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      Interferon-stimulated genes and their antiviral effector functions

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      Author(s): ,
      Publication date (Electronic):
      Journal: Current Opinion in Virology
      Publisher: Elsevier

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          Highlights

          ► IFN induces a diverse range of antiviral effectors. ► Each virus has a unique, but partially overlapping, antiviral ‘ISG profile’. ► IFN effectors target multiple stages in the virus life cycle. ► The IFN signaling pathway is highly self-reinforcing. ► Viruses may hijack IFN effectors to promote replication.

          Abstract

          Many viruses trigger the type I interferon (IFN) system, leading to the transcription of hundreds of interferon-stimulated genes (ISGs). The products of these ISGs exert numerous antiviral effector functions, many of which are still not fully described. Recent efforts have been aimed at identifying which ISGs are antiviral and further characterizing their mechanisms of action. IFN effectors vary widely in their magnitude of inhibitory activity and display combinatorial antiviral properties. Collectively, ISGs can target almost any step in a virus life cycle. Some of the most potent antiviral effectors reinforce the system by further inducing IFN or ISGs. Other genes enhance or facilitate viral replication, suggesting that some viruses may have evolved to co-opt IFN effectors for a survival advantage.

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          Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures.

          Richard E Randall, Stephen Goodbourn (2008)
          The interferon (IFN) system is an extremely powerful antiviral response that is capable of controlling most, if not all, virus infections in the absence of adaptive immunity. However, viruses can still replicate and cause disease in vivo, because they have some strategy for at least partially circumventing the IFN response. We reviewed this topic in 2000 [Goodbourn, S., Didcock, L. & Randall, R. E. (2000). J Gen Virol 81, 2341-2364] but, since then, a great deal has been discovered about the molecular mechanisms of the IFN response and how different viruses circumvent it. This information is of fundamental interest, but may also have practical application in the design and manufacture of attenuated virus vaccines and the development of novel antiviral drugs. In the first part of this review, we describe how viruses activate the IFN system, how IFNs induce transcription of their target genes and the mechanism of action of IFN-induced proteins with antiviral action. In the second part, we describe how viruses circumvent the IFN response. Here, we reflect upon possible consequences for both the virus and host of the different strategies that viruses have evolved and discuss whether certain viruses have exploited the IFN response to modulate their life cycle (e.g. to establish and maintain persistent/latent infections), whether perturbation of the IFN response by persistent infections can lead to chronic disease, and the importance of the IFN system as a species barrier to virus infections. Lastly, we briefly describe applied aspects that arise from an increase in our knowledge in this area, including vaccine design and manufacture, the development of novel antiviral drugs and the use of IFN-sensitive oncolytic viruses in the treatment of cancer.
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            Identification of genes differentially regulated by interferon alpha, beta, or gamma using oligonucleotide arrays.

            S. Der, A. Zhou, B R Williams … (1998)
            The pleiotropic activities of interferons (IFNs) are mediated primarily through the transcriptional regulation of many downstream effector genes. The mRNA profiles from IFN-alpha, -beta, or -gamma treatments of the human fibrosarcoma cell line, HT1080, were determined by using oligonucleotide arrays with probe sets corresponding to more than 6,800 human genes. Among these were transcripts for known IFN-stimulated genes (ISGs), the expression of which were consistent with previous studies in which the particular ISG was characterized as responsive to either Type I (alpha, beta) or Type II (gamma) IFNs, or both. Importantly, many novel IFN-stimulated genes were identified that were diverse in their known biological functions. For instance, several novel ISGs were identified that are implicated in apoptosis (including RAP46/Bag-1, phospholipid scramblase, and hypoxia inducible factor-1alpha). Furthermore, several IFN-repressed genes also were identified. These results demonstrate the usefulness of oligonucleotide arrays in monitoring mammalian gene expression on a broad and unprecedented scale. In particular, these findings provide insights into the basic mechanisms of IFN actions and ultimately may contribute to better therapeutic uses for IFNs.
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              Peroxisomes are signaling platforms for antiviral innate immunity.

              Evelyn Dixit, Steeve Boulant, Yijing Zhang … (2010)
              Peroxisomes have long been established to play a central role in regulating various metabolic activities in mammalian cells. These organelles act in concert with mitochondria to control the metabolism of lipids and reactive oxygen species. However, while mitochondria have emerged as an important site of antiviral signal transduction, a role for peroxisomes in immune defense is unknown. Here, we report that the RIG-I-like receptor (RLR) adaptor protein MAVS is located on peroxisomes and mitochondria. We find that peroxisomal and mitochondrial MAVS act sequentially to create an antiviral cellular state. Upon viral infection, peroxisomal MAVS induces the rapid interferon-independent expression of defense factors that provide short-term protection, whereas mitochondrial MAVS activates an interferon-dependent signaling pathway with delayed kinetics, which amplifies and stabilizes the antiviral response. The interferon regulatory factor IRF1 plays a crucial role in regulating MAVS-dependent signaling from peroxisomes. These results establish that peroxisomes are an important site of antiviral signal transduction. Copyright (c) 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                John W Schoggins
                Charles M Rice
                Journal
                Journal ID (nlm-ta): Curr Opin Virol
                Journal ID (iso-abbrev): Curr Opin Virol
                Title: Current Opinion in Virology
                Publisher: Elsevier
                ISSN (Print): 1879-6257
                ISSN (Electronic): 1879-6265
                Publication date PMC-release: 28 October 2011
                Publication date (Print): December 2011
                Publication date (Electronic): 28 October 2011
                Volume: 1
                Issue: 6
                Pages: 519-525
                Affiliations
                Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University, 1230 York Avenue, New York, NY 10065, United States
                Article
                Publisher ID: S1879-6257(11)00127-1
                DOI: 10.1016/j.coviro.2011.10.008
                PMC ID: 3274382
                PubMed ID: 22328912
                SO-VID: 5c5bd30e-847d-461f-b3c6-dd475fbca159
                Copyright © Copyright © 2011 Elsevier B.V. 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.

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