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      T Cell Distribution in Relation to HIV/HBV/HCV Coinfections and Intravenous Drug Use

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          Abstract

          Intravenous drug use (IDU) is one of the most important transmission routes for blood borne viruses, including human immunodeficiency virus (HIV), hepatitis B virus (HBV), and hepatitis C virus (HCV). These infections alter the subset distributions of T cells; however, knowledge of such effects during HIV, HBV, and or HCV coinfection is limited. Therefore, we aimed to evaluate any associations between T cell distribution and the presence of HIV, HBV, and HCV coinfections among persons who inject drugs (PWID). Blood samples from 88 Caucasian PWID (mean age 30; 82% male) and 47 age-matched subjects negative for all three infections (mean age of 29; 83% male) were analyzed. The T cell markers CD3, CD4, CD8, CD45RA, CCR7, HLA-DR, and CCR5 were assessed using flow cytometry. Of the PWID, 40% were HIV+HBV+HCV+, 20% HBV+HCV+, 19% HCV+, and 13% negative for all three infections. The HIV+HBV+HCV+ PWID had lower percentages of CD4 + and higher percentages of CD8 + cells compared to triple negative PWID ( p < 0.001 in all cases). The only difference between HBV+HCV+ with triple negative PWID was the lower CD4 + cell percentages among the former (52.1% and 58.6%, p = 0.021). Triple negative PWID had higher immune activation and number of CCR5 + cells compared to the controls. We suggest that the altered T cell subset distribution among PWID is mainly triggered by HIV infection and or IDU, while HBV and or HCV seropositivity has minimal additional effects on CD4 + cell distribution.

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          Author and article information

          Journal
          Viral Immunol
          Viral Immunol
          vim
          Viral Immunology
          Mary Ann Liebert, Inc. (140 Huguenot Street, 3rd FloorNew Rochelle, NY 10801USA )
          0882-8245
          1557-8976
          01 October 2016
          01 October 2016
          : 29
          : 8
          : 464-470
          Affiliations
          [ 1 ]Department of Microbiology, Institute of Biomedicine and Translational Medicine, Faculty of Medicine, University of Tartu , Tartu, Estonia.
          [ 2 ]Department of Immunology, Institute of Biomedicine and Translational Medicine, Faculty of Medicine, University of Tartu , Tartu, Estonia.
          [ 3 ] Icahn School of Medicine at Mount Sinai , New York, New York.
          [ 4 ]Institute of Family Medicine and Public Health, Faculty of Medicine, University of Tartu , Tartu, Estonia.
          Author notes
          Address correspondence to: Eveli Kallas, Department of Microbiology, Institute of Biomedicine and Translational Medicine, Faculty of Medicine, University of Tartu Ravila 19, Tartu 50411, Estonia

          E-mail: eveli.kallas@ 123456ut.ee
          Article
          PMC5065031 PMC5065031 5065031 10.1089/vim.2016.0057
          10.1089/vim.2016.0057
          5065031
          27564643
          040f3d83-296e-420a-823d-deda2ec57f7c
          Copyright 2016, Mary Ann Liebert, Inc.
          History
          Page count
          Figures: 2, Tables: 2, References: 35, Pages: 7
          Categories
          Original Research Articles

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