The Causes and Consequences of Changes in Virulence following Pathogen Host Shifts
Identifieur interne : 001390 ( Pmc/Curation ); précédent : 001389; suivant : 001391The Causes and Consequences of Changes in Virulence following Pathogen Host Shifts
Auteurs : Ben Longdon [Royaume-Uni] ; Jarrod D. Hadfield [Royaume-Uni] ; Jonathan P. Day [Royaume-Uni] ; Sophia C. L. Smith [Royaume-Uni] ; John E. Mcgonigle [Royaume-Uni] ; Rodrigo Cogni [Royaume-Uni, Brésil] ; Chuan Cao [Royaume-Uni] ; Francis M. Jiggins [Royaume-Uni]Source :
- PLoS Pathogens [ 1553-7366 ] ; 2015.
Abstract
Emerging infectious diseases are often the result of a host shift, where the pathogen originates from a different host species. Virulence—the harm a pathogen does to its host—can be extremely high following a host shift (for example Ebola, HIV, and SARs), while other host shifts may go undetected as they cause few symptoms in the new host. Here we examine how virulence varies across host species by carrying out a large cross infection experiment using 48 species of Drosophilidae and an RNA virus. Host shifts resulted in dramatic variation in virulence, with benign infections in some species and rapid death in others. The change in virulence was highly predictable from the host phylogeny, with hosts clustering together in distinct clades displaying high or low virulence. High levels of virulence are associated with high viral loads, and this may determine the transmission rate of the virus.
Url:
DOI: 10.1371/journal.ppat.1004728
PubMed: 25774803
PubMed Central: 4361674
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Virulence—the harm a pathogen does to its host—can be extremely high following a host shift (for example Ebola, HIV, and SARs), while other host shifts may go undetected as they cause few symptoms in the new host. Here we examine how virulence varies across host species by carrying out a large cross infection experiment using 48 species of Drosophilidae and an RNA virus. Host shifts resulted in dramatic variation in virulence, with benign infections in some species and rapid death in others. The change in virulence was highly predictable from the host phylogeny, with hosts clustering together in distinct clades displaying high or low virulence. High levels of virulence are associated with high viral loads, and this may determine the transmission rate of the virus.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Jones, Ke" uniqKey="Jones K">KE Jones</name></author><author><name sortKey="Patel, Ng" uniqKey="Patel N">NG Patel</name></author><author><name sortKey="Levy, Ma" uniqKey="Levy M">MA Levy</name></author><author><name sortKey="Storeygard, A" uniqKey="Storeygard A">A Storeygard</name></author><author><name sortKey="Balk, D" uniqKey="Balk D">D Balk</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Woolhouse, Me" uniqKey="Woolhouse M">ME Woolhouse</name></author><author><name sortKey="Haydon, Dt" uniqKey="Haydon D">DT Haydon</name></author><author><name sortKey="Antia, R" uniqKey="Antia R">R Antia</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Leroy, Em" uniqKey="Leroy E">EM 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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, CA USA</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">25774803</article-id><article-id pub-id-type="pmc">4361674</article-id><article-id pub-id-type="doi">10.1371/journal.ppat.1004728</article-id><article-id pub-id-type="publisher-id">PPATHOGENS-D-14-02458</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>The Causes and Consequences of Changes in Virulence following Pathogen Host Shifts</article-title><alt-title alt-title-type="running-head">Virulence following 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="aff001"><sup>1</sup></xref><xref rid="cor001" ref-type="corresp">*</xref></contrib><contrib contrib-type="author"><name><surname>Hadfield</surname><given-names>Jarrod D.</given-names></name><xref ref-type="aff" rid="aff002"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Day</surname><given-names>Jonathan P.</given-names></name><xref ref-type="aff" rid="aff001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Smith</surname><given-names>Sophia C. L.</given-names></name><xref ref-type="aff" rid="aff001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>McGonigle</surname><given-names>John E.</given-names></name><xref ref-type="aff" rid="aff001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Cogni</surname><given-names>Rodrigo</given-names></name><xref ref-type="aff" rid="aff001"><sup>1</sup></xref><xref ref-type="aff" rid="aff003"><sup>3</sup></xref></contrib><contrib contrib-type="author"><name><surname>Cao</surname><given-names>Chuan</given-names></name><xref ref-type="aff" rid="aff001"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Jiggins</surname><given-names>Francis M.</given-names></name><xref ref-type="aff" rid="aff001"><sup>1</sup></xref></contrib></contrib-group><aff id="aff001"><label>1</label><addr-line>Department of Genetics, University of Cambridge, Cambridge, United Kingdom</addr-line></aff><aff id="aff002"><label>2</label><addr-line>Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, United Kingdom</addr-line></aff><aff id="aff003"><label>3</label><addr-line>Department of Ecology, University of São Paulo, São Paulo, Brazil</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"><addr-line>Stanford University, UNITED STATES</addr-line></aff><author-notes><fn fn-type="COI-statement" id="coi001"><p>The authors have declared that no competing interests exist.</p></fn><fn fn-type="con" id="contrib001"><p>Conceived and designed the experiments: BL. Performed the experiments: BL JPD SCLS. Analyzed the data: BL JDH FMJ. Wrote the paper: BL JDH FMJ. Assisted with experiments: RC JEM CC. Provided comments on manuscript: JPD SCLS RC JEM CC.</p></fn><corresp id="cor001">* E-mail: <email>b.longdon@gen.cam.ac.uk</email></corresp></author-notes><pub-date pub-type="epub"><day>16</day><month>3</month><year>2015</year></pub-date><pub-date pub-type="collection"><month>3</month><year>2015</year></pub-date><volume>11</volume><issue>3</issue><elocation-id>e1004728</elocation-id><history><date date-type="received"><day>13</day><month>10</month><year>2014</year></date><date date-type="accepted"><day>4</day><month>2</month><year>2015</year></date></history><permissions><copyright-statement>© 2015 Longdon et al</copyright-statement><copyright-year>2015</copyright-year><copyright-holder>Longdon et al</copyright-holder><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><self-uri content-type="pdf" xlink:type="simple" xlink:href="ppat.1004728.pdf"></self-uri><abstract><p>Emerging infectious diseases are often the result of a host shift, where the pathogen originates from a different host species. Virulence—the harm a pathogen does to its host—can be extremely high following a host shift (for example Ebola, HIV, and SARs), while other host shifts may go undetected as they cause few symptoms in the new host. Here we examine how virulence varies across host species by carrying out a large cross infection experiment using 48 species of Drosophilidae and an RNA virus. Host shifts resulted in dramatic variation in virulence, with benign infections in some species and rapid death in others. The change in virulence was highly predictable from the host phylogeny, with hosts clustering together in distinct clades displaying high or low virulence. High levels of virulence are associated with high viral loads, and this may determine the transmission rate of the virus.</p></abstract><abstract abstract-type="summary"><title>Author Summary</title><p>Many emerging infectious diseases are the result of a host shift, with the pathogen jumping into the new host from another species. Virulence—the harm a pathogen does to its host—can be extremely high following a host shift (for example HIV, SARs and Ebola), while other host shifts may go undetected as they cause few symptoms in the new host. We have found that variation in virulence following host shifts can be extremely large and were highly predictable from the host phylogeny, with hosts clustering together in distinct clades displaying high or low virulence. These changes in virulence result from changes in viral load, and therefore the transmission potential of the virus. This suggests there is no clear rule to predict whether a pathogen will be virulent in a novel host. However, it does suggest a simple rule of thumb may be that if a pathogen causes high levels of virulence in any given host species, it will typically cause similar levels of virulence in closely related hosts.</p></abstract><funding-group><funding-statement>BL and FMJ are supported by a NERC grant (NE/L004232/1), a European Research Council grant (281668, DrosophilaInfection), a Junior Research Fellowship from Christ’s College, Cambridge (BL) and a Royal Society University Research Fellowship (FMJ). JDH is supported by a Royal Society University Research Fellowship. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.</funding-statement></funding-group><counts><fig-count count="4"></fig-count><table-count count="0"></table-count><page-count count="18"></page-count></counts><custom-meta-group><custom-meta id="data-availability"><meta-name>Data Availability</meta-name><meta-value>All data is available in online repositories- sequence data is in Genbank (for accessions see table S2), figshare (<ext-link ext-link-type="uri" xlink:href="http://dx.doi.org/10.6084/m9.figshare.1192890">http://dx.doi.org/10.6084/m9.figshare.1192890</ext-link> and <ext-link ext-link-type="uri" xlink:href="http://dx.doi.org/10.6084/m9.figshare.1112749">http://dx.doi.org/10.6084/m9.figshare.1112749</ext-link>) or as supplementary materials.</meta-value></custom-meta></custom-meta-group></article-meta><notes><title>Data Availability</title><p>All data is available in online repositories- sequence data is in Genbank (for accessions see table S2), figshare (<ext-link ext-link-type="uri" xlink:href="http://dx.doi.org/10.6084/m9.figshare.1192890">http://dx.doi.org/10.6084/m9.figshare.1192890</ext-link> and <ext-link ext-link-type="uri" xlink:href="http://dx.doi.org/10.6084/m9.figshare.1112749">http://dx.doi.org/10.6084/m9.figshare.1112749</ext-link>) or as supplementary materials.</p></notes></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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