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HIV infection and the intestinal mucosal barrier

Authors

  • Hans-Jörg Epple,

    1. Department of Gastroenterology, Infectious Diseases and Rheumatology, Charité– Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany
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  • Martin Zeitz

    1. Department of Gastroenterology, Infectious Diseases and Rheumatology, Charité– Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany
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Hans-Jörg Epple, M.D., Medical Clinic, Gastroenterology, Infectious Diseases and Rheumatology, Charité– Universitätsmedizin Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany. hans-joerg.epple@charite.de

Abstract

HIV infection induces a barrier defect of the intestinal mucosa, which is closely linked to immune activation and CD4 T cell depletion. The HIV-induced barrier defect is initiated in early acute and maintained through chronic infection. In acute infection, increased epithelial permeability is associated with increased epithelial apoptosis possibly caused by perforin-expressing cytotoxic T cells. In chronic infection, mucosal production of inflammatory cytokines is associated with increased epithelial permeability, epithelial apoptosis, and alterations of epithelial tight junctions. In addition to HIV-induced immune-mediated effects, viral proteins have the potential to directly affect epithelial barrier function. After prolonged viral suppression by antiretroviral therapy, there is, at least partial, restoration of the HIV-associated intestinal mucosal barrier defect despite persisting alterations of the mucosal immune system.

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