The causes and consequences of changes in virulence following pathogen host shifts.
Identifieur interne : 000D38 ( PubMed/Checkpoint ); précédent : 000D37; suivant : 000D39The 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 [Brésil] ; Chuan Cao [Royaume-Uni] ; Francis M. Jiggins [Royaume-Uni]Source :
- PLoS pathogens [ 1553-7374 ] ; 2015.
Descripteurs français
- KwdFr :
- MESH :
- génétique : Drosophila, Spécificité d'hôte, Virulence.
- pathogénicité : Virus à ARN.
- virologie : Drosophila.
- Animaux, Charge virale, Phylogénie, RT-PCR.
English descriptors
- KwdEn :
- MESH :
- genetics : Drosophila, Host Specificity, Virulence.
- pathogenicity : RNA Viruses.
- virology : Drosophila.
- Animals, Phylogeny, Reverse Transcriptase Polymerase Chain Reaction, Viral Load.
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.
DOI: 10.1371/journal.ppat.1004728
PubMed: 25774803
Affiliations:
- Brésil, Royaume-Uni
- Angleterre, Angleterre de l'Est, Écosse, État de São Paulo
- Cambridge, São Paulo, Édimbourg
- Université d'Édimbourg, Université de Cambridge
Links toward previous steps (curation, corpus...)
Links to Exploration step
pubmed:25774803Le document en format XML
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Jiggins</name><affiliation wicri:level="4"><nlm:affiliation>Department of Genetics, University of Cambridge, Cambridge, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Genetics, University of Cambridge, Cambridge</wicri:regionArea><orgName type="university">Université de Cambridge</orgName><placeName><settlement type="city">Cambridge</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Angleterre de l'Est</region></placeName></affiliation></author></analytic><series><title level="j">PLoS pathogens</title><idno type="eISSN">1553-7374</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Drosophila (genetics)</term><term>Drosophila (virology)</term><term>Host Specificity (genetics)</term><term>Phylogeny</term><term>RNA Viruses (pathogenicity)</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Viral Load</term><term>Virulence (genetics)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Charge virale</term><term>Drosophila (génétique)</term><term>Drosophila (virologie)</term><term>Phylogénie</term><term>RT-PCR</term><term>Spécificité d'hôte (génétique)</term><term>Virulence (génétique)</term><term>Virus à ARN (pathogénicité)</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Drosophila</term><term>Host Specificity</term><term>Virulence</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Drosophila</term><term>Spécificité d'hôte</term><term>Virulence</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>RNA Viruses</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus à ARN</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Drosophila</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Drosophila</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Phylogeny</term><term>Reverse Transcriptase Polymerase Chain Reaction</term><term>Viral Load</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Charge virale</term><term>Phylogénie</term><term>RT-PCR</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25774803</PMID><DateCompleted><Year>2015</Year><Month>07</Month><Day>31</Day></DateCompleted><DateRevised><Year>2019</Year><Month>02</Month><Day>02</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1553-7374</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><Issue>3</Issue><PubDate><Year>2015</Year><Month>Mar</Month></PubDate></JournalIssue><Title>PLoS pathogens</Title><ISOAbbreviation>PLoS Pathog.</ISOAbbreviation></Journal><ArticleTitle>The causes and consequences of changes in virulence following pathogen host shifts.</ArticleTitle><Pagination><MedlinePgn>e1004728</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.ppat.1004728</ELocationID><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Longdon</LastName><ForeName>Ben</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Genetics, University of Cambridge, Cambridge, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hadfield</LastName><ForeName>Jarrod D</ForeName><Initials>JD</Initials><AffiliationInfo><Affiliation>Institute of Evolutionary Biology, University of Edinburgh, Edinburgh, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Day</LastName><ForeName>Jonathan P</ForeName><Initials>JP</Initials><AffiliationInfo><Affiliation>Department of Genetics, University of Cambridge, Cambridge, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smith</LastName><ForeName>Sophia C L</ForeName><Initials>SC</Initials><AffiliationInfo><Affiliation>Department of Genetics, University of Cambridge, Cambridge, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>McGonigle</LastName><ForeName>John E</ForeName><Initials>JE</Initials><AffiliationInfo><Affiliation>Department of Genetics, University of Cambridge, Cambridge, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cogni</LastName><ForeName>Rodrigo</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Genetics, University of Cambridge, Cambridge, United Kingdom; Department of Ecology, University of São Paulo, São Paulo, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cao</LastName><ForeName>Chuan</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Genetics, University of Cambridge, Cambridge, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jiggins</LastName><ForeName>Francis M</ForeName><Initials>FM</Initials><AffiliationInfo><Affiliation>Department of Genetics, University of Cambridge, Cambridge, United Kingdom.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>03</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS Pathog</MedlineTA><NlmUniqueID>101238921</NlmUniqueID><ISSNLinking>1553-7366</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004330" MajorTopicYN="N">Drosophila</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D058507" MajorTopicYN="N">Host Specificity</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010802" MajorTopicYN="N">Phylogeny</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012328" MajorTopicYN="N">RNA Viruses</DescriptorName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019562" MajorTopicYN="N">Viral Load</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName><QualifierName UI="Q000235" 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Chuan" uniqKey="Cao C" first="Chuan" last="Cao">Chuan Cao</name><name sortKey="Day, Jonathan P" sort="Day, Jonathan P" uniqKey="Day J" first="Jonathan P" last="Day">Jonathan P. Day</name><name sortKey="Hadfield, Jarrod D" sort="Hadfield, Jarrod D" uniqKey="Hadfield J" first="Jarrod D" last="Hadfield">Jarrod D. Hadfield</name><name sortKey="Jiggins, Francis M" sort="Jiggins, Francis M" uniqKey="Jiggins F" first="Francis M" last="Jiggins">Francis M. Jiggins</name><name sortKey="Mcgonigle, John E" sort="Mcgonigle, John E" uniqKey="Mcgonigle J" first="John E" last="Mcgonigle">John E. Mcgonigle</name><name sortKey="Smith, Sophia C L" sort="Smith, Sophia C L" uniqKey="Smith S" first="Sophia C L" last="Smith">Sophia C L. Smith</name></country><country name="Brésil"><region name="État de São Paulo"><name sortKey="Cogni, Rodrigo" sort="Cogni, Rodrigo" uniqKey="Cogni R" first="Rodrigo" last="Cogni">Rodrigo Cogni</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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