HIV infection and the intestinal mucosal barrier
Department of Gastroenterology, Infectious Diseases and Rheumatology, Charité- Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany. Annals of the New York Academy of Sciences
(Impact Factor: 4.38).
07/2012; 1258(1):19-24. DOI: 10.1111/j.1749-6632.2012.06512.x
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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Available from: Natalie L. Wilson
- "Inflammation of the GI epithelial barrier leads to symptoms including diarrhea, bloating, and abdominal pain (Berkes, Viswanathan, Savkovic, & Hecht, 2003; Epple & Zeitz, 2012). In IBD/ IBS, inflammation leads to the translocation of microbes naturally residing in the gut into the bloodstream, as seen in HIV disease where microbial products residing in the gut translocate through the GALT into the bloodstream (Brenchley et al., 2006; Epple & Zeitz, 2012). "
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ABSTRACT: Microbial translocation within the context of HIV disease has been described as one of the contributing causes of inflammation and disease progression in HIV infection. HIV-associated symptoms have been related to inflammatory markers and sCD14, a surrogate marker for microbial translocation, suggesting a plausible link between microbial translocation and symptom burden in HIV disease. Similar pathophysiological responses and symptoms have been reported in inflammatory bowel disease (IBD). We provide a comprehensive review of microbial translocation, HIV-associated symptoms, and symptoms connected with inflammation. We identify studies showing a relationship among inflammatory markers, sCD14, and symptoms reported in HIV disease. A conceptual framework and rationale to investigate the link between microbial translocation and symptoms is presented. The impact of inflammation on symptoms supports recommendations to reduce inflammation as part of HIV symptom management. Research in reducing microbial translocation-induced inflammation is limited, but needed, to further promote positive health outcomes among HIV-infected patients.
Journal of the Association of Nurses in AIDS Care 11/2014; 25(6). DOI:10.1016/j.jana.2014.07.004 · 1.27 Impact Factor
Available from: Michael Schindler
- "There is strong evidence that most of the CD4+ T cells in the GALT, including CD4+ memory T cells are directly depleted by massive HIV-1 propagation, accompanied by the loss of integrity of the intestinal barrier
[51,52]. This causes translocation of lipopolysaccharide (LPS) and other bacterial products into the blood stream, driving generalized immune activation associated with rapid AIDS progression
[51,53]. When compared to other macrophages like those of the vaginal mucosal tissue, intestinal macrophages seem to be relatively resistant against HIV-1 infection
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ABSTRACT: Macrophages are important target cells for the Human Immunodeficiency Virus Type I (HIV-1) in vivo. Several studies have assessed the molecular biology of the virus in this cell type, and a number of differences towards HIV-1 infection of CD4+ T cells have been described. There is a broad consensus that macrophages resist HIV-1 infection much better than CD4+ T cells. Among other reasons, this is due to the presence of the recently identified host cell restriction factor SamHD1, which is strongly expressed in cells of the myeloid lineage. Furthermore, macrophages produce and release relatively low amounts of infectious HIV-1 and are less sensitive to viral cytotoxicity in comparison to CD4+ T cells. Nevertheless, macrophages play a crucial role in the different phases of HIV-1 infection. In this review, we summarize and discuss the significance of macrophages for HIV-1 transmission, the acute and chronic phases of HIV-1 infection, the development of acquired immunodeficiency syndrome (AIDS) and HIV-associated diseases, including neurocognitive disorders. We propose that interaction of HIV-1 with macrophages is crucial during all stages of HIV-1 infection. Thus, long-term successful treatment of HIV-1 infected individuals requires potent strategies to prevent HIV-1 from entering and persisting in these cells.
Retrovirology 10/2012; 9(1):82. DOI:10.1186/1742-4690-9-82 · 4.19 Impact Factor
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ABSTRACT: Clostridium difficile infection (CDI) affects significant numbers of hospitalized patients and is an increasing problem in the community. It is also among the most commonly isolated pathogens in HIV patients with diarrheal illness and is ≥2 fold more common in HIV-seropositive individuals. This association is stronger in those with low absolute CD4 T cell counts or meeting clinical criteria for an AIDS diagnosis, and was most pronounced before the wide availability of highly active antiretroviral therapy. The presentation and outcome of CDI in HIV appears similar to the general population. The increased risk can in part be attributed to increased hospitalization and antimicrobial use, but HIV related alterations in fecal microbiota, gut mucosal integrity, and humoral and cell mediated immunity are also likely to play a role. Here we review the evidence for these observations and the relevance of recent advances in the diagnosis and management of CDI for the HIV clinician.
Current HIV/AIDS Reports 05/2013; DOI:10.1007/s11904-013-0162-z · 3.80 Impact Factor
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