Cited by 2,743interferon and immune responsesCytokine Signaling Pathways and InteractionsImmune Response and Inflammation

Antiviral Actions of Interferons

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Samuel, Charles E.·2001·Clinical Microbiology Reviews

Abstract

SUMMARY: 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-α, IFN-β, and IFN-γ, 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.

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Crossref · 10.1128/cmr.14.4.778-809.2001

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  • NO inhibits rhinovirus replication and virus-induced cytokine expression through inhibition of IRF-1 and NF-kB pathways in airway epithelial cells.

    “NO inhibits rhinovirus replication and virus-induced cytokine expression through inhibition of IRF-1 and NF-κB pathways in airway epithelial cells (146, 247), but other transcription factors may be involved (248).”

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  1. [4]Alberts B, Bray D, Lewis J, Raff M, Roberts K, Watson J D. Molecular biology of the cell. 3rd ed. New York, N.Y: Garland Publishing; 1994. [Google Scholar]
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Authors
Samuel, C. E.
Affiliations
University of California, Santa Barbara (US)
Corresponding author
Samuel, Charles E.
Venue
Clinical Microbiology Reviews
Published
2001-10
Volume
14
Issue
4
Pages
778-809
ISSN
  • 0893-8512 (ISSN-L)
  • 1098-6618
OpenAlex
W2160063406
Cited by
2,743
References
474
Citations by year
2026: 42 · 2025: 64 · 2024: 81 · 2023: 93 · 2022: 105 · 2021: 157 · 2020: 166 · 2019: 67 · 2018: 60 · 2017: 61 · 2016: 78 · 2015: 89 · 2014: 116 · 2013: 108 · 2012: 140
FWCI
7.18
Type
journal article
Language
en
Open access
Locations
  • Clinical Microbiology Reviews (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Allergy and Infectious Diseases (AI-20611, R01AI012520, AI 12520, R37AI012520, R01AI020611)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
interferon, antiviral mechanism, interferon-induced proteins, PKR, 2',5'-oligoadenylate synthetase, RNase L, ADAR1, double-stranded RNA, inducible nitric oxide synthase, MHC class I and II, JAK/STAT signaling, interferon receptor, interferon-gamma, host-virus interaction, interferon therapy
MeSH terms
Antiviral Agents, Humans, Interferons, Virus Diseases, Signal Transduction, Transcriptional Activation, Apoptosis, Receptors, Interferon

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