Host Phylogeny Determines Viral Persistence and Replication in Novel Hosts
Identifieur interne : 001403 ( Pmc/Curation ); précédent : 001402; suivant : 001404Host Phylogeny Determines Viral Persistence and Replication in Novel Hosts
Auteurs : Ben Longdon [Royaume-Uni] ; Jarrod D. Hadfield [Royaume-Uni] ; Claire L. Webster [Royaume-Uni] ; Darren J. Obbard [Royaume-Uni] ; Francis M. Jiggins [Royaume-Uni]Source :
- PLoS Pathogens [ 1553-7366 ] ; 2011.
Abstract
Pathogens switching to new hosts can result in the emergence of new infectious diseases, and determining which species are likely to be sources of such host shifts is essential to understanding disease threats to both humans and wildlife. However, the factors that determine whether a pathogen can infect a novel host are poorly understood. We have examined the ability of three host-specific RNA-viruses (
Url:
DOI: 10.1371/journal.ppat.1002260
PubMed: 21966271
PubMed Central: 3178573
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Jiggins</name><affiliation wicri:level="1"><nlm:aff id="aff3"><addr-line>Department of Genetics, University of Cambridge, Cambridge, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Genetics, University of Cambridge, Cambridge</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">21966271</idno><idno type="pmc">3178573</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3178573</idno><idno type="RBID">PMC:3178573</idno><idno type="doi">10.1371/journal.ppat.1002260</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">001403</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">001403</idno><idno type="wicri:Area/Pmc/Curation">001403</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">001403</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Host Phylogeny Determines Viral Persistence and Replication in Novel Hosts</title><author><name sortKey="Longdon, Ben" sort="Longdon, Ben" uniqKey="Longdon B" first="Ben" last="Longdon">Ben Longdon</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Institute of Evolutionary Biology, University of Edinburgh, Ashworth Labs, Edinburgh, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Evolutionary Biology, University of Edinburgh, Ashworth Labs, Edinburgh</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><addr-line>Centre for Immunity, Infection and Evolution, University of Edinburgh, Ashworth Labs, Edinburgh, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Centre for Immunity, Infection and Evolution, University of Edinburgh, Ashworth Labs, Edinburgh</wicri:regionArea></affiliation></author><author><name sortKey="Hadfield, Jarrod D" sort="Hadfield, Jarrod D" uniqKey="Hadfield J" first="Jarrod D." last="Hadfield">Jarrod D. Hadfield</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Institute of Evolutionary Biology, University of Edinburgh, Ashworth Labs, Edinburgh, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Evolutionary Biology, University of Edinburgh, Ashworth Labs, Edinburgh</wicri:regionArea></affiliation></author><author><name sortKey="Webster, Claire L" sort="Webster, Claire L" uniqKey="Webster C" first="Claire L." last="Webster">Claire L. Webster</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Institute of Evolutionary Biology, University of Edinburgh, Ashworth Labs, Edinburgh, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Evolutionary Biology, University of Edinburgh, Ashworth Labs, Edinburgh</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><addr-line>Centre for Immunity, Infection and Evolution, University of Edinburgh, Ashworth Labs, Edinburgh, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Centre for Immunity, Infection and Evolution, University of Edinburgh, Ashworth Labs, Edinburgh</wicri:regionArea></affiliation></author><author><name sortKey="Obbard, Darren J" sort="Obbard, Darren J" uniqKey="Obbard D" first="Darren J." last="Obbard">Darren J. Obbard</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Institute of Evolutionary Biology, University of Edinburgh, Ashworth Labs, Edinburgh, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Institute of Evolutionary Biology, University of Edinburgh, Ashworth Labs, Edinburgh</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><addr-line>Centre for Immunity, Infection and Evolution, University of Edinburgh, Ashworth Labs, Edinburgh, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Centre for Immunity, Infection and Evolution, University of Edinburgh, Ashworth Labs, Edinburgh</wicri:regionArea></affiliation></author><author><name sortKey="Jiggins, Francis M" sort="Jiggins, Francis M" uniqKey="Jiggins F" first="Francis M." last="Jiggins">Francis M. Jiggins</name><affiliation wicri:level="1"><nlm:aff id="aff3"><addr-line>Department of Genetics, University of Cambridge, Cambridge, United Kingdom</addr-line></nlm:aff><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Genetics, University of Cambridge, Cambridge</wicri:regionArea></affiliation></author></analytic><series><title level="j">PLoS Pathogens</title><idno type="ISSN">1553-7366</idno><idno type="eISSN">1553-7374</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Pathogens switching to new hosts can result in the emergence of new infectious diseases, and determining which species are likely to be sources of such host shifts is essential to understanding disease threats to both humans and wildlife. However, the factors that determine whether a pathogen can infect a novel host are poorly understood. We have examined the ability of three host-specific RNA-viruses (<italic>Drosophila</italic> sigma viruses from the family <italic>Rhabdoviridae</italic>) to persist and replicate in 51 different species of Drosophilidae. Using a novel analytical approach we found that the host phylogeny could explain most of the variation in viral replication and persistence between different host species. This effect is partly driven by viruses reaching a higher titre in those novel hosts most closely related to the original host. However, there is also a strong effect of host phylogeny that is independent of the distance from the original host, with viral titres being similar in groups of related hosts. Most of this effect could be explained by variation in general susceptibility to all three sigma viruses, as there is a strong phylogenetic correlation in the titres of the three viruses. These results suggest that the source of new emerging diseases may often be predictable from the host phylogeny, but that the effect may be more complex than simply causing most host shifts to occur between closely related hosts.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Hahn, Bh" uniqKey="Hahn B">BH Hahn</name></author><author><name sortKey="Shaw, Gm" uniqKey="Shaw G">GM Shaw</name></author><author><name sortKey="De Cock, Km" uniqKey="De Cock K">KM De Cock</name></author><author><name sortKey="Sharp, Pm" uniqKey="Sharp P">PM Sharp</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Webby, Rj" uniqKey="Webby R">RJ Webby</name></author><author><name sortKey="Webster, Rg" uniqKey="Webster R">RG Webster</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, Wm" uniqKey="Liu W">WM Liu</name></author><author><name sortKey="Li, Yy" uniqKey="Li Y">YY 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<front><journal-meta><journal-id journal-id-type="nlm-ta">PLoS Pathog</journal-id><journal-id journal-id-type="iso-abbrev">PLoS Pathog</journal-id><journal-id journal-id-type="publisher-id">plos</journal-id><journal-id journal-id-type="pmc">plospath</journal-id><journal-title-group><journal-title>PLoS Pathogens</journal-title></journal-title-group><issn pub-type="ppub">1553-7366</issn><issn pub-type="epub">1553-7374</issn><publisher><publisher-name>Public Library of Science</publisher-name><publisher-loc>San Francisco, USA</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">21966271</article-id><article-id pub-id-type="pmc">3178573</article-id><article-id pub-id-type="publisher-id">PPATHOGENS-D-11-00774</article-id><article-id pub-id-type="doi">10.1371/journal.ppat.1002260</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="Discipline-v2"><subject>Biology</subject><subj-group><subject>Evolutionary Biology</subject></subj-group></subj-group><subj-group subj-group-type="Discipline-v2"><subject>Medicine</subject><subj-group><subject>Epidemiology</subject></subj-group></subj-group></article-categories><title-group><article-title>Host Phylogeny Determines Viral Persistence and Replication in Novel Hosts</article-title><alt-title alt-title-type="running-head">Phylogenetic Determinants of Host Shifts</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Longdon</surname><given-names>Ben</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib><contrib contrib-type="author"><name><surname>Hadfield</surname><given-names>Jarrod D.</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Webster</surname><given-names>Claire L.</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib contrib-type="author" equal-contrib="yes"><name><surname>Obbard</surname><given-names>Darren J.</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib contrib-type="author" equal-contrib="yes"><name><surname>Jiggins</surname><given-names>Francis M.</given-names></name><xref ref-type="aff" rid="aff3"><sup>3</sup></xref></contrib></contrib-group><aff id="aff1"><label>1</label><addr-line>Institute of Evolutionary Biology, University of Edinburgh, Ashworth Labs, Edinburgh, United Kingdom</addr-line></aff><aff id="aff2"><label>2</label><addr-line>Centre for Immunity, Infection and Evolution, University of Edinburgh, Ashworth Labs, Edinburgh, United Kingdom</addr-line></aff><aff id="aff3"><label>3</label><addr-line>Department of Genetics, University of Cambridge, Cambridge, United Kingdom</addr-line></aff><contrib-group><contrib contrib-type="editor"><name><surname>Schneider</surname><given-names>David S.</given-names></name><role>Editor</role><xref ref-type="aff" rid="edit1"></xref></contrib></contrib-group><aff id="edit1">Stanford University, United States of America</aff><author-notes><corresp id="cor1">* E-mail: <email>B.Longdon@ed.ac.uk</email></corresp><fn fn-type="con"><p>Conceived and designed the experiments: BL DJO FMJ. Performed the experiments: BL CLW DJO. Analyzed the data: BL FMJ DJO JDH. Contributed reagents/materials/analysis tools: BL FMJ DJO JDH. Wrote the paper: BL FMJ DJO JDH CLW. Fly rearing, injections, molecular work: BL. Fly rearing and sorting: CLW DJO.</p></fn></author-notes><pub-date pub-type="collection"><month>9</month><year>2011</year></pub-date><pub-date pub-type="epub"><day>22</day><month>9</month><year>2011</year></pub-date><volume>7</volume><issue>9</issue><elocation-id>e1002260</elocation-id><history><date date-type="received"><day>14</day><month>4</month><year>2011</year></date><date date-type="accepted"><day>25</day><month>7</month><year>2011</year></date></history><permissions><copyright-statement>Longdon et al.</copyright-statement><copyright-year>2011</copyright-year><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.</license-p></license></permissions><abstract><p>Pathogens switching to new hosts can result in the emergence of new infectious diseases, and determining which species are likely to be sources of such host shifts is essential to understanding disease threats to both humans and wildlife. However, the factors that determine whether a pathogen can infect a novel host are poorly understood. We have examined the ability of three host-specific RNA-viruses (<italic>Drosophila</italic> sigma viruses from the family <italic>Rhabdoviridae</italic>) to persist and replicate in 51 different species of Drosophilidae. Using a novel analytical approach we found that the host phylogeny could explain most of the variation in viral replication and persistence between different host species. This effect is partly driven by viruses reaching a higher titre in those novel hosts most closely related to the original host. However, there is also a strong effect of host phylogeny that is independent of the distance from the original host, with viral titres being similar in groups of related hosts. Most of this effect could be explained by variation in general susceptibility to all three sigma viruses, as there is a strong phylogenetic correlation in the titres of the three viruses. These results suggest that the source of new emerging diseases may often be predictable from the host phylogeny, but that the effect may be more complex than simply causing most host shifts to occur between closely related hosts.</p></abstract><abstract abstract-type="summary"><title>Author Summary</title><p>Emerging infectious diseases such as SARS, HIV and swine-origin influenza have all been recently acquired by humans from other species. Understanding the reasons why parasites jump between different host species is essential to allow us to predict future threats and understand the causes of disease emergence. Here we ask how host-relatedness might determine when host-shifts can occur in the most important group of emerging diseases—RNA viruses. We show that the relationship between host species is the primary factor in determining a virus's ability to persist and replicate in a novel host following exposure. This can be broken down into two components. Firstly, species closely related to the virus's natural host are more susceptible than distantly related species. Secondly, independent of the distance effect, groups of closely related host species have similar levels of susceptibility. This has important implications for our understanding of disease-emergence, and until now the only large-scale studies of viruses have been correlative rather than experimental. We also found groups of related species that are susceptible to these viruses but are distantly related to the natural hosts, which may explain why viruses sometimes jump between distantly related species.</p></abstract><counts><page-count count="9"></page-count></counts></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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