Human Immunodeficiency Virus-Related Microbial Translocation and Progression of Hepatitis C

Ashwin Balagopal, Frances H. Philp, Jacquie Astemborski, Timothy M. Block, Anand Mehta, Ronald Long, Gregory D. Kirk, Shruti H. Mehta, Andrea L. Cox, David L. Thomas, Stuart C. Ray

Research output: Contribution to journalArticlepeer-review


Background & Aims: Human immunodeficiency virus (HIV)-1 infection has been associated with enhanced microbial translocation, and microbial translocation is a mechanism through which alcohol and some enteric conditions cause liver disease. We hypothesized that HIV promotes liver disease by enhancing microbial translocation. Methods: We studied human cohorts in which hepatitis C virus (HCV) and HIV outcomes were carefully characterized. Results: HIV-related CD4+ lymphocyte depletion was strongly associated with microbial translocation as indicated by elevated levels of circulating lipopolysaccharide (LPS), LPS-binding protein, soluble CD14, and fucose-binding lectin (AAL) reactive to immunoglobulin G specific for the α-galactose epitope and suppressed levels of endotoxin core antibodies (EndoCAb IgM) in HIV-infected subjects compared with the same persons before they had HIV infection and compared with HIV-uninfected subjects. The same measures of microbial translocation were strongly associated with HCV-related liver disease progression (cirrhosis), eg, LPS, odds ratio, 19.0 (P = .002); AAL, odds ratio, 27.8 (P < .0001); in addition, levels of LPS were elevated prior to recognition of cirrhosis. Conclusions: Microbial translocation may be a fundamental mechanism through which HIV accelerates progression of chronic liver disease.

Original languageEnglish (US)
Pages (from-to)226-233
Number of pages8
Issue number1
StatePublished - Jul 2008

ASJC Scopus subject areas

  • Hepatology
  • Gastroenterology


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