High Levels of Chronic Immune Activation in the T-Cell Compartments of Patients Coinfected with Hepatitis C Virus and Human Immunodeficiency Virus Type 1 and on Highly Active Antiretroviral Therapy Are Reverted by Alpha Interferon and Ribavirin Treatment
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Published in | Journal of Virology Vol. 83; no. 21; pp. 11407 - 11411 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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Washington, DC
American Society for Microbiology
01.11.2009
American Society for Microbiology (ASM) |
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ISSN | 0022-538X 1098-5514 1098-5514 |
DOI | 10.1128/JVI.01211-09 |
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AbstractList | Chronic immune activation is a driver of human immunodeficiency virus type 1 (HIV-1) disease progression. Here, we describe that subjects with chronic hepatitis C virus (HCV)/HIV-1 coinfection display sharply elevated immune activation as determined by CD38 expression in T cells. This occurs, despite effective antiretroviral therapy, in both CD8 and CD4 T cells and is more pronounced than in the appropriate monoinfected control groups. Interestingly, the suppression of HCV by pegylated alpha interferon and ribavirin treatment reduces activation. High HCV loads and elevated levels of chronic immune activation may contribute to the high rates of viral disease progression observed in HCV/HIV-1-coinfected patients. Chronic immune activation is a driver of human immunodeficiency virus type 1 (HIV-1) disease progression. Here, we describe that subjects with chronic hepatitis C virus (HCV)/HIV-1 coinfection display sharply elevated immune activation as determined by CD38 expression in T cells. This occurs, despite effective antiretroviral therapy, in both CD8 and CD4 T cells and is more pronounced than in the appropriate monoinfected control groups. Interestingly, the suppression of HCV by pegylated alpha interferon and ribavirin treatment reduces activation. High HCV loads and elevated levels of chronic immune activation may contribute to the high rates of viral disease progression observed in HCV/HIV-1-coinfected patients.Chronic immune activation is a driver of human immunodeficiency virus type 1 (HIV-1) disease progression. Here, we describe that subjects with chronic hepatitis C virus (HCV)/HIV-1 coinfection display sharply elevated immune activation as determined by CD38 expression in T cells. This occurs, despite effective antiretroviral therapy, in both CD8 and CD4 T cells and is more pronounced than in the appropriate monoinfected control groups. Interestingly, the suppression of HCV by pegylated alpha interferon and ribavirin treatment reduces activation. High HCV loads and elevated levels of chronic immune activation may contribute to the high rates of viral disease progression observed in HCV/HIV-1-coinfected patients. Article Usage Stats Services JVI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue JVI About JVI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy JVI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0022-538X Online ISSN: 1098-5514 Copyright © 2014 by the American Society for Microbiology. For an alternate route to JVI .asm.org, visit: JVI |
Author | Alex Lund Laursen Annette Alaeus Johan K. Sandberg Kim G. Blom Birgitte Mørn Olle Reichard Nina Weis Karolin Falconer Veronica D. Gonzalez |
AuthorAffiliation | Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, 14186 Stockholm, Sweden, 1 Unit of Infectious Diseases, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Solna, 17176 Stockholm, Sweden, 2 Department of Infectious Diseases, Aalborg University Hospital, Aalborg, Denmark, 3 Department of Infectious Diseases, Aarhus University Hospital, Aarhus, Denmark, 4 Department of Infectious Diseases, Hvidovre University Hospital, Copenhagen, Denmark, 5 Department of Infectious Diseases, Rigshospitalet, Copenhagen, Denmark 6 |
AuthorAffiliation_xml | – name: Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, 14186 Stockholm, Sweden, 1 Unit of Infectious Diseases, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Solna, 17176 Stockholm, Sweden, 2 Department of Infectious Diseases, Aalborg University Hospital, Aalborg, Denmark, 3 Department of Infectious Diseases, Aarhus University Hospital, Aarhus, Denmark, 4 Department of Infectious Diseases, Hvidovre University Hospital, Copenhagen, Denmark, 5 Department of Infectious Diseases, Rigshospitalet, Copenhagen, Denmark 6 |
Author_xml | – sequence: 1 givenname: Veronica D. surname: Gonzalez fullname: Gonzalez, Veronica D. organization: Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, 14186 Stockholm, Sweden – sequence: 2 givenname: Karolin surname: Falconer fullname: Falconer, Karolin organization: Unit of Infectious Diseases, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Solna, 17176 Stockholm, Sweden – sequence: 3 givenname: Kim G. surname: Blom fullname: Blom, Kim G. organization: Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, 14186 Stockholm, Sweden – sequence: 4 givenname: Olle surname: Reichard fullname: Reichard, Olle organization: Unit of Infectious Diseases, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Solna, 17176 Stockholm, Sweden – sequence: 5 givenname: Birgitte surname: Mørn fullname: Mørn, Birgitte organization: Department of Infectious Diseases, Aalborg University Hospital, Aalborg, Denmark – sequence: 6 givenname: Alex Lund surname: Laursen fullname: Laursen, Alex Lund organization: Department of Infectious Diseases, Aarhus University Hospital, Aarhus, Denmark – sequence: 7 givenname: Nina surname: Weis fullname: Weis, Nina organization: Department of Infectious Diseases, Hvidovre University Hospital, Copenhagen, Denmark, Department of Infectious Diseases, Rigshospitalet, Copenhagen, Denmark – sequence: 8 givenname: Annette surname: Alaeus fullname: Alaeus, Annette organization: Unit of Infectious Diseases, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Solna, 17176 Stockholm, Sweden – sequence: 9 givenname: Johan K. surname: Sandberg fullname: Sandberg, Johan K. organization: Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, 14186 Stockholm, Sweden |
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Mendeley... Chronic immune activation is a driver of human immunodeficiency virus type 1 (HIV-1) disease progression. Here, we describe that subjects with chronic... |
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SubjectTerms | ADP-ribosyl Cyclase 1 - immunology Adult Antiretroviral Therapy, Highly Active Antiviral Agents - therapeutic use Biological and medical sciences Disease Progression Female Fundamental and applied biological sciences. Psychology Hepacivirus - immunology Hepatitis C, Chronic - drug therapy Hepatitis C, Chronic - immunology Hepatitis C, Chronic - virology HIV Infections - drug therapy HIV Infections - immunology HIV Infections - virology HIV-1 - immunology Humans Interferon-alpha - immunology Interferon-alpha - therapeutic use Lymphocyte Activation - immunology Male Microbiology Middle Aged Miscellaneous Pathogenesis and Immunity Ribavirin - therapeutic use T-Lymphocyte Subsets - immunology T-Lymphocyte Subsets - virology T-Lymphocytes - immunology T-Lymphocytes - virology Viral Load Virology Young Adult |
Title | High Levels of Chronic Immune Activation in the T-Cell Compartments of Patients Coinfected with Hepatitis C Virus and Human Immunodeficiency Virus Type 1 and on Highly Active Antiretroviral Therapy Are Reverted by Alpha Interferon and Ribavirin Treatment |
URI | http://jvi.asm.org/content/83/21/11407.abstract https://www.ncbi.nlm.nih.gov/pubmed/19710147 https://www.proquest.com/docview/733945806 https://pubmed.ncbi.nlm.nih.gov/PMC2772767 http://kipublications.ki.se/Default.aspx?queryparsed=id:119466298 |
Volume | 83 |
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