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      The interferon response circuit: Induction and suppression by pathogenic viruses

      review-article
      Author(s): * , ,
      Publication date (Electronic):
      Journal: Virology
      Publisher: Elsevier Inc.
      Keywords: AdV, adenovirus, BDV, Borna disease virus, BUNV, Bunyamwera virus, CSFV, classical swine fever virus, DHFV, Dengue hemorrhagic fever virus, EBOV, Ebola virus, EBV, Epstein–Barr virus, FLUAV, influenza A virus, FLUBV, influenza B virus, HCV, Hepatitis C virus, HHV-8, human herpes virus 8, HIV, human immunodeficiency virus, HPV16, human papilloma virus 16, HPV18, human papilloma virus 18, HSV-1, herpes simplex virus 1, JEV, Japanese encephalitis virus, PV, Polio virus, RV, Rabies virus, RSV, respiratory syncytial virus, RVFV, Rift valley fever virus, THOV, Thogoto virus, TMEV, Theiler's meningoencephalitis virus, VV, Vaccinia virus, VSV, vesicular stomatitis virus, WNV, West Nile virus, YFV, Yellow fever virus

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          Abstract

          Type I interferons (IFN-α/β) are potent antiviral cytokines and modulators of the adaptive immune system. They are induced by viral infection or by double-stranded RNA (dsRNA), a by-product of viral replication, and lead to the production of a broad range of antiviral proteins and immunoactive cytokines. Viruses, in turn, have evolved multiple strategies to counter the IFN system which would otherwise stop virus growth early in infection. Here we discuss the current view on the balancing act between virus-induced IFN responses and the viral counterplayers.

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          Antiviral actions of interferons.

          C Samuel (2001)
          Tremendous progress has been made in understanding the molecular basis of the antiviral actions of interferons (IFNs), as well as strategies evolved by viruses to antagonize the actions of IFNs. Furthermore, advances made while elucidating the IFN system have contributed significantly to our understanding in multiple areas of virology and molecular cell biology, ranging from pathways of signal transduction to the biochemical mechanisms of transcriptional and translational control to the molecular basis of viral pathogenesis. IFNs are approved therapeutics and have moved from the basic research laboratory to the clinic. Among the IFN-induced proteins important in the antiviral actions of IFNs are the RNA-dependent protein kinase (PKR), the 2',5'-oligoadenylate synthetase (OAS) and RNase L, and the Mx protein GTPases. Double-stranded RNA plays a central role in modulating protein phosphorylation and RNA degradation catalyzed by the IFN-inducible PKR kinase and the 2'-5'-oligoadenylate-dependent RNase L, respectively, and also in RNA editing by the IFN-inducible RNA-specific adenosine deaminase (ADAR1). IFN also induces a form of inducible nitric oxide synthase (iNOS2) and the major histocompatibility complex class I and II proteins, all of which play important roles in immune response to infections. Several additional genes whose expression profiles are altered in response to IFN treatment and virus infection have been identified by microarray analyses. The availability of cDNA and genomic clones for many of the components of the IFN system, including IFN-alpha, IFN-beta, and IFN-gamma, their receptors, Jak and Stat and IRF signal transduction components, and proteins such as PKR, 2',5'-OAS, Mx, and ADAR, whose expression is regulated by IFNs, has permitted the generation of mutant proteins, cells that overexpress different forms of the proteins, and animals in which their expression has been disrupted by targeted gene disruption. The use of these IFN system reagents, both in cell culture and in whole animals, continues to provide important contributions to our understanding of the virus-host interaction and cellular antiviral response.
          Article 0 comments Cited 623 times – based on 0 reviews     Review now
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            Triggering the interferon antiviral response through an IKK-related pathway.

            Sonia Sharma, Benjamin tenOever, Nathalie Grandvaux … (2003)
            Rapid induction of type I interferon expression, a central event in establishing the innate antiviral response, requires cooperative activation of numerous transcription factors. Although signaling pathways that activate the transcription factors nuclear factor kappaB and ATF-2/c-Jun have been well characterized, activation of the interferon regulatory factors IRF-3 and IRF-7 has remained a critical missing link in understanding interferon signaling. We report here that the IkappaB kinase (IKK)-related kinases IKKepsilon and TANK-binding kinase 1 are components of the virus-activated kinase that phosphorylate IRF-3 and IRF-7. These studies illustrate an essential role for an IKK-related kinase pathway in triggering the host antiviral response to viral infection.
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              Cell type-specific involvement of RIG-I in antiviral response.

              Hiroki Kato, Shintaro Sato, Mitsutoshi Yoneyama … (2005)
              Toll-like receptors (TLRs) play an important role in antiviral response by recognizing viral components. Recently, a RNA helicase, RIG-I, was also suggested to recognize viral double-stranded RNA. However, how these molecules contribute to viral recognition in vivo is poorly understood. We show by gene targeting that RIG-I is essential for induction of type I interferons (IFNs) after infection with RNA viruses in fibroblasts and conventional dendritic cells (DCs). RIG-I induces type I IFNs by activating IRF3 via IkappaB kinase-related kinases. In contrast, plasmacytoid DCs, which produce large amounts of IFN-alpha, use the TLR system rather than RIG-I for viral detection. Taken together, RIG-I and the TLR system exert antiviral responses in a cell type-specific manner.
              Article 0 comments Cited 318 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Otto Haller
                Journal
                Journal ID (nlm-ta): Virology
                Journal ID (iso-abbrev): Virology
                Title: Virology
                Publisher: Elsevier Inc.
                ISSN (Print): 0042-6822
                ISSN (Electronic): 1096-0341
                Publication date PMC-release: 16 December 2005
                Publication date (Print): 5 January 2006
                Publication date (Electronic): 16 December 2005
                Volume: 344
                Issue: 1
                Pages: 119-130
                Affiliations
                Abteilung Virologie, Institut für Medizinische Mikrobiologie und Hygiene, Universität Freiburg, D-79008 Freiburg, Germany
                Author notes
                [* ]Corresponding author. Fax: +49 761 2036626. otto.haller@ 123456uniklinik-freiburg.de
                Article
                Publisher ID: S0042-6822(05)00581-7
                DOI: 10.1016/j.virol.2005.09.024
                PMC ID: 7125643
                PubMed ID: 16364743
                SO-VID: 1cccdba5-7c28-47c0-a076-d9750883a3ec
                Copyright © Copyright © 2005 Elsevier Inc. 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 : 6 September 2005
                Date accepted : 10 September 2005
                Categories
                Subject: Article

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: adv, adenovirus,bdv, borna disease virus,bunv, bunyamwera virus,csfv, classical swine fever virus,dhfv, dengue hemorrhagic fever virus,ebov, ebola virus,ebv, epstein–barr virus,fluav, influenza a virus,flubv, influenza b virus,hcv, hepatitis c virus,hhv-8, human herpes virus 8,hiv, human immunodeficiency virus,hpv16, human papilloma virus 16,hpv18, human papilloma virus 18,hsv-1, herpes simplex virus 1,jev, japanese encephalitis virus,pv, polio virus,rv, rabies virus,rsv, respiratory syncytial virus,rvfv, rift valley fever virus,thov, thogoto virus,tmev, theiler's meningoencephalitis virus,vv, vaccinia virus,vsv, vesicular stomatitis virus,wnv, west nile virus,yfv, yellow fever virus
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: adv, adenovirus, bdv, borna disease virus, bunv, bunyamwera virus, csfv, classical swine fever virus, dhfv, dengue hemorrhagic fever virus, ebov, ebola virus, ebv, epstein–barr virus, fluav, influenza a virus, flubv, influenza b virus, hcv, hepatitis c virus, hhv-8, human herpes virus 8, hiv, human immunodeficiency virus, hpv16, human papilloma virus 16, hpv18, human papilloma virus 18, hsv-1, herpes simplex virus 1, jev, japanese encephalitis virus, pv, polio virus, rv, rabies virus, rsv, respiratory syncytial virus, rvfv, rift valley fever virus, thov, thogoto virus, tmev, theiler's meningoencephalitis virus, vv, vaccinia virus, vsv, vesicular stomatitis virus, wnv, west nile virus, yfv, yellow fever virus

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