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      Altered Virome and Bacterial Microbiome in Human Immunodeficiency Virus-Associated Acquired Immunodeficiency Syndrome.

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          Abstract

          Human immunodeficiency virus (HIV) infection is associated with increased intestinal translocation of microbial products and enteropathy as well as alterations in gut bacterial communities. However, whether the enteric virome contributes to this infection and resulting immunodeficiency remains unknown. We characterized the enteric virome and bacterial microbiome in a cohort of Ugandan patients, including HIV-uninfected or HIV-infected subjects and those either treated with anti-retroviral therapy (ART) or untreated. Low peripheral CD4 T cell counts were associated with an expansion of enteric adenovirus sequences and this increase was independent of ART treatment. Additionally, the enteric bacterial microbiome of patients with lower CD4 T counts exhibited reduced phylogenetic diversity and richness with specific bacteria showing differential abundance, including increases in Enterobacteriaceae, which have been associated with inflammation. Thus, immunodeficiency in progressive HIV infection is associated with alterations in the enteric virome and bacterial microbiome, which may contribute to AIDS-associated enteropathy and disease progression.

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          Author and article information

          Journal
          Cell Host Microbe
          Cell host & microbe
          1934-6069
          1931-3128
          Mar 9 2016
          : 19
          : 3
          Affiliations
          [1 ] Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
          [2 ] Ragon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA.
          [3 ] Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, 63110, USA.
          [4 ] Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, 63110, USA; Department of Molecular Microbiology, Washington University School of Medicine, Saint Louis, MO 63110, USA.
          [5 ] Division of Infectious Diseases, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.
          [6 ] Vedanta Biosciences, Cambridge, MA 02139, USA.
          [7 ] Médecins Sans Frontières Epicentre, 1956 Mbarara, Uganda.
          [8 ] Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA 94143, USA.
          [9 ] Department of Medicine, University of California San Francisco, San Francisco, CA 94110, USA.
          [10 ] Division of Infectious Diseases, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA; Harvard School of Public Health, Boston, MA 02114, USA.
          [11 ] Ragon Institute of MGH, MIT, and Harvard, Cambridge, MA 02139, USA; Division of Infectious Diseases, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Electronic address: dkwon@mgh.harvard.edu.
          [12 ] Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, 63110, USA. Electronic address: virgin@wustl.edu.
          Article
          S1931-3128(16)30052-X NIHMS764192
          10.1016/j.chom.2016.02.011
          26962942
          Copyright © 2016 Elsevier Inc. All rights reserved.

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