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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Epidemics-in-waiting</title><author><name sortKey="Bull, Jim" sort="Bull, Jim" uniqKey="Bull J" first="Jim" last="Bull">Jim Bull</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.89336.37</institution-id><institution-id institution-id-type="ISNI">0000 0004 1936 9924</institution-id><institution>Section of Integrative Biology and the Institute of Cellular and Molecular Biology, University of Texas,</institution></institution-wrap>Austin, 78712 Texas USA</nlm:aff></affiliation></author><author><name sortKey="Dykhuizen, Dan" sort="Dykhuizen, Dan" uniqKey="Dykhuizen D" first="Dan" last="Dykhuizen">Dan Dykhuizen</name><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="GRID">grid.36425.36</institution-id><institution-id institution-id-type="ISNI">0000 0001 2216 9681</institution-id><institution>Department of Ecology and Evolution,</institution><institution>State University of New York at Stony Brook,</institution></institution-wrap>Stony Brook, 11794 New York USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">14668840</idno><idno type="pmc">7095089</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7095089</idno><idno type="RBID">PMC:7095089</idno><idno type="doi">10.1038/426609a</idno><date when="2003">2003</date><idno type="wicri:Area/Pmc/Corpus">000059</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000059</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Epidemics-in-waiting</title><author><name sortKey="Bull, Jim" sort="Bull, Jim" uniqKey="Bull J" first="Jim" last="Bull">Jim Bull</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="GRID">grid.89336.37</institution-id><institution-id institution-id-type="ISNI">0000 0004 1936 9924</institution-id><institution>Section of Integrative Biology and the Institute of Cellular and Molecular Biology, University of Texas,</institution></institution-wrap>Austin, 78712 Texas USA</nlm:aff></affiliation></author><author><name sortKey="Dykhuizen, Dan" sort="Dykhuizen, Dan" uniqKey="Dykhuizen D" first="Dan" last="Dykhuizen">Dan Dykhuizen</name><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="GRID">grid.36425.36</institution-id><institution-id institution-id-type="ISNI">0000 0001 2216 9681</institution-id><institution>Department of Ecology and Evolution,</institution><institution>State University of New York at Stony Brook,</institution></institution-wrap>Stony Brook, 11794 New York USA</nlm:aff></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">Could the next SARS-like virus reach epidemic proportions? Quantifying the likely threat of emerging diseases isn't easy, but evolution is a crucial factor that may tip the balance in favour of such human parasites.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Antia, R" uniqKey="Antia R">R Antia</name></author><author><name sortKey="Regoes, Rr" uniqKey="Regoes R">RR Regoes</name></author><author><name sortKey="Koella, Jc" uniqKey="Koella J">JC Koella</name></author><author><name sortKey="Bergstrom, Ct" uniqKey="Bergstrom C">CT Bergstrom</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Garrett, L" uniqKey="Garrett L">L Garrett</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Preston, R" uniqKey="Preston R">R Preston</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Frank, Sa" uniqKey="Frank S">SA Frank</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Frank, Sa" uniqKey="Frank S">SA Frank</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ewald, Pw" uniqKey="Ewald P">PW Ewald</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wallace, B" uniqKey="Wallace B">B Wallace</name></author></analytic></biblStruct></listBibl></div1></back></TEI><pmc article-type="brief-report"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Nature</journal-id><journal-id journal-id-type="iso-abbrev">Nature</journal-id><journal-title-group><journal-title>Nature</journal-title></journal-title-group><issn pub-type="ppub">0028-0836</issn><issn pub-type="epub">1476-4687</issn><publisher><publisher-name>Nature Publishing Group UK</publisher-name><publisher-loc>London</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">14668840</article-id><article-id pub-id-type="pmc">7095089</article-id><article-id pub-id-type="publisher-id">BF426609a</article-id><article-id pub-id-type="doi">10.1038/426609a</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Epidemics-in-waiting</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Bull</surname><given-names>Jim</given-names></name><address><email>bull@bull.biosci.utexas.edu</email></address><xref ref-type="aff" rid="Aff1">1</xref></contrib><contrib contrib-type="author"><name><surname>Dykhuizen</surname><given-names>Dan</given-names></name><address><email>dandyk@life.bio.sunysb.edu</email></address><xref ref-type="aff" rid="Aff2">2</xref></contrib><aff id="Aff1"><label>1</label><institution-wrap><institution-id institution-id-type="GRID">grid.89336.37</institution-id><institution-id institution-id-type="ISNI">0000 0004 1936 9924</institution-id><institution>Section of Integrative Biology and the Institute of Cellular and Molecular Biology, University of Texas,</institution></institution-wrap>Austin, 78712 Texas USA</aff><aff id="Aff2"><label>2</label><institution-wrap><institution-id institution-id-type="GRID">grid.36425.36</institution-id><institution-id institution-id-type="ISNI">0000 0001 2216 9681</institution-id><institution>Department of Ecology and Evolution,</institution><institution>State University of New York at Stony Brook,</institution></institution-wrap>Stony Brook, 11794 New York USA</aff></contrib-group><pub-date pub-type="ppub"><year>2003</year></pub-date><volume>426</volume><issue>6967</issue><fpage>609</fpage><lpage>610</lpage><permissions><copyright-statement>© Nature Publishing Group 2003</copyright-statement><license><license-p>This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.</license-p></license></permissions><abstract id="Abs1" abstract-type="Standfirst"><p id="Par1">Could the next SARS-like virus reach epidemic proportions? Quantifying the likely threat of emerging diseases isn't easy, but evolution is a crucial factor that may tip the balance in favour of such human parasites.</p></abstract><custom-meta-group><custom-meta><meta-name>issue-copyright-statement</meta-name><meta-value>© Springer Nature Limited 2003</meta-value></custom-meta></custom-meta-group></article-meta></front><body><p id="Par2">One of the oldest tenets of evolutionary biology is that it is easier to change a little than a lot. We also know that evolutionary change is more easily selected for in a large population than in a small one. On <ext-link ext-link-type="uri" xlink:href="https://www.nature.com/articles/nature02104">page 658</ext-link> of this issue, Antia <italic>et al</italic>.<sup><xref ref-type="bibr" rid="CR1">1</xref></sup> combine these facts to reach a previously unappreciated conclusion about emerging infectious diseases: some types of infectious parasites that attack the human population may pose a serious threat even if they are not initially able to cause epidemics. The reason is that certain parasites are specially poised to evolve so that they can cause epidemics.</p><p id="Par3">In epidemiological models, an infectious agent can be characterized by its basic reproductive rate, <italic>R</italic><sub>0</sub>. This is the average number of new infections caused by the first infected individual in the population. The epidemic threshold is <italic>R</italic><sub>0</sub>=1, above which the disease spreads (neglecting random effects) and below which it eventually dies out. <italic>R</italic><sub>0</sub> is not, however, a measure of virulence or of the harm inflicted on the host by infection. In humans, for example, <italic>R</italic><sub>0</sub> is virtually zero for some diseases with a high mortality rate (such as rabies, and hantavirus respiratory infections); but <italic>R</italic><sub>0</sub> is well above unity for other diseases that also have high mortality rates (such as measles in undernourished populations, AIDS and smallpox).</p><p id="Par4">Antia <italic>et al</italic>.<sup><xref ref-type="bibr" rid="CR1">1</xref></sup> point out that, because of evolution, parasites with an <italic>R</italic><sub>0</sub> value that is hovering just below one can be epidemics-in-waiting. An obvious reason for this is that it takes less change to achieve an <italic>R</italic><sub>0</sub> of more than one if the initial <italic>R</italic><sub>0</sub> is just below one. A less obvious reason — and the focus of Antia and colleagues' paper — is that the length of time a parasite persists in the population before disappearing increases with <italic>R</italic><sub>0</sub>; parasites with <italic>R</italic><sub>0</sub> nearly at unity can persist for a considerable time by chance. The longer the parasite persists, the greater will be its opportunity to evolve to a higher <italic>R</italic><sub>0</sub>. This is merely a population size effect: each additional host infected before the parasite dies out provides yet another opportunity for a mutation that might push <italic>R</italic><sub>0</sub> over the epidemic threshold.</p><p id="Par5">The model is tractable because of its reliance on the single parameter <italic>R</italic><sub>0</sub>, but the biology behind it is potentially complicated. <italic>R</italic><sub>0</sub> encapsulates the long chain of events involved in the parasite's association with its host — its first contact, entry, growth in the initial tissue infected, infection of secondary tissues, and so on, until the final stage of its dissemination to make contact with other hosts. A mutation that increases <italic>R</italic><sub>0</sub> may arise at any stage in this chain, provided that it ultimately leads to an increase in the number of infections. For instance, an increase in <italic>R</italic><sub>0</sub> may evolve through changes in surface molecules that improve parasite infection of new hosts directly, or it may evolve through improved growth within the host (possibly increasing virulence) so that more parasite progeny are disseminated from the host, resulting in higher numbers of secondary infections.</p><p id="Par6">The rabies and hantavirus examples mentioned above are characterized by good within-host growth of the parasite but poor dissemination to new hosts. The 1976 outbreak of Ebola virus in southern Sudan (which spread from an initial infection of a cotton factory worker to the owner of the local jazz club, then to others at the club, giving at least eight generations of transmission<sup><xref ref-type="bibr" rid="CR2">2</xref></sup>) is a case in which within-host growth was good and the dissemination–infection stage brought the parasite perilously close to the epidemic threshold. However, a parasite could also begin its foray into humans by being fairly infectious but poor at surviving the onslaught of our immune system (as seems to have been the case with the Ebola virus that, in 1989, destroyed an imported Philippine monkey colony in Reston, Virginia<sup><xref ref-type="bibr" rid="CR3">3</xref></sup>). Mutations that increase <italic>R</italic><sub>0</sub> might then improve within-human growth. This type of emerging pathogen is the most easily missed and potentially the most dangerous. Efforts to understand the relationship between parasite adaptation to hosts, virulence and transmission have developed into a small industry in evolutionary biology. The relationship is complicated because it involves group versus individual selection, population bottlenecks and trade-offs<sup><xref ref-type="bibr" rid="CR4">4</xref>,<xref ref-type="bibr" rid="CR5">5</xref></sup>.</p><p id="Par7">Antia and colleagues' result<sup><xref ref-type="bibr" rid="CR1">1</xref></sup> contributes to a growing awareness of the evolutionary and ecological factors surrounding the emergence of new diseases. We have already had warnings that virulence itself may evolve in response to changes in cultural practices<sup><xref ref-type="bibr" rid="CR6">6</xref></sup>, and that immunocompromised patients may act as stepping stones to foster evolution of new pathogens capable of attacking people with healthy immune systems<sup><xref ref-type="bibr" rid="CR7">7</xref></sup>. With the possibility of using grafts from non-human species to replace tissues in humans, we also need to be aware of the potential for activation and genetic recombination of otherwise dormant retroviruses in the human genome or in the graft.</p><p id="Par8">Antia <italic>et al.</italic> do not, however, emphasize cultural factors in disease emergence. Instead, they provide a way of identifying which agents are most worthy of attention — those closest to the epidemic threshold. An example suggested by Antia <italic>et al.</italic> is the threat of monkeypox in a world with little resistance to its relative smallpox, because of a lack of either vaccination or exposure. Furthermore, the result draws attention to the neglected topic of parasite dynamics in the pre-epidemic stages. This was brought into focus earlier this year when it was realized that the initial spread of severe acute respiratory syndrome (SARS; <xref rid="Fig1" ref-type="fig">Fig. 1</xref>) depended heavily on the social connectivity of the first (index) case in a community. Such results and realizations give us a better understanding of how to contain infectious diseases, through early prevention rather than cure. Ultimately, we should learn where and when to apply our efforts to block transmission and so prevent an epidemic.<fig id="Fig1"><label>Figure 1</label><caption><title>Danger ahead?</title><p>The virus (inset) causing severe acute respiratory syndrome, or SARS, emerged in southeast Asia in late 2002. As the infection spread, face masks became a common sight on the streets of Hong Kong and elsewhere. Antia <italic>et al.</italic><sup><xref ref-type="bibr" rid="CR1">1</xref></sup> describe a way to help identify other viruses with epidemic potential.</p><p>P.PARKS/AFP</p></caption><graphic xlink:href="41586_2003_Article_BF426609a_Fig1_HTML" id="d29e350"></graphic></fig></p><p id="Par9">Currently, the resources and public attention devoted to an infectious disease depend on a combination of social, biological, economic and political factors specific to that disease. Disease virulence, transmissibility and incidence are included in such considerations. The complacency of the pre-HIV and pre-bioterrorism eras has yielded to a growing acceptance of the need to monitor pathogens and even pre-pathogens in our environment. It is not beyond imagination that, even with existing technology, methods could be developed for monitoring emerging pathogens, potentially distinguishing between strains with differing <italic>R</italic><sub>0</sub> values. The means, provided by Antia <italic>et al</italic>.<sup><xref ref-type="bibr" rid="CR1">1</xref></sup>, of identifying these epidemics-in-waiting could become a critical tool in a global defence strategy against emerging pathogens.</p><fig id="Figa"><caption><p>CAMR/A.B.DOWSETT/SPL</p></caption><graphic xlink:href="41586_2003_Article_BF426609a_Figa_HTML" id="d29e372"></graphic></fig></body><back><ref-list id="Bib1"><title>References</title><ref id="CR1"><label>1</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Antia</surname><given-names>R</given-names></name><name><surname>Regoes</surname><given-names>RR</given-names></name><name><surname>Koella</surname><given-names>JC</given-names></name><name><surname>Bergstrom</surname><given-names>CT</given-names></name></person-group><source>Nature</source><year>2003</year><volume>426</volume><fpage>658</fpage><lpage>661</lpage><pub-id pub-id-type="doi">10.1038/nature02104</pub-id><pub-id pub-id-type="pmid">14668863</pub-id></element-citation></ref><ref id="CR2"><label>2</label><element-citation publication-type="book"><person-group person-group-type="author"><name><surname>Garrett</surname><given-names>L</given-names></name></person-group><source>The Coming Plague</source><year>1994</year></element-citation></ref><ref id="CR3"><label>3</label><element-citation publication-type="book"><person-group person-group-type="author"><name><surname>Preston</surname><given-names>R</given-names></name></person-group><source>The Hot Zone</source><year>1994</year></element-citation></ref><ref id="CR4"><label>4</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Frank</surname><given-names>SA</given-names></name></person-group><source>Q. Rev. Biol.</source><year>1996</year><volume>71</volume><fpage>37</fpage><lpage>78</lpage><pub-id pub-id-type="doi">10.1086/419267</pub-id><pub-id pub-id-type="pmid">8919665</pub-id></element-citation></ref><ref id="CR5"><label>5</label><element-citation publication-type="book"><person-group person-group-type="author"><name><surname>Frank</surname><given-names>SA</given-names></name></person-group><source>Immunology and Evolution of Infectious Disease</source><year>2002</year></element-citation></ref><ref id="CR6"><label>6</label><element-citation publication-type="book"><person-group person-group-type="author"><name><surname>Ewald</surname><given-names>PW</given-names></name></person-group><source>Evolution of Infectious Disease</source><year>1994</year></element-citation></ref><ref id="CR7"><label>7</label><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wallace</surname><given-names>B</given-names></name></person-group><source>Am. Nat.</source><year>1989</year><volume>133</volume><fpage>578</fpage><lpage>579</lpage><pub-id pub-id-type="doi">10.1086/284937</pub-id></element-citation></ref></ref-list></back></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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