دورية أكاديمية
أعرض في EDS

Disruption of Type I Interferon Induction by HIV Infection of T Cells.

التفاصيل البيبلوغرافية
العنوان: Disruption of Type I Interferon Induction by HIV Infection of T Cells.
المؤلفون: Sanchez DJ; Pharmaceutical Sciences Department, College of Pharmacy, Western University of Health Sciences, Pomona, California, United States of America., Miranda D Jr; Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, California, United States of America; UCLA AIDS Institute, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America., Marsden MD; UCLA AIDS Institute, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America; Department of Medicine, Division of Hematology and Oncology, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America., Dizon TM; Pharmaceutical Sciences Department, College of Pharmacy, Western University of Health Sciences, Pomona, California, United States of America., Bontemps JR; Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, California, United States of America., Davila SJ; Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, California, United States of America., Del Mundo LE; Pharmaceutical Sciences Department, College of Pharmacy, Western University of Health Sciences, Pomona, California, United States of America., Ha T; Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, California, United States of America., Senaati A; Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, California, United States of America., Zack JA; Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, California, United States of America; UCLA AIDS Institute, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America; Department of Medicine, Division of Hematology and Oncology, David Geffen School of Medicine at UCLA, Los Angeles, California, United States of America., Cheng G; Department of Microbiology, Immunology and Molecular Genetics, University of California Los Angeles, Los Angeles, California, United States of America.
المصدر: PloS one [PLoS One] 2015 Sep 16; Vol. 10 (9), pp. e0137951. Date of Electronic Publication: 2015 Sep 16 (Print Publication: 2015).
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: CD4-Positive T-Lymphocytes/*immunology , HIV Infections/*immunology , HIV-1/*immunology , Host-Pathogen Interactions/*immunology , Immunity, Innate/*immunology , Interferon Type I/*immunology , Virus Replication/*immunology, CD4-Positive T-Lymphocytes/pathology ; Cells, Cultured ; Cytokines/metabolism ; HIV Infections/pathology ; HIV Infections/virology ; Human Immunodeficiency Virus Proteins/immunology ; Humans ; Signal Transduction
مستخلص: Our main objective of this study was to determine how Human Immunodeficiency Virus (HIV) avoids induction of the antiviral Type I Interferon (IFN) system. To limit viral infection, the innate immune system produces important antiviral cytokines such as the IFN. IFN set up a critical roadblock to virus infection by limiting further replication of a virus. Usually, IFN production is induced by the recognition of viral nucleic acids by innate immune receptors and subsequent downstream signaling. However, the importance of IFN in the defense against viruses has lead most pathogenic viruses to evolve strategies to inhibit host IFN induction or responses allowing for increased pathogenicity and persistence of the virus. While the adaptive immune responses to HIV infection have been extensively studied, less is known about the balance between induction and inhibition of innate immune defenses, including the antiviral IFN response, by HIV infection. Here we show that HIV infection of T cells does not induce significant IFN production even IFN I Interferon production. To explain this paradox, we screened HIV proteins and found that two HIV encoded proteins, Vpu and Nef, strongly antagonize IFN induction, with expression of these proteins leading to loss of expression of the innate immune viral RNA sensing adaptor protein, IPS-1 (IFN-β promoter stimulator-1). We hypothesize that with lower levels of IPS-1 present, infected cells are defective in mounting antiviral responses allowing HIV to replicate without the normal antiviral actions of the host IFN response. Using cell lines as well as primary human derived cells, we show that HIV targeting of IPS-1 is key to limiting IFN induction. These findings describe how HIV infection modulates IFN induction providing insight into the mechanisms by which HIV establishes infection and persistence in a host.
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معلومات مُعتمدة: R25 GM055052 United States GM NIGMS NIH HHS; 5T32AI060567-05 United States AI NIAID NIH HHS; T34 GM008563 United States GM NIGMS NIH HHS; T32 CA009056 United States CA NCI NIH HHS; AI069120-03 United States AI NIAID NIH HHS; AI70010 United States AI NIAID NIH HHS; R01 AI069120 United States AI NIAID NIH HHS; T32 AI007126 United States AI NIAID NIH HHS; 5T32CA009056-29 United States CA NCI NIH HHS; 5T34GM008563-13 United States GM NIGMS NIH HHS; 5T32AI007126-30 United States AI NIAID NIH HHS; P30 AI028697 United States AI NIAID NIH HHS; N01AI70010 United States AI NIAID NIH HHS; AI028697 United States AI NIAID NIH HHS; T32 AI060567 United States AI NIAID NIH HHS; 5R25GM055052-10 United States GM NIGMS NIH HHS
المشرفين على المادة: 0 (Cytokines)
0 (Human Immunodeficiency Virus Proteins)
0 (Interferon Type I)
تواريخ الأحداث: Date Created: 20150917 Date Completed: 20160526 Latest Revision: 20201215
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC4574156
DOI: 10.1371/journal.pone.0137951
PMID: 26375588
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0137951