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Viruses 2010, 2(10), 2154-2168; doi:10.3390/v2102154
Antiviral Properties of ISG15
1 Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA 2 Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA
Received: 2 August 2010; in revised form: 8 September 2010 / Accepted: 15 September 2010 / Published: 28 September 2010
(This article belongs to the Special Issue Ubiquitination/Deubiquitination in Viral Infection)
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Abstract: The type I interferon system plays a critical role in limiting the spread of viral infection. Viruses induce the production of interferon (IFN), which after binding to the IFN-α/β receptor (IFNAR), and triggering of the JAK/STAT signaling cascade, results in the induction of interferon-stimulated genes (ISGs). These ISGs function to inhibit viral replication and to regulate the host immune response. Among these ISGs, the ubiquitin-like molecule, ISG15, is one of the most strongly induced proteins. Similar to ubiquitin, through an IFN induced conjugation cascade, ISG15 is covalently linked to a variety of cellular proteins, suggesting regulation of different cellular processes. Studies performed over the past several years have shown that ISG15 plays a central role in the host’s antiviral response against many viruses. Mice lacking ISG15 display increased susceptibility to multiple viruses. Furthermore, several viruses have developed immune evasion strategies that directly target the ISG15 pathway. Work is now underway to determine the mechanism by which ISG15 functions as an antiviral molecule, such that therapies targeting this pathway can be developed in the future.
Keywords: ISG15; interferon; antiviral; ubiquitin-like molecule
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MDPI and ACS Style
Lenschow, D.J. Antiviral Properties of ISG15. Viruses 2010, 2, 2154-2168.AMA Style
Lenschow DJ. Antiviral Properties of ISG15. Viruses. 2010; 2(10):2154-2168.Chicago/Turabian Style
Lenschow, Deborah J. 2010. "Antiviral Properties of ISG15." Viruses 2, no. 10: 2154-2168.