ISG15 in antiviral immunity and beyond

The host response to viral infection includes the induction of type I interferons and the subsequent upregulation of hundreds of interferon-stimulated genes. Ubiquitin-like protein ISG15 is an interferon-induced protein that has been implicated as a central player in the host antiviral response. Ove...

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Published inNature reviews. Microbiology Vol. 16; no. 7; pp. 423 - 439
Main Authors Perng, Yi-Chieh, Lenschow, Deborah J.
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.07.2018
Nature Publishing Group
Subjects
13
13/1
631/250/255/2514
631/326/596/2553
631/326/596/2557
82/58
Antiviral agents
Antiviral drugs
Biological response modifiers
Biomedical and Life Sciences
Care and treatment
Cell receptors
Cellular proteins
Cytokines - immunology
Cytokines - metabolism
Development and progression
Genes
Genetic aspects
Health aspects
Host-virus relationships
Humans
Immune response
Immune system
Immunity
Infection
Infections
Infectious Diseases
Interferon
Life Sciences
Medical Microbiology
Microbiology
Parasitology
Proteins
Review
Review Article
Signal transduction
Ubiquitin
Ubiquitins - immunology
Ubiquitins - metabolism
Viral infections
Virology
Virus diseases
Virus Diseases - immunology
Virus Physiological Phenomena
Virus replication
Viruses - immunology
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Abstract The host response to viral infection includes the induction of type I interferons and the subsequent upregulation of hundreds of interferon-stimulated genes. Ubiquitin-like protein ISG15 is an interferon-induced protein that has been implicated as a central player in the host antiviral response. Over the past 15 years, efforts to understand how ISG15 protects the host during infection have revealed that its actions are diverse and pathogen-dependent. In this Review, we describe new insights into how ISG15 directly inhibits viral replication and discuss the recent finding that ISG15 modulates the host damage and repair response, immune response and other host signalling pathways. We also explore the viral immune-evasion strategies that counteract the actions of ISG15. These findings are integrated with a discussion of the recent identification of ISG15-deficient individuals and a cellular receptor for ISG15 that provides new insights into how ISG15 shapes the host response to viral infection. Ubiquitin-like protein ISG15 is an interferon-induced protein that has been implicated as a central player in the host antiviral response. In this Review, Perng and Lenschow provide new insights into how ISG15 restricts and shapes the host response to viral infection and the viral immune-evasion strategies that counteract ISG15.
AbstractList The host response to viral infection includes the induction of type I interferons and the subsequent upregulation of hundreds of interferon-stimulated genes. Ubiquitin-like protein ISG15 is an interferon-induced protein that has been implicated as a central player in the host antiviral response. Over the past 15 years, efforts to understand how ISG15 protects the host during infection have revealed that its actions are diverse and pathogen-dependent. In this Review, we describe new insights into how ISG15 directly inhibits viral replication and discuss the recent finding that ISG15 modulates the host damage and repair response, immune response and other host signalling pathways. We also explore the viral immune-evasion strategies that counteract the actions of ISG15. These findings are integrated with a discussion of the recent identification of ISG15-deficient individuals and a cellular receptor for ISG15 that provides new insights into how ISG15 shapes the host response to viral infection. Ubiquitin-like protein ISG15 is an interferon-induced protein that has been implicated as a central player in the host antiviral response. In this Review, Perng and Lenschow provide new insights into how ISG15 restricts and shapes the host response to viral infection and the viral immune-evasion strategies that counteract ISG15.
The host response to viral infection includes the induction of type I interferons and the subsequent upregulation of hundreds of interferon-stimulated genes. Ubiquitin-like protein ISG15 is an interferon-induced protein that has been implicated as a central player in the host antiviral response. Over the past 15 years, efforts to understand how ISG15 protects the host during infection have revealed that its actions are diverse and pathogen-dependent. In this Review, we describe new insights into how ISG15 directly inhibits viral replication and discuss the recent finding that ISG15 modulates the host damage and repair response, immune response and other host signalling pathways. We also explore the viral immune-evasion strategies that counteract the actions of ISG15. These findings are integrated with a discussion of the recent identification of ISG15-deficient individuals and a cellular receptor for ISG15 that provides new insights into how ISG15 shapes the host response to viral infection.
The host response to viral infection includes the induction of type I interferons and the subsequent upregulation of hundreds of interferon-stimulated genes. Ubiquitin-like protein ISG15 is an interferon-induced protein that has been implicated as a central player in the host antiviral response. Over the past 15 years, efforts to understand how ISG15 protects the host during infection have revealed that its actions are diverse and pathogen-dependent. In this Review, we describe new insights into how ISG15 directly inhibits viral replication and discuss the recent finding that ISG15 modulates the host damage and repair response, immune response and other host signalling pathways. We also explore the viral immune-evasion strategies that counteract the actions of ISG15. These findings are integrated with a discussion of the recent identification of ISG15-deficient individuals and a cellular receptor for ISG15 that provides new insights into how ISG15 shapes the host response to viral infection. Ubiquitin-like protein ISG15 is an interferon-induced protein that has been implicated as a central player in the host antiviral response. In this Review, Perng and Lenschow provide new insights into how ISG15 restricts and shapes the host response to viral infection and the viral immune-evasion strategies that counteract ISG15.
Audience Academic
Author Perng, Yi-Chieh
Lenschow, Deborah J.
Author_xml – sequence: 1
  givenname: Yi-Chieh
  surname: Perng
  fullname: Perng, Yi-Chieh
  organization: Department of Internal Medicine, Washington University School of Medicine
– sequence: 2
  givenname: Deborah J.
  surname: Lenschow
  fullname: Lenschow, Deborah J.
  email: dlenschow@wustl.edu
  organization: Department of Internal Medicine, Washington University School of Medicine, Department of Pathology and Immunology, Washington University School of Medicine
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29769653$$D View this record in MEDLINE/PubMed
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– name: Nature Publishing Group
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Snippet The host response to viral infection includes the induction of type I interferons and the subsequent upregulation of hundreds of interferon-stimulated genes....
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SubjectTerms 13
13/1
631/250/255/2514
631/326/596/2553
631/326/596/2557
82/58
Antiviral agents
Antiviral drugs
Biological response modifiers
Biomedical and Life Sciences
Care and treatment
Cell receptors
Cellular proteins
Cytokines - immunology
Cytokines - metabolism
Development and progression
Genes
Genetic aspects
Health aspects
Host-virus relationships
Humans
Immune response
Immune system
Immunity
Infection
Infections
Infectious Diseases
Interferon
Life Sciences
Medical Microbiology
Microbiology
Parasitology
Proteins
Review
Review Article
Signal transduction
Ubiquitin
Ubiquitins - immunology
Ubiquitins - metabolism
Viral infections
Virology
Virus diseases
Virus Diseases - immunology
Virus Physiological Phenomena
Virus replication
Viruses - immunology
Title ISG15 in antiviral immunity and beyond
URI https://link.springer.com/article/10.1038/s41579-018-0020-5
https://www.ncbi.nlm.nih.gov/pubmed/29769653
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https://search.proquest.com/docview/2040763825
https://pubmed.ncbi.nlm.nih.gov/PMC7097117
Volume 16
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