and risk factors for hepatic flare (HF) after the initiation of hepatitis B virus (HBV)–active antiretroviral therapy (ART) in HIV/HBV-coinfected individuals is not well understood Methods: We studied HF in ART-naive HIV/HBV-coinfected individuals in Thailand (n=36) who were beginning HBV-active ART as part of a prospective clinical trial. HF was defined as an alanine aminotransferase (ALT) level >5 times the upper limit of normal or >200 IU/L higher than that at baseline. Immune mediators (interleukin [IL]–18, IL-2, IL-6, IL-8, IL-10, soluble CD26 [sCD26], sCD30, sCD8, CXCL-10, CCL-2, tumor necrosis factor–α, interferon [IFN]–γ, and IFN-α) and activated NK cells were quantified Results: HBV DNA and ALT levels at baseline were higher in patients with HF (n=8) than in patients without HF (n=28) (P=.01). After the initiation of ART, CXCL-10 levels remained elevated in patients with HF but decreased in patients without HF (P
    Original languageEnglish
    Pages (from-to)974-981
    JournalJournal of Infectious Diseases
    Volume199
    Issue number7
    DOIs
    Publication statusPublished - 2009

    Fingerprint Dive into the research topics of 'Immunopathogenesis of Hepatic Flare in HIV/Hepatitis B Virus (HBV)-Coinfected Individuals after the Initiation of HBV-Active Antiretroviral Therapy'. Together they form a unique fingerprint.

    Cite this