Legacy of the influenza pandemic 1918: Introduction
Identifieur interne : 000475 ( Pmc/Corpus ); précédent : 000474; suivant : 000476Legacy of the influenza pandemic 1918: Introduction
Auteurs : Siamon GordonSource :
- Biomedical Journal [ 2319-4170 ] ; 2019.
Url:
DOI: 10.1016/j.bj.2019.01.006
PubMed: 30987705
PubMed Central: 6468111
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Legacy of the influenza pandemic 1918: Introduction</title><author><name sortKey="Gordon, Siamon" sort="Gordon, Siamon" uniqKey="Gordon S" first="Siamon" last="Gordon">Siamon Gordon</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">30987705</idno><idno type="pmc">6468111</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6468111</idno><idno type="RBID">PMC:6468111</idno><idno type="doi">10.1016/j.bj.2019.01.006</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000475</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000475</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Legacy of the influenza pandemic 1918: Introduction</title><author><name sortKey="Gordon, Siamon" sort="Gordon, Siamon" uniqKey="Gordon S" first="Siamon" last="Gordon">Siamon Gordon</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></TEI><pmc article-type="editorial"><pmc-dir>properties open_access</pmc-dir>
<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">30987705</article-id><article-id pub-id-type="pmc">6468111</article-id><article-id pub-id-type="publisher-id">S2319-4170(19)30034-4</article-id><article-id pub-id-type="doi">10.1016/j.bj.2019.01.006</article-id><article-categories><subj-group subj-group-type="heading"><subject>Special Edition</subject></subj-group></article-categories><title-group><article-title>Legacy of the influenza pandemic 1918: Introduction</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Gordon</surname><given-names>Siamon</given-names></name><email>siamon.gordon@path.ox.ac.uk</email><xref rid="cor1" ref-type="corresp">∗</xref></contrib></contrib-group><aff id="aff1">Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan</aff><aff id="aff2">Exeter College Emeritus Fellow in Pathology, and Emeritus GlaxoWellcome Professor of Cellular Pathology, University of Oxford, UK</aff><author-notes><corresp id="cor1"><label>∗</label><italic>Corresponding author</italic>. Graduate Institute of Biomedical Sciences, Chang Gung University, 259, Wenhua 1st Rd., Gueishan, Taoyuan 333, Taiwan. <email>siamon.gordon@path.ox.ac.uk</email></corresp></author-notes><pub-date pub-type="pmc-release"><day>28</day><month>2</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>28</day><month>2</month><year>2019</year></pub-date><volume>42</volume><issue>1</issue><fpage>5</fpage><lpage>7</lpage><history><date date-type="received"><day>18</day><month>1</month><year>2019</year></date><date date-type="accepted"><day>18</day><month>1</month><year>2019</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><kwd-group id="kwrds0010"><title>Keywords</title><kwd>Influenza</kwd><kwd>Pandemic anniversary</kwd><kwd>Immunity</kwd></kwd-group></article-meta></front><body><p id="p0010">This guest edited issue contains the articles follow the earlier group of articles to mark the centennial of the influenza pandemic which swept the world in 1918, continuing into the following year. The following section provides brief personal background, perspectives and references provided by the two corresponding authors.<boxed-text id="dtbox1"><caption><title>Carmelo Biondo, Germana Lentini, Concetta Beninati, Giuseppe Teti: The dual role of innate immunity during influenza</title></caption><p id="p0015"><fig id="undfig1"><alt-text id="alttext0010">Image 1</alt-text><graphic xlink:href="fx1"></graphic></fig></p><p id="p0040">Giuseppe Teti is currently acting as Scientific Director of Scylla Biotech S.r.l, a spin off of the University of Messina, Messina, Italy involved in research on innate immunity, epitope mapping and vaccine development. A native of Naples, Italy, he obtained his medical degree at the Catholic University of Rome and worked for several years in microbiology and basic immunology at the Medical University of South Carolina in Charleston, South Carolina. He later worked at the University of Messina as Professor of Medical Microbiology.</p><p id="p0045">Our understanding of the mechanisms underlying host defence against infection continues to grow at a fast pace and it is time now to consider how we can apply this knowledge to control influenza and the associated secondary bacterial infections, which still represent a major public health problem. Drs Biondo, Lentini, Beninati and Teti are interested in how the innate immune system recognizes extracellular bacteria, such as those causing secondary infections during influenza, and in identifying the major arms of the host defence system that are predominantly involved in clearing these infections <xref rid="bib1" ref-type="bibr">[1]</xref>, <xref rid="bib2" ref-type="bibr">[2]</xref>. They are now studying how previous exposure to influenza virus affects subsequent anti-bacterial activities. In the context of this broad field, Drs Biondo, Lentini, Beninati and Teti are particularly focusing on the role of nucleic acid-sensing Toll-like receptors in inducing type I interferons <xref rid="bib1" ref-type="bibr">[1]</xref>, <xref rid="bib3" ref-type="bibr">[3]</xref> and interleukin-1 beta <xref rid="bib4" ref-type="bibr">[4]</xref>, <xref rid="bib5" ref-type="bibr">[5]</xref> responses and in activating neutrophils <xref rid="bib6" ref-type="bibr">[6]</xref>, <xref rid="bib7" ref-type="bibr">[7]</xref>. While type I interferons have been traditionally viewed as playing a major role in anti-viral defences only, it was recently found that inferferon beta production occurs very early during bacterial infection and is crucial for priming phagocytes for increased antibacterial activity <xref rid="bib8" ref-type="bibr">[8]</xref>. Drs Biondo, Lentini, Beninati and Teti are currently based at the Metchnikoff Laboratory, a public-private research unit hosted by the University of Messina in Messina, Italy.</p><ref-list id="cebib0010"><title>References</title><ref id="bib1"><label>1</label><element-citation publication-type="journal" id="sref1"><person-group person-group-type="author"><name><surname>Signorino</surname><given-names>G.</given-names></name><name><surname>Mohammadi</surname><given-names>N.</given-names></name><name><surname>Patane</surname><given-names>F.</given-names></name><name><surname>Buscetta</surname><given-names>M.</given-names></name><name><surname>Venza</surname><given-names>M.</given-names></name><name><surname>Venza</surname><given-names>I.</given-names></name></person-group><article-title>Role of toll-like receptor 13 in innate immune recognition of group B streptococci</article-title><source>Infect 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person-group-type="author"><name><surname>Mancuso</surname><given-names>G.</given-names></name><name><surname>Midiri</surname><given-names>A.</given-names></name><name><surname>Biondo</surname><given-names>C.</given-names></name><name><surname>Beninati</surname><given-names>C.</given-names></name><name><surname>Zummo</surname><given-names>S.</given-names></name><name><surname>Galbo</surname><given-names>R.</given-names></name></person-group><article-title>Type I IFN signaling is crucial for host resistance against different species of pathogenic bacteria</article-title><source>J Immunol</source><volume>178</volume><year>2007</year><fpage>3126</fpage><lpage>3133</lpage><pub-id pub-id-type="pmid">17312160</pub-id></element-citation></ref></ref-list></boxed-text></p><p id="p0050"><boxed-text id="dtbox2"><caption><title>Dannielle Wellington and Tao Dong: IFITM3: How genetics influence Influenza infection demographically</title></caption><p id="p0055"><fig id="undfig5"><alt-text id="alttext0030">Image 5</alt-text><graphic xlink:href="fx2"></graphic></fig></p><p id="p0070">Tao Dong is a Professor of Immunology at the MRC Human Immunology Unit and founding director (Oxford) of CAMS-Oxford Institute and Director of Center for translational Immunology, Oxford University and Senior Fellow in University College. She gained a BSc (Physiology) from Fudan University, Shanghai, China in 1987 and D. Phil in Oxford University in 1998.</p><p id="p0075">Tao Dong's main research interest is to understand the key factors required for efficient viral control by the T cell response in a number of different viral infections and cancer, with the aim to augment and control the immune response as a way of improving the outcome in several important human diseases. Her group has uncovered novel mechanisms by which virus and host (HLA) genetic variation controls antigen processing and presentation to T cells, and also described how host genetic variation has an impact on HIV virus evolution and Influenza virus infection such as IFITM3.</p><p id="p0080">The role of host genetic variability in the susceptibility to influenza virus has not been widely investigated due to the influence of confounding factors and a lack of conclusive association between the host and virus. However, following reports of a single nucleotide polymorphism within the anti-viral protein IFITM3 <xref rid="bib9" ref-type="bibr">[1]</xref>, Prof. Tao Dong decided to investigate the association of this SNP, rs12252, with influenza in a Chinese cohort <xref rid="bib10" ref-type="bibr">[2]</xref>. They found a significant association between the development of severe influenza and homozygosity for the minor allele <italic>C</italic>. Consequently, this association has been confirmed in further studies <xref rid="bib11" ref-type="bibr">[3]</xref>. The <italic>IFITM3</italic> rs12252-CC genotype is only common in Asian populations, suggesting that genetic variation of the host is confounded by ethnic background <xref rid="bib12" ref-type="bibr">[4]</xref>. The mechanism of how the synonymous SNP rs12252 alters IFITM3 viral restriction is still unknown and a key focus of the research by Prof. Dong and a postdoctoral fellow Dr Dannielle Wellington. In this review they explain the role of host genetic variation in influenza infection severity with a focus on the role IFITM3 plays, summarising what is known about IFITM3 and the open questions that surround this important anti-viral protein.</p><ref-list id="fread0010"><title>References</title><ref id="bib9"><label>1</label><element-citation publication-type="journal" id="sref9"><person-group person-group-type="author"><name><surname>Everitt</surname><given-names>A.R.</given-names></name><name><surname>Clare</surname><given-names>S.</given-names></name><name><surname>Pertel</surname><given-names>T.</given-names></name><name><surname>John</surname><given-names>S.P.</given-names></name><name><surname>Wash</surname><given-names>R.S.</given-names></name><name><surname>Smith</surname><given-names>S.E.</given-names></name></person-group><article-title>IFITM3 restricts the morbidity and mortality associated with influenza</article-title><source>Nature</source><volume>484</volume><year>2012</year><fpage>519</fpage><lpage>523</lpage><pub-id pub-id-type="pmid">22446628</pub-id></element-citation></ref><ref id="bib10"><label>2</label><element-citation publication-type="journal" id="sref10"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>Y.H.</given-names></name><name><surname>Zhao</surname><given-names>Y.</given-names></name><name><surname>Li</surname><given-names>N.</given-names></name><name><surname>Peng</surname><given-names>Y.C.</given-names></name><name><surname>Giannoulatou</surname><given-names>E.</given-names></name><name><surname>Jin</surname><given-names>R.H.</given-names></name></person-group><article-title>Interferon-induced transmembrane protein-3 genetic variant rs12252-C is associated with severe influenza in Chinese individuals</article-title><source>Nat Commun</source><volume>4</volume><year>2013</year><fpage>1418</fpage><pub-id pub-id-type="pmid">23361009</pub-id></element-citation></ref><ref id="bib11"><label>3</label><element-citation publication-type="journal" id="sref11"><person-group person-group-type="author"><name><surname>Prabhu</surname><given-names>S.S.</given-names></name><name><surname>Chakraborty</surname><given-names>T.T.</given-names></name><name><surname>Kumar</surname><given-names>N.</given-names></name><name><surname>Banerjee</surname><given-names>I.</given-names></name></person-group><article-title>Association between IFITM3 rs12252 polymorphism and influenza susceptibility and severity: a meta-analysis</article-title><source>Gene</source><volume>674</volume><year>2018</year><fpage>70</fpage><lpage>79</lpage><pub-id pub-id-type="pmid">29940276</pub-id></element-citation></ref><ref id="bib12"><label>4</label><element-citation publication-type="journal" id="sref12"><person-group person-group-type="author"><name><surname>Zerbino</surname><given-names>D.R.</given-names></name><name><surname>Achuthan</surname><given-names>P.</given-names></name><name><surname>Akanni</surname><given-names>W.</given-names></name><name><surname>Amode</surname><given-names>M.R.</given-names></name><name><surname>Barrell</surname><given-names>D.</given-names></name><name><surname>Bhai</surname><given-names>J.</given-names></name></person-group><article-title>Ensembl 2018</article-title><source>Nucleic Acids Res</source><volume>46</volume><year>2018</year><fpage>D754</fpage><lpage>D761</lpage><pub-id pub-id-type="pmid">29155950</pub-id></element-citation></ref></ref-list></boxed-text></p></body><back><fn-group><fn id="d31e14"><p id="ntpara0010p">Peer review under responsibility of Chang Gung University.</p></fn></fn-group></back></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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