The DOI matches its Crossref record; 474 of the 474 references it cites were found in a registry or an index.
Antiviral Actions of Interferons
Open accessAbstract
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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“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).”
From The airway epithelium: soldier in the fight against respiratory viruses (2011) · cites this paper as [248]
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Metadata
- Authors
- Samuel, C. E.
- Affiliations
- University of California, Santa Barbara (US)
- Corresponding author
- Samuel, Charles E.
- ORCID
- Samuel, Charles E.
- Venue
- Clinical Microbiology Reviews
- Publisher
- American Society for Microbiology
- Published
- 2001-10
- Volume
- 14
- Issue
- 4
- Pages
- 778-809
- ISSN
- 0893-8512 (ISSN-L)
- 1098-6618
- PMC
- PMC89003
- 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
- green
- www.ncbi.nlm.nih.gov
- 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
- Life Sciences › Immunology and Microbiology › Immunology › 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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