The role of evolution in the emergence of infectious diseases.
Identifieur interne : 003020 ( PubMed/Checkpoint ); précédent : 003019; suivant : 003021The role of evolution in the emergence of infectious diseases.
Auteurs : Rustom Antia [États-Unis] ; Roland R. Regoes ; Jacob C. Koella ; Carl T. BergstromSource :
- Nature [ 1476-4687 ] ; 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 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.
DOI: 10.1038/nature02104
PubMed: 14668863
Affiliations:
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pubmed:14668863Le document en format XML
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Koella</name></author><author><name sortKey="Bergstrom, Carl T" sort="Bergstrom, Carl T" uniqKey="Bergstrom C" first="Carl T" last="Bergstrom">Carl T. 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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><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">14668863</PMID><DateCompleted><Year>2004</Year><Month>01</Month><Day>05</Day></DateCompleted><DateRevised><Year>2020</Year><Month>03</Month><Day>27</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1476-4687</ISSN><JournalIssue CitedMedium="Internet"><Volume>426</Volume><Issue>6967</Issue><PubDate><Year>2003</Year><Month>Dec</Month><Day>11</Day></PubDate></JournalIssue><Title>Nature</Title><ISOAbbreviation>Nature</ISOAbbreviation></Journal><ArticleTitle>The role of evolution in the emergence of infectious diseases.</ArticleTitle><Pagination><MedlinePgn>658-61</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Antia</LastName><ForeName>Rustom</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Biology, Emory University, Atlanta, Georgia 30322, USA. rantia@emory.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Regoes</LastName><ForeName>Roland R</ForeName><Initials>RR</Initials></Author><Author ValidYN="Y"><LastName>Koella</LastName><ForeName>Jacob C</ForeName><Initials>JC</Initials></Author><Author ValidYN="Y"><LastName>Bergstrom</LastName><ForeName>Carl T</ForeName><Initials>CT</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType 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Bergstrom</name><name sortKey="Koella, Jacob C" sort="Koella, Jacob C" uniqKey="Koella J" first="Jacob C" last="Koella">Jacob C. Koella</name><name sortKey="Regoes, Roland R" sort="Regoes, Roland R" uniqKey="Regoes R" first="Roland R" last="Regoes">Roland R. Regoes</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Antia, Rustom" sort="Antia, Rustom" uniqKey="Antia R" first="Rustom" last="Antia">Rustom Antia</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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