For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
14
views
192
references
 Top references
cited by
73
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
1 collections
    0
    shares
      235
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      Global virus outbreaks: Interferons as 1st responders

      review-article
      Author(s): a , b , c , *
      Publication date (Electronic):
      Journal: Seminars in Immunology
      Publisher: Published by Elsevier Ltd.
      Keywords: Interferons-α/β, Antiviral, Immune response

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Highlights

          • •

            IFNs-α/β exhibit direct antiviral effects on viral replication.

          • •

            IFNs-α/β activate innate and adaptive immune responses.

          • •

            IFNs-α/β present as ideal broad-spectrum antivirals for acute virus infections.

          Abstract

          Outbreaks of severe virus infections with the potential to cause global pandemics are increasing. In many instances these outbreaks have been newly emerging (SARS coronavirus), re-emerging (Ebola virus, Zika virus) or zoonotic (avian influenza H5N1) virus infections. In the absence of a targeted vaccine or a pathogen-specific antiviral, broad-spectrum antivirals would function to limit virus spread. Given the direct antiviral effects of type I interferons (IFNs) in inhibiting the replication of both DNA and RNA viruses at different stages of their replicative cycles, and the effects of type I IFNs on activating immune cell populations to clear virus infections, IFNs-α/β present as ideal candidate broad-spectrum antivirals.

          Related collections

          Most cited references192

          • Record: found
          • Abstract: found
          • Article: not found

          Tetherin inhibits retrovirus release and is antagonized by HIV-1 Vpu.

          Stuart J D Neil, Trinity Zang, Paul D. Bieniasz (2008)
          Human cells possess an antiviral activity that inhibits the release of retrovirus particles, and other enveloped virus particles, and is antagonized by the HIV-1 accessory protein, Vpu. This antiviral activity can be constitutively expressed or induced by interferon-alpha, and it consists of protein-based tethers, which we term 'tetherins', that cause retention of fully formed virions on infected cell surfaces. Using deductive constraints and gene expression analyses, we identify CD317 (also called BST2 or HM1.24), a membrane protein of previously unknown function, as a tetherin. Specifically, CD317 expression correlated with, and induced, a requirement for Vpu during HIV-1 and murine leukaemia virus particle release. Furthermore, in cells where HIV-1 virion release requires Vpu expression, depletion of CD317 abolished this requirement. CD317 caused retention of virions on cell surfaces and, after endocytosis, in CD317-positive compartments. Vpu co-localized with CD317 and inhibited these effects. Inhibition of Vpu function and consequent mobilization of tetherin's antiviral activity is a potential therapeutic strategy in HIV/AIDS.
          Article 0 comments Cited 697 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            IFNalpha activates dormant haematopoietic stem cells in vivo.

            Marieke Essers, Sandra Offner, William E. Blanco-Bose … (2009)
            Maintenance of the blood system is dependent on dormant haematopoietic stem cells (HSCs) with long-term self-renewal capacity. After injury these cells are induced to proliferate to quickly re-establish homeostasis. The signalling molecules promoting the exit of HSCs out of the dormant stage remain largely unknown. Here we show that in response to treatment of mice with interferon-alpha (IFNalpha), HSCs efficiently exit G(0) and enter an active cell cycle. HSCs respond to IFNalpha treatment by the increased phosphorylation of STAT1 and PKB/Akt (also known as AKT1), the expression of IFNalpha target genes, and the upregulation of stem cell antigen-1 (Sca-1, also known as LY6A). HSCs lacking the IFNalpha/beta receptor (IFNAR), STAT1 (ref. 3) or Sca-1 (ref. 4) are insensitive to IFNalpha stimulation, demonstrating that STAT1 and Sca-1 mediate IFNalpha-induced HSC proliferation. Although dormant HSCs are resistant to the anti-proliferative chemotherapeutic agent 5-fluoro-uracil, HSCs pre-treated (primed) with IFNalpha and thus induced to proliferate are efficiently eliminated by 5-fluoro-uracil exposure in vivo. Conversely, HSCs chronically activated by IFNalpha are functionally compromised and are rapidly out-competed by non-activatable Ifnar(-/-) cells in competitive repopulation assays. Whereas chronic activation of the IFNalpha pathway in HSCs impairs their function, acute IFNalpha treatment promotes the proliferation of dormant HSCs in vivo. These data may help to clarify the so far unexplained clinical effects of IFNalpha on leukaemic cells, and raise the possibility for new applications of type I interferons to target cancer stem cells.
            Article 0 comments Cited 487 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found
              Is Open Access

              INTERFEROME v2.0: an updated database of annotated interferon-regulated genes

              Irina Rusinova, Sam Forster, Simon Yu … (2012)
              Interferome v2.0 (http://interferome.its.monash.edu.au/interferome/) is an update of an earlier version of the Interferome DB published in the 2009 NAR database edition. Vastly improved computational infrastructure now enables more complex and faster queries, and supports more data sets from types I, II and III interferon (IFN)-treated cells, mice or humans. Quantitative, MIAME compliant data are collected, subjected to thorough, standardized, quantitative and statistical analyses and then significant changes in gene expression are uploaded. Comprehensive manual collection of metadata in v2.0 allows flexible, detailed search capacity including the parameters: range of -fold change, IFN type, concentration and time, and cell/tissue type. There is no limit to the number of genes that can be used to search the database in a single query. Secondary analysis such as gene ontology, regulatory factors, chromosomal location or tissue expression plots of IFN-regulated genes (IRGs) can be performed in Interferome v2.0, or data can be downloaded in convenient text formats compatible with common secondary analysis programs. Given the importance of IFN to innate immune responses in infectious, inflammatory diseases and cancer, this upgrade of the Interferome to version 2.0 will facilitate the identification of gene signatures of importance in the pathogenesis of these diseases.
              Article 0 comments Cited 420 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Eleanor N. Fish
                Journal
                Journal ID (nlm-ta): Semin Immunol
                Journal ID (iso-abbrev): Semin. Immunol
                Title: Seminars in Immunology
                Publisher: Published by Elsevier Ltd.
                ISSN (Print): 1044-5323
                ISSN (Electronic): 1096-3618
                Publication date PMC-release: 23 November 2019
                Publication date (Print): June 2019
                Publication date (Electronic): 23 November 2019
                Volume: 43
                Page: 101300
                Affiliations
                [a ]Princess Margaret Cancer Center, Tumor Immunotherapy Program, University Health Network, Toronto, ON M5G 2M9, Canada
                [b ]Toronto General Hospital Research Institute, University Health Network, 67 College Street, Toronto, ON M5G 2M1, Canada
                [c ]Department of Immunology, University of Toronto, 1 King’s College Circle, Toronto, ON M5S 1A8, Canada
                Author notes
                [* ]Corresponding author at: Toronto General Hospital Research Institute, University Health Network, 67 College Street, Toronto, ON M5G 2M1, Canada. en.fish@ 123456utoronto.ca
                Article
                Publisher ID: S1044-5323(19)30006-5 Publisher ID: 101300
                DOI: 10.1016/j.smim.2019.101300
                PMC ID: 7128104
                PubMed ID: 31771760
                SO-VID: 178ed189-0c85-47e7-81d0-19ee1af05ff8
                Copyright © Crown Copyright © 2019 Published by Elsevier Ltd. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                Date received : 12 August 2019
                Date accepted : 19 August 2019
                Categories
                Subject: Article

                ScienceOpen disciplines: Immunology
                Keywords: interferons-α/β,antiviral,immune response
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: interferons-α/β, antiviral, immune response

                Comments

                Comment on this article

                scite_

                Similar content235

                See all similar

                Cited by72

                See all cited by

                Most referenced authors3,572

                See all reference authors