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Lipopolysaccharide, immune activation, and liver abnormalities in HIV/hepatitis B virus (HBV)-coinfected individuals receiving HBV-active combination antiretroviral therapy.

Crane M, Avihingsanon A, Rajasuriar R, Velayudham P, Iser D, Solomon A, Sebolao B, Tran A, Spelman T, Matthews G, Cameron P, Tangkijvanich P, Dore GJ, Ruxrungtham K, Lewin SR

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  • Journal The Journal of infectious diseases

  • Published 28 Feb 2014

  • Volume 210

  • ISSUE 5

  • Pagination 745-51

  • DOI 10.1093/infdis/jiu119

Abstract

We investigated the relationship between microbial translocation, immune activation, and liver disease in human immunodeficiency virus (HIV)/hepatitis B virus (HBV) coinfection. Lipopolysaccharide (LPS), soluble CD14, CXCL10, and CCL-2 levels were elevated in patients with HIV/HBV coinfection. Levels of LPS, soluble CD14, and CCL-2 declined following receipt of HBV-active combination antiretroviral therapy (cART), but the CXCL10 level remained elevated. No markers were associated with liver disease severity on liver biopsy (n = 96), but CXCL10, interleukin 6 (IL-6), interleukin 10 (IL-10), tumor necrosis factor α, and interferon γ (IFN-γ) were all associated with elevated liver enzyme levels during receipt of HBV-active cART. Stimulation of hepatocyte cell lines in vitro with IFN-γ and LPS induced a profound synergistic increase in the production of CXCL10. LPS may contribute to liver disease via stimulating persistent production of CXCL10.