IFITM-Family Proteins: The Cell's First Line of Antiviral Defense.
Identifieur interne : 001635 ( Main/Exploration ); précédent : 001634; suivant : 001636IFITM-Family Proteins: The Cell's First Line of Antiviral Defense.
Auteurs : Charles C. Bailey [États-Unis] ; Guocai Zhong [États-Unis] ; I-Chueh Huang [États-Unis] ; Michael Farzan [États-Unis]Source :
- Annual review of virology [ 2327-056X ] ; 2014.
Abstract
Animal cells use a wide variety of mechanisms to slow or prevent replication of viruses. These mechanisms are usually mediated by antiviral proteins whose expression and activities can be constitutive but are frequently amplified by interferon induction. Among these interferon-stimulated proteins, members of the IFITM (interferon-induced transmembrane) family are unique because they prevent infection before a virus can traverse the lipid bilayer of the cell. At least three human IFITM proteins-IFITM1, IFITM2, and IFITM3-have antiviral activities. These activities limit infection in cultured cells by many viruses, including dengue virus, Ebola virus, influenza A virus, severe acute respiratory syndrome coronavirus, and West Nile virus. Murine Ifitm3 controls influenza A virus infection in vivo, and polymorphisms in human IFITM3 correlate with the severity of both seasonal and highly pathogenic avian influenza virus. Here we review the discovery and characterization of the IFITM proteins, describe the spectrum of their antiviral activities, and discuss potential mechanisms underlying these effects.
DOI: 10.1146/annurev-virology-031413-085537
PubMed: 25599080
Affiliations:
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Bailey</name><affiliation wicri:level="2"><nlm:affiliation>Department of Infectious Diseases, The Scripps Research Institute, Jupiter, Florida 33458.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Floride</region></placeName><wicri:cityArea>Department of Infectious Diseases, The Scripps Research Institute, Jupiter</wicri:cityArea></affiliation></author><author><name sortKey="Zhong, Guocai" sort="Zhong, Guocai" uniqKey="Zhong G" first="Guocai" last="Zhong">Guocai Zhong</name><affiliation wicri:level="2"><nlm:affiliation>Department of Infectious Diseases, The Scripps Research Institute, Jupiter, Florida 33458.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Floride</region></placeName><wicri:cityArea>Department of Infectious Diseases, The Scripps Research Institute, Jupiter</wicri:cityArea></affiliation></author><author><name sortKey="Huang, I Chueh" sort="Huang, I Chueh" uniqKey="Huang I" first="I-Chueh" last="Huang">I-Chueh Huang</name><affiliation wicri:level="2"><nlm:affiliation>Department of Cell Biology and Neuroscience, College of Natural and Agricultural Sciences, University of California, Riverside, California 92521.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Californie</region></placeName><wicri:cityArea>Department of Cell Biology and Neuroscience, College of Natural and Agricultural Sciences, University of California, Riverside</wicri:cityArea></affiliation></author><author><name sortKey="Farzan, Michael" sort="Farzan, Michael" uniqKey="Farzan M" first="Michael" last="Farzan">Michael Farzan</name><affiliation wicri:level="2"><nlm:affiliation>Department of Infectious Diseases, The Scripps Research Institute, Jupiter, Florida 33458.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Floride</region></placeName><wicri:cityArea>Department of Infectious Diseases, The Scripps Research Institute, Jupiter</wicri:cityArea></affiliation></author></analytic><series><title level="j">Annual review of virology</title><idno type="ISSN">2327-056X</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Animal cells use a wide variety of mechanisms to slow or prevent replication of viruses. These mechanisms are usually mediated by antiviral proteins whose expression and activities can be constitutive but are frequently amplified by interferon induction. Among these interferon-stimulated proteins, members of the IFITM (interferon-induced transmembrane) family are unique because they prevent infection before a virus can traverse the lipid bilayer of the cell. At least three human IFITM proteins-IFITM1, IFITM2, and IFITM3-have antiviral activities. These activities limit infection in cultured cells by many viruses, including dengue virus, Ebola virus, influenza A virus, severe acute respiratory syndrome coronavirus, and West Nile virus. Murine Ifitm3 controls influenza A virus infection in vivo, and polymorphisms in human <i>IFITM3</i> correlate with the severity of both seasonal and highly pathogenic avian influenza virus. Here we review the discovery and characterization of the IFITM proteins, describe the spectrum of their antiviral activities, and discuss potential mechanisms underlying these effects.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li><li>Floride</li></region></list><tree><country name="États-Unis"><region name="Floride"><name sortKey="Bailey, Charles C" sort="Bailey, Charles C" uniqKey="Bailey C" first="Charles C" last="Bailey">Charles C. Bailey</name></region><name sortKey="Farzan, Michael" sort="Farzan, Michael" uniqKey="Farzan M" first="Michael" last="Farzan">Michael Farzan</name><name sortKey="Huang, I Chueh" sort="Huang, I Chueh" uniqKey="Huang I" first="I-Chueh" last="Huang">I-Chueh Huang</name><name sortKey="Zhong, Guocai" sort="Zhong, Guocai" uniqKey="Zhong G" first="Guocai" last="Zhong">Guocai Zhong</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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