The role of evolution in the emergence of infectious diseases
Identifieur interne : 000499 ( Ncbi/Merge ); précédent : 000498; suivant : 000500The role of evolution in the emergence of infectious diseases
Auteurs : Rustom Antia [États-Unis] ; Roland R. Regoes [États-Unis] ; Jacob C. Koella [France] ; Carl T. Bergstrom [États-Unis]Source :
- Nature [ 0028-0836 ] ; 2003.
Descripteurs français
- KwdFr :
- MESH :
- génétique : Maladies transmissibles, Mutation.
- épidémiologie : Maladies transmissibles.
- Animaux, Humains, Interactions hôte-parasite, Modèles biologiques, Probabilité, Processus stochastiques, Écosystème, Évolution biologique.
English descriptors
- KwdEn :
- MESH :
- epidemiology : Communicable Diseases.
- genetics : Communicable Diseases, Mutation.
- transmission : Communicable Diseases.
- Animals, Biological Evolution, Ecosystem, Host-Parasite Interactions, Humans, Models, Biological, Probability, Stochastic Processes.
Abstract
It is unclear when, where and how novel pathogens such as human immunodeficiency virus (HIV), monkeypox and severe acute respiratory syndrome (SARS) will cross the barriers that separate their natural reservoirs from human populations and ignite the epidemic spread of novel infectious diseases. New pathogens are believed to emerge from animal reservoirs when ecological changes increase the pathogen's opportunities to enter the human population
The online version of this article (doi:10.1038/nature02104) contains supplementary material, which is available to authorized users.
Url:
DOI: 10.1038/nature02104
PubMed: 14668863
PubMed Central: 7095141
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PMC:7095141Le document en format XML
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New pathogens are believed to emerge from animal reservoirs when ecological changes increase the pathogen's opportunities to enter the human population<sup><xref ref-type="bibr" rid="CR1">1</xref></sup> and to generate subsequent human-to-human transmission<sup><xref ref-type="bibr" rid="CR2">2</xref></sup>. Effective human-to-human transmission requires that the pathogen's basic reproductive number, <italic>R</italic><sub>0</sub>, should exceed one, where <italic>R</italic><sub>0</sub> is the average number of secondary infections arising from one infected individual in a completely susceptible population<sup><xref ref-type="bibr" rid="CR3">3</xref></sup>. However, an increase in <italic>R</italic><sub>0</sub>, even when insufficient to generate an epidemic, nonetheless increases the number of subsequently infected individuals. Here we show that, as a consequence of this, the probability of pathogen evolution to <italic>R</italic><sub>0</sub> > 1 and subsequent disease emergence can increase markedly.</p><sec><title>Supplementary information</title><p>The online version of this article (doi:10.1038/nature02104) contains supplementary material, which is available to authorized users.</p></sec></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="May, Rm" uniqKey="May R">RM May</name></author><author><name sortKey="Gupta, S" uniqKey="Gupta S">S Gupta</name></author><author><name sortKey="Mclean, Ar" uniqKey="Mclean A">AR 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uniqKey="Sigmund K">K Sigmund</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stivers, Dn" uniqKey="Stivers D">DN Stivers</name></author><author><name sortKey="Kimmel, M" uniqKey="Kimmel M">M Kimmel</name></author><author><name sortKey="Axelrod, De" uniqKey="Axelrod D">DE Axelrod</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wilke, Co" uniqKey="Wilke C">CO Wilke</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wright, S" uniqKey="Wright S">S Wright</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Holmes, Ec" uniqKey="Holmes E">EC Holmes</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Peeters, M" uniqKey="Peeters M">M Peeters</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Guan, Y" uniqKey="Guan Y">Y 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Koella</name><affiliation wicri:level="1"><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="GRID">grid.462844.8</institution-id><institution-id institution-id-type="ISNI">0000 0001 2308 1657</institution-id><institution>Laboratoire de Parasitologie Evolutive,</institution><institution>Université Pierre et Marie Curie,</institution></institution-wrap>75252 Paris, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea>75252 Paris</wicri:regionArea></affiliation></author><author><name sortKey="Bergstrom, Carl T" sort="Bergstrom, Carl T" uniqKey="Bergstrom C" first="Carl T." last="Bergstrom">Carl T. Bergstrom</name><affiliation wicri:level="1"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="GRID">grid.34477.33</institution-id><institution-id institution-id-type="ISNI">0000000122986657</institution-id><institution>Department of Biology,</institution><institution>University of Washington,</institution></institution-wrap>Washington 98195 Seattle, USA</nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Washington 98195 Seattle</wicri:regionArea></affiliation></author></analytic><series><title level="j">Nature</title><idno type="ISSN">0028-0836</idno><idno type="eISSN">1476-4687</idno><imprint><date when="2003">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">It is unclear when, where and how novel pathogens such as human immunodeficiency virus (HIV), monkeypox and severe acute respiratory syndrome (SARS) will cross the barriers that separate their natural reservoirs from human populations and ignite the epidemic spread of novel infectious diseases. New pathogens are believed to emerge from animal reservoirs when ecological changes increase the pathogen's opportunities to enter the human population<sup><xref ref-type="bibr" rid="CR1">1</xref></sup> and to generate subsequent human-to-human transmission<sup><xref ref-type="bibr" rid="CR2">2</xref></sup>. Effective human-to-human transmission requires that the pathogen's basic reproductive number, <italic>R</italic><sub>0</sub>, should exceed one, where <italic>R</italic><sub>0</sub> is the average number of secondary infections arising from one infected individual in a completely susceptible population<sup><xref ref-type="bibr" rid="CR3">3</xref></sup>. However, an increase in <italic>R</italic><sub>0</sub>, even when insufficient to generate an epidemic, nonetheless increases the number of subsequently infected individuals. Here we show that, as a consequence of this, the probability of pathogen evolution to <italic>R</italic><sub>0</sub> > 1 and subsequent disease emergence can increase markedly.</p><sec><title>Supplementary information</title><p>The online version of this article (doi:10.1038/nature02104) contains supplementary material, which is available to authorized users.</p></sec></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="May, Rm" uniqKey="May R">RM May</name></author><author><name sortKey="Gupta, S" uniqKey="Gupta S">S Gupta</name></author><author><name sortKey="Mclean, Ar" uniqKey="Mclean A">AR McLean</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Anderson, R" uniqKey="Anderson R">R Anderson</name></author><author><name sortKey="May, R" uniqKey="May R">R May</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schrag, S" uniqKey="Schrag S">S Schrag</name></author><author><name sortKey="Wiener, P" uniqKey="Wiener P">P Wiener</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wallace, B" uniqKey="Wallace B">B Wallace</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Athreya, Kb" uniqKey="Athreya K">KB Athreya</name></author><author><name sortKey="Ney, P" uniqKey="Ney P">P Ney</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Demetrius, L" uniqKey="Demetrius L">L Demetrius</name></author><author><name sortKey="Schuster, P" uniqKey="Schuster P">P Schuster</name></author><author><name sortKey="Sigmund, K" uniqKey="Sigmund K">K Sigmund</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stivers, Dn" uniqKey="Stivers D">DN Stivers</name></author><author><name sortKey="Kimmel, M" uniqKey="Kimmel M">M Kimmel</name></author><author><name sortKey="Axelrod, De" uniqKey="Axelrod D">DE Axelrod</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wilke, Co" uniqKey="Wilke C">CO Wilke</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wright, S" uniqKey="Wright S">S Wright</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Holmes, Ec" uniqKey="Holmes E">EC Holmes</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Peeters, M" uniqKey="Peeters M">M Peeters</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Guan, Y" uniqKey="Guan Y">Y Guan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cyranoski, D" uniqKey="Cyranoski D">D Cyranoski</name></author><author><name sortKey="Abbott, A" uniqKey="Abbott A">A Abbott</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Enserink, M" uniqKey="Enserink M">M Enserink</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Riley, S" uniqKey="Riley S">S Riley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lipsitch, M" uniqKey="Lipsitch M">M Lipsitch</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Heymann, Dl" uniqKey="Heymann D">DL Heymann</name></author><author><name sortKey="Szczeniowski, M" uniqKey="Szczeniowski M">M Szczeniowski</name></author><author><name sortKey="Esteves, K" uniqKey="Esteves K">K Esteves</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Fine, Pe" uniqKey="Fine P">PE Fine</name></author><author><name sortKey="Jezek, Z" uniqKey="Jezek Z">Z Jezek</name></author><author><name sortKey="Grab, B" uniqKey="Grab B">B Grab</name></author><author><name sortKey="Dixon, H" uniqKey="Dixon H">H Dixon</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Breman, Jg" uniqKey="Breman J">JG Breman</name></author><author><name sortKey="Henderson, Da" uniqKey="Henderson D">DA Henderson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hutin, Yj" uniqKey="Hutin Y">YJ Hutin</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Enserink, M" uniqKey="Enserink M">M Enserink</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chua, Kb" uniqKey="Chua K">KB Chua</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Enserink, M" uniqKey="Enserink M">M Enserink</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="May, R" uniqKey="May R">R May</name></author><author><name sortKey="Anderson, R" uniqKey="Anderson R">R Anderson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lloyd, Al" uniqKey="Lloyd A">AL Lloyd</name></author><author><name sortKey="May, Rm" uniqKey="May R">RM May</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dobson, A" uniqKey="Dobson A">A Dobson</name></author><author><name sortKey="Foufopoulos, J" uniqKey="Foufopoulos J">J Foufopoulos</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Elton, Cs" uniqKey="Elton C">CS Elton</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kornberg, H" uniqKey="Kornberg H">H Kornberg</name></author><author><name sortKey="Williamson, M" uniqKey="Williamson M">M Williamson</name></author></analytic></biblStruct></listBibl></div1></back></TEI></pmc><pubmed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">The role of evolution in the emergence of infectious diseases.</title><author><name sortKey="Antia, Rustom" sort="Antia, Rustom" uniqKey="Antia R" first="Rustom" last="Antia">Rustom Antia</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biology, Emory University, Atlanta, Georgia 30322, USA. rantia@emory.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biology, Emory University, Atlanta, Georgia 30322</wicri:regionArea><wicri:noRegion>Georgia 30322</wicri:noRegion></affiliation></author><author><name sortKey="Regoes, Roland R" sort="Regoes, Roland R" uniqKey="Regoes R" first="Roland R" last="Regoes">Roland R. Regoes</name></author><author><name sortKey="Koella, Jacob C" sort="Koella, Jacob C" uniqKey="Koella J" first="Jacob C" last="Koella">Jacob C. Koella</name></author><author><name sortKey="Bergstrom, Carl T" sort="Bergstrom, Carl T" uniqKey="Bergstrom C" first="Carl T" last="Bergstrom">Carl T. Bergstrom</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:14668863</idno><idno type="pmid">14668863</idno><idno type="doi">10.1038/nature02104</idno><idno type="wicri:Area/PubMed/Corpus">003050</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">003050</idno><idno type="wicri:Area/PubMed/Curation">003050</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">003050</idno><idno type="wicri:Area/PubMed/Checkpoint">003020</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">003020</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The role of evolution in the emergence of infectious diseases.</title><author><name sortKey="Antia, Rustom" sort="Antia, Rustom" uniqKey="Antia R" first="Rustom" last="Antia">Rustom Antia</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biology, Emory University, Atlanta, Georgia 30322, USA. rantia@emory.edu</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biology, Emory University, Atlanta, Georgia 30322</wicri:regionArea><wicri:noRegion>Georgia 30322</wicri:noRegion></affiliation></author><author><name sortKey="Regoes, Roland R" sort="Regoes, Roland R" uniqKey="Regoes R" first="Roland R" last="Regoes">Roland R. Regoes</name></author><author><name sortKey="Koella, Jacob C" sort="Koella, Jacob C" uniqKey="Koella J" first="Jacob C" last="Koella">Jacob C. Koella</name></author><author><name sortKey="Bergstrom, Carl T" sort="Bergstrom, Carl T" uniqKey="Bergstrom C" first="Carl T" last="Bergstrom">Carl T. Bergstrom</name></author></analytic><series><title level="j">Nature</title><idno type="eISSN">1476-4687</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Biological Evolution</term><term>Communicable Diseases (epidemiology)</term><term>Communicable Diseases (genetics)</term><term>Communicable Diseases (transmission)</term><term>Ecosystem</term><term>Host-Parasite Interactions</term><term>Humans</term><term>Models, Biological</term><term>Mutation (genetics)</term><term>Probability</term><term>Stochastic Processes</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Interactions hôte-parasite</term><term>Maladies transmissibles (génétique)</term><term>Maladies transmissibles (transmission)</term><term>Maladies transmissibles (épidémiologie)</term><term>Modèles biologiques</term><term>Mutation (génétique)</term><term>Probabilité</term><term>Processus stochastiques</term><term>Écosystème</term><term>Évolution biologique</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Communicable Diseases</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Communicable Diseases</term><term>Mutation</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Maladies transmissibles</term><term>Mutation</term></keywords><keywords scheme="MESH" qualifier="transmission" xml:lang="en"><term>Communicable Diseases</term></keywords><keywords scheme="MESH" qualifier="épidémiologie" xml:lang="fr"><term>Maladies transmissibles</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Biological Evolution</term><term>Ecosystem</term><term>Host-Parasite Interactions</term><term>Humans</term><term>Models, Biological</term><term>Probability</term><term>Stochastic Processes</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Interactions hôte-parasite</term><term>Modèles biologiques</term><term>Probabilité</term><term>Processus stochastiques</term><term>Écosystème</term><term>Évolution biologique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">It is unclear when, where and how novel pathogens such as human immunodeficiency virus (HIV), monkeypox and severe acute respiratory syndrome (SARS) will cross the barriers that separate their natural reservoirs from human populations and ignite the epidemic spread of novel infectious diseases. New pathogens are believed to emerge from animal reservoirs when ecological changes increase the pathogen's opportunities to enter the human population and to generate subsequent human-to-human transmission. Effective human-to-human transmission requires that the pathogen's basic reproductive number, R(0), should exceed one, where R(0) is the average number of secondary infections arising from one infected individual in a completely susceptible population. However, an increase in R(0), even when insufficient to generate an epidemic, nonetheless increases the number of subsequently infected individuals. Here we show that, as a consequence of this, the probability of pathogen evolution to R(0) > 1 and subsequent disease emergence can increase markedly.</div></front></TEI></pubmed></double></record>Pour manipuler ce document sous Unix (Dilib)
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