The dual role of innate immunity during influenza
Identifieur interne : 000F75 ( Ncbi/Merge ); précédent : 000F74; suivant : 000F76The dual role of innate immunity during influenza
Auteurs : Carmelo Biondo ; Germana Lentini ; Concetta Beninati ; Giuseppe TetiSource :
- Biomedical Journal [ 2319-4170 ] ; 2019.
Abstract
One of the distinguishing features of the 1918 pandemic is the occurrence of massive, potentially detrimental, activation of the innate immune system in critically ill patients. Whether this reflects an intrinsic capacity of the virus to induce an exaggerated inflammatory responses or its remarkable ability to reproduce
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DOI: 10.1016/j.bj.2018.12.009
PubMed: 30987709
PubMed Central: 6468094
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The dual role of innate immunity during influenza</title><author><name sortKey="Biondo, Carmelo" sort="Biondo, Carmelo" uniqKey="Biondo C" first="Carmelo" last="Biondo">Carmelo Biondo</name></author><author><name sortKey="Lentini, Germana" sort="Lentini, Germana" uniqKey="Lentini G" first="Germana" last="Lentini">Germana Lentini</name></author><author><name sortKey="Beninati, Concetta" sort="Beninati, Concetta" uniqKey="Beninati C" first="Concetta" last="Beninati">Concetta Beninati</name></author><author><name sortKey="Teti, Giuseppe" sort="Teti, Giuseppe" uniqKey="Teti G" first="Giuseppe" last="Teti">Giuseppe Teti</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">30987709</idno><idno type="pmc">6468094</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468094</idno><idno type="RBID">PMC:6468094</idno><idno type="doi">10.1016/j.bj.2018.12.009</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000D06</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000D06</idno><idno type="wicri:Area/Pmc/Curation">000D06</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000D06</idno><idno type="wicri:Area/Pmc/Checkpoint">000017</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000017</idno><idno type="wicri:Area/Ncbi/Merge">000F75</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The dual role of innate immunity during influenza</title><author><name sortKey="Biondo, Carmelo" sort="Biondo, Carmelo" uniqKey="Biondo C" first="Carmelo" last="Biondo">Carmelo Biondo</name></author><author><name sortKey="Lentini, Germana" sort="Lentini, Germana" uniqKey="Lentini G" first="Germana" last="Lentini">Germana Lentini</name></author><author><name sortKey="Beninati, Concetta" sort="Beninati, Concetta" uniqKey="Beninati C" first="Concetta" last="Beninati">Concetta Beninati</name></author><author><name sortKey="Teti, Giuseppe" sort="Teti, Giuseppe" uniqKey="Teti G" first="Giuseppe" last="Teti">Giuseppe Teti</name></author></analytic><series><title level="j">Biomedical Journal</title><idno type="ISSN">2319-4170</idno><idno type="eISSN">2320-2890</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>One of the distinguishing features of the 1918 pandemic is the occurrence of massive, potentially detrimental, activation of the innate immune system in critically ill patients. Whether this reflects an intrinsic capacity of the virus to induce an exaggerated inflammatory responses or its remarkable ability to reproduce <italic>in vivo</italic> is still open to debate. Tremendous progress has recently been made in our understanding of innate immune responses to influenza infection and it is now time to translate this knowledge into therapeutic strategies, particularly in view of the possible occurrence of future outbreaks caused by virulent strains.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Olive, C" uniqKey="Olive C">C. Olive</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Krammer, F" uniqKey="Krammer F">F. Krammer</name></author><author><name sortKey="Smith, G J D" uniqKey="Smith G">G.J.D. Smith</name></author><author><name sortKey="Fouchier, R A M" uniqKey="Fouchier R">R.A.M. Fouchier</name></author><author><name sortKey="Peiris, M" uniqKey="Peiris M">M. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Biomed J</journal-id><journal-id journal-id-type="iso-abbrev">Biomed J</journal-id><journal-title-group><journal-title>Biomedical Journal</journal-title></journal-title-group><issn pub-type="ppub">2319-4170</issn><issn pub-type="epub">2320-2890</issn><publisher><publisher-name>Chang Gung University</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">30987709</article-id><article-id pub-id-type="pmc">6468094</article-id><article-id pub-id-type="publisher-id">S2319-4170(18)30648-6</article-id><article-id pub-id-type="doi">10.1016/j.bj.2018.12.009</article-id><article-categories><subj-group subj-group-type="heading"><subject>Special Edition</subject></subj-group></article-categories><title-group><article-title>The dual role of innate immunity during influenza</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Biondo</surname><given-names>Carmelo</given-names></name></contrib><contrib contrib-type="author"><name><surname>Lentini</surname><given-names>Germana</given-names></name></contrib><contrib contrib-type="author"><name><surname>Beninati</surname><given-names>Concetta</given-names></name></contrib><contrib contrib-type="author"><name><surname>Teti</surname><given-names>Giuseppe</given-names></name><email>gioteti@mac.com</email><xref rid="cor1" ref-type="corresp">∗</xref></contrib></contrib-group><aff id="aff1">Metchnikoff Laboratory, University of Messina, Messina, Italy</aff><author-notes><corresp id="cor1"><label>∗</label><italic>Corresponding author</italic>. Metchnikoff Laboratory, University of Messina, Torre Biologica IIp, Policlinico Universitario, Via C. Valeria, 1, Messina, 98125, Italy. <email>gioteti@mac.com</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>20</day><month>3</month><year>2019</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on .</pmc-comment>
<pub-date pub-type="ppub"><month>2</month><year>2019</year></pub-date><pub-date pub-type="epub"><day>20</day><month>3</month><year>2019</year></pub-date><volume>42</volume><issue>1</issue><fpage>8</fpage><lpage>18</lpage><history><date date-type="received"><day>13</day><month>11</month><year>2018</year></date><date date-type="accepted"><day>20</day><month>12</month><year>2018</year></date></history><permissions><copyright-statement>© 2019 Chang Gung University. Publishing services by Elsevier B.V.</copyright-statement><copyright-year>2019</copyright-year><copyright-holder>Chang Gung University</copyright-holder><license license-type="CC BY-NC-ND" xlink:href="http://creativecommons.org/licenses/by-nc-nd/4.0/"><license-p>This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).</license-p></license></permissions><abstract id="abs0010"><p>One of the distinguishing features of the 1918 pandemic is the occurrence of massive, potentially detrimental, activation of the innate immune system in critically ill patients. Whether this reflects an intrinsic capacity of the virus to induce an exaggerated inflammatory responses or its remarkable ability to reproduce <italic>in vivo</italic> is still open to debate. Tremendous progress has recently been made in our understanding of innate immune responses to influenza infection and it is now time to translate this knowledge into therapeutic strategies, particularly in view of the possible occurrence of future outbreaks caused by virulent strains.</p></abstract><abstract abstract-type="teaser" id="abs0015"><p>We summarize here current knowledge of the mechanisms whereby the human body detects the presence of influenza virus infection, controls viral replication and repairs damaged tissue. We discuss the possibility of using this knowledge to treat patients with severe forms of the disease.</p></abstract><kwd-group id="kwrds0010"><title>Keywords</title><kwd>Toll-like receptors</kwd><kwd>RIG-I-like receptors</kwd><kwd>Interferon</kwd><kwd>Inflammasome</kwd><kwd>Inflammation</kwd></kwd-group></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Beninati, Concetta" sort="Beninati, Concetta" uniqKey="Beninati C" first="Concetta" last="Beninati">Concetta Beninati</name><name sortKey="Biondo, Carmelo" sort="Biondo, Carmelo" uniqKey="Biondo C" first="Carmelo" last="Biondo">Carmelo Biondo</name><name sortKey="Lentini, Germana" sort="Lentini, Germana" uniqKey="Lentini G" first="Germana" last="Lentini">Germana Lentini</name><name sortKey="Teti, Giuseppe" sort="Teti, Giuseppe" uniqKey="Teti G" first="Giuseppe" last="Teti">Giuseppe Teti</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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