Epidemic mechanisms of Type A influenza
Identifieur interne : 000229 ( Istex/Corpus ); précédent : 000228; suivant : 000230Epidemic mechanisms of Type A influenza
Auteurs : R. E. Hope-SimpsonSource :
- Journal of Hygiene [ 0022-1724 ] ; 1979-08.
Abstract
The antigenic varieties of influenza A virus isolated from 1968 to 1976 in a surveillance of a small, rather remote population were similar to those from England and Wales as a whole, despite frequent antigenic changes during the period. Household studies in the first two H3N2 influenza A epidemics found low attack rates within households, a high proportion (70%) of affected households with only one case of influenza, similar distributions of affected households in the two epidemics by the number of cases of influenza and similar distributions of the influenza cases by the day of their onset in the household outbreak. No serial interval could be demonstrated by cumulating household outbreaks. More than one minor variant was causing influenza contemporaneously in the same villages in several seasons, and different variants were on one occasion found on successive days in bedfellows. The regular occurrence of epidemics in winter was often accompanied by the disappearance of the epidemic variants and their replacement, after a virus-free interval, by new variants. These epidemiological findings seem best interpreted on the following tentative hypothesis. Influenza A sufferers do not transmit the virus during their illness; instead it rapidly becomes latent in their tissues so that they become symptomless carrier-hosts and develop specific immunity. Next season an extraneous seasonally mediated stimulus reactivates the latent virus residues so that the carrier-host becomes briefly infectious, though symptomless. Antigenic drift occurs because particles reconstituted to be identical with the progenitor virus cannot escape the specific immunity it has provoked in the carrier host. He can shed only mutants also determined by the progenitor virus. From the assortment of mutants shed by the carrier-host, his non-immune companions select that (those) which is best fitted to survive, and it rapidly causes influenzal illness. Epidemics consist largely or entirely of such persons sick with influenza caused by reactivated virus caught from symptomless carrier-hosts.
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DOI: 10.1017/S002217240002578X
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Epidemic mechanisms of Type A influenza</title><author><name sortKey="Hope Simpson, R E" sort="Hope Simpson, R E" uniqKey="Hope Simpson R" first="R. E." last="Hope-Simpson">R. E. Hope-Simpson</name><affiliation><mods:affiliation>Epidemiological Research Unit, 86 Dyer Street, Cirencester, Gloucestershire, England</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:2105ADD361658E5FCDA3862C9BB3E414A99DDAE7</idno><date when="1979" year="1979">1979</date><idno type="doi">10.1017/S002217240002578X</idno><idno type="url">https://api.istex.fr/ark:/67375/6GQ-90WZ3G4R-C/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000229</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000229</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Epidemic mechanisms of Type A influenza</title><author><name sortKey="Hope Simpson, R E" sort="Hope Simpson, R E" uniqKey="Hope Simpson R" first="R. E." last="Hope-Simpson">R. E. Hope-Simpson</name><affiliation><mods:affiliation>Epidemiological Research Unit, 86 Dyer Street, Cirencester, Gloucestershire, England</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Hygiene</title><title level="j" type="abbrev">J. Hyg.</title><idno type="ISSN">0022-1724</idno><imprint><publisher>Cambridge University Press</publisher><pubPlace>Cambridge, UK</pubPlace><date type="published" when="1979-08">1979-08</date><biblScope unit="volume">83</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="11">11</biblScope><biblScope unit="page" to="26">26</biblScope></imprint><idno type="ISSN">0022-1724</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-1724</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">The antigenic varieties of influenza A virus isolated from 1968 to 1976 in a surveillance of a small, rather remote population were similar to those from England and Wales as a whole, despite frequent antigenic changes during the period. Household studies in the first two H3N2 influenza A epidemics found low attack rates within households, a high proportion (70%) of affected households with only one case of influenza, similar distributions of affected households in the two epidemics by the number of cases of influenza and similar distributions of the influenza cases by the day of their onset in the household outbreak. No serial interval could be demonstrated by cumulating household outbreaks. More than one minor variant was causing influenza contemporaneously in the same villages in several seasons, and different variants were on one occasion found on successive days in bedfellows. The regular occurrence of epidemics in winter was often accompanied by the disappearance of the epidemic variants and their replacement, after a virus-free interval, by new variants. These epidemiological findings seem best interpreted on the following tentative hypothesis. Influenza A sufferers do not transmit the virus during their illness; instead it rapidly becomes latent in their tissues so that they become symptomless carrier-hosts and develop specific immunity. Next season an extraneous seasonally mediated stimulus reactivates the latent virus residues so that the carrier-host becomes briefly infectious, though symptomless. Antigenic drift occurs because particles reconstituted to be identical with the progenitor virus cannot escape the specific immunity it has provoked in the carrier host. He can shed only mutants also determined by the progenitor virus. From the assortment of mutants shed by the carrier-host, his non-immune companions select that (those) which is best fitted to survive, and it rapidly causes influenzal illness. Epidemics consist largely or entirely of such persons sick with influenza caused by reactivated virus caught from symptomless carrier-hosts.</div></front></TEI><istex><corpusName>cambridge</corpusName><author><json:item><name>R. E. Hope-simpson</name><affiliations><json:string>Epidemiological Research Unit, 86 Dyer Street, Cirencester, Gloucestershire, England</json:string></affiliations></json:item></author><articleId><json:string>02578</json:string></articleId><arkIstex>ark:/67375/6GQ-90WZ3G4R-C</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>The antigenic varieties of influenza A virus isolated from 1968 to 1976 in a surveillance of a small, rather remote population were similar to those from England and Wales as a whole, despite frequent antigenic changes during the period. Household studies in the first two H3N2 influenza A epidemics found low attack rates within households, a high proportion (70%) of affected households with only one case of influenza, similar distributions of affected households in the two epidemics by the number of cases of influenza and similar distributions of the influenza cases by the day of their onset in the household outbreak. No serial interval could be demonstrated by cumulating household outbreaks. More than one minor variant was causing influenza contemporaneously in the same villages in several seasons, and different variants were on one occasion found on successive days in bedfellows. The regular occurrence of epidemics in winter was often accompanied by the disappearance of the epidemic variants and their replacement, after a virus-free interval, by new variants. These epidemiological findings seem best interpreted on the following tentative hypothesis. Influenza A sufferers do not transmit the virus during their illness; instead it rapidly becomes latent in their tissues so that they become symptomless carrier-hosts and develop specific immunity. Next season an extraneous seasonally mediated stimulus reactivates the latent virus residues so that the carrier-host becomes briefly infectious, though symptomless. Antigenic drift occurs because particles reconstituted to be identical with the progenitor virus cannot escape the specific immunity it has provoked in the carrier host. He can shed only mutants also determined by the progenitor virus. From the assortment of mutants shed by the carrier-host, his non-immune companions select that (those) which is best fitted to survive, and it rapidly causes influenzal illness. Epidemics consist largely or entirely of such persons sick with influenza caused by reactivated virus caught from symptomless carrier-hosts.</abstract><qualityIndicators><score>10</score><pdfWordCount>5959</pdfWordCount><pdfCharCount>36346</pdfCharCount><pdfVersion>1.4</pdfVersion><pdfPageCount>16</pdfPageCount><pdfPageSize>523.44 x 769.68 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>310</abstractWordCount><abstractCharCount>2088</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>Epidemic mechanisms of Type A influenza</title><pii><json:string>S002217240002578X</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Journal of Hygiene</title><language><json:string>unknown</json:string></language><issn><json:string>0022-1724</json:string></issn><publisherId><json:string>HYG</json:string></publisherId><volume>83</volume><issue>1</issue><pages><first>11</first><last>26</last><total>16</total></pages><genre><json:string>journal</json:string></genre></host><ark><json:string>ark:/67375/6GQ-90WZ3G4R-C</json:string></ark><categories><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>1979</publicationDate><copyrightDate>1979</copyrightDate><doi><json:string>10.1017/S002217240002578X</json:string></doi><id>2105ADD361658E5FCDA3862C9BB3E414A99DDAE7</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6GQ-90WZ3G4R-C/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6GQ-90WZ3G4R-C/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6GQ-90WZ3G4R-C/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">Epidemic mechanisms of Type A influenza</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">Cambridge University Press</publisher><pubPlace>Cambridge, UK</pubPlace><availability><licence><p>Copyright © Cambridge University Press 1979</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-G3RCRD03-V">cambridge</p></availability><date>1979</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Epidemic mechanisms of Type A influenza</title><author xml:id="author-0000"><persName><forename type="first">R. E.</forename><surname>Hope-simpson</surname></persName><affiliation>Epidemiological Research Unit, 86 Dyer Street, Cirencester, Gloucestershire, England</affiliation></author><idno type="istex">2105ADD361658E5FCDA3862C9BB3E414A99DDAE7</idno><idno type="ark">ark:/67375/6GQ-90WZ3G4R-C</idno><idno type="DOI">10.1017/S002217240002578X</idno><idno type="PII">S002217240002578X</idno><idno type="article-id">02578</idno></analytic><monogr><title level="j">Journal of Hygiene</title><title level="j" type="abbrev">J. Hyg.</title><idno type="pISSN">0022-1724</idno><idno type="publisher-id">HYG</idno><imprint><publisher>Cambridge University Press</publisher><pubPlace>Cambridge, UK</pubPlace><date type="published" when="1979-08"></date><biblScope unit="volume">83</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="11">11</biblScope><biblScope unit="page" to="26">26</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1979</date></creation><langUsage><language ident="en">en</language></langUsage><abstract style="normal"><p>The antigenic varieties of influenza A virus isolated from 1968 to 1976 in a surveillance of a small, rather remote population were similar to those from England and Wales as a whole, despite frequent antigenic changes during the period. Household studies in the first two H3N2 influenza A epidemics found low attack rates within households, a high proportion (70%) of affected households with only one case of influenza, similar distributions of affected households in the two epidemics by the number of cases of influenza and similar distributions of the influenza cases by the day of their onset in the household outbreak. No serial interval could be demonstrated by cumulating household outbreaks. More than one minor variant was causing influenza contemporaneously in the same villages in several seasons, and different variants were on one occasion found on successive days in bedfellows. The regular occurrence of epidemics in winter was often accompanied by the disappearance of the epidemic variants and their replacement, after a virus-free interval, by new variants. These epidemiological findings seem best interpreted on the following tentative hypothesis. Influenza A sufferers do not transmit the virus during their illness; instead it rapidly becomes latent in their tissues so that they become symptomless carrier-hosts and develop specific immunity. Next season an extraneous seasonally mediated stimulus reactivates the latent virus residues so that the carrier-host becomes briefly infectious, though symptomless. Antigenic drift occurs because particles reconstituted to be identical with the progenitor virus cannot escape the specific immunity it has provoked in the carrier host. He can shed only mutants also determined by the progenitor virus. From the assortment of mutants shed by the carrier-host, his non-immune companions select that (those) which is best fitted to survive, and it rapidly causes influenzal illness. Epidemics consist largely or entirely of such persons sick with influenza caused by reactivated virus caught from symptomless carrier-hosts.</p></abstract></profileDesc><revisionDesc><change when="1979-08">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6GQ-90WZ3G4R-C/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus cambridge not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="US-ASCII"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.2 20060430//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article dtd-version="2.2" article-type="research-article"><front><journal-meta><journal-id journal-id-type="publisher-id">HYG</journal-id><journal-title>Journal of Hygiene</journal-title><abbrev-journal-title>J. Hyg.</abbrev-journal-title><issn pub-type="ppub">0022-1724</issn><publisher><publisher-name>Cambridge University Press</publisher-name><publisher-loc>Cambridge, UK</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1017/S002217240002578X</article-id><article-id pub-id-type="pii">S002217240002578X</article-id><article-id pub-id-type="publisher-id">02578</article-id><title-group><article-title>Epidemic mechanisms of Type A influenza</article-title><alt-title alt-title-type="left-running">R. E. Hope-Simpson</alt-title><alt-title alt-title-type="right-running">Epidemic mechanisms of type A influenza</alt-title></title-group><contrib-group><contrib><name><surname>Hope-simpson</surname><given-names>R. E.</given-names></name><xref ref-type="aff" rid="aff1"></xref></contrib></contrib-group><aff id="aff1"><addr-line>Epidemiological Research Unit</addr-line>, <addr-line>86 Dyer Street</addr-line>, <addr-line>Cirencester</addr-line>, <addr-line>Gloucestershire</addr-line>, <country>England</country></aff><pub-date pub-type="ppub"><month>08</month><year>1979</year></pub-date><volume>83</volume><issue>1</issue><fpage seq="4">11</fpage><lpage>26</lpage><history><date date-type="received"><day>18</day><month>05</month><year>1978</year></date></history><permissions><copyright-statement>Copyright © Cambridge University Press 1979</copyright-statement><copyright-year>1979</copyright-year><copyright-holder>Cambridge University Press</copyright-holder></permissions><abstract abstract-type="normal"><title>SUMMARY</title><p>The antigenic varieties of influenza A virus isolated from 1968 to 1976 in a surveillance of a small, rather remote population were similar to those from England and Wales as a whole, despite frequent antigenic changes during the period. Household studies in the first two H3N2 influenza A epidemics found low attack rates within households, a high proportion (70%) of affected households with only one case of influenza, similar distributions of affected households in the two epidemics by the number of cases of influenza and similar distributions of the influenza cases by the day of their onset in the household outbreak. No serial interval could be demonstrated by cumulating household outbreaks. More than one minor variant was causing influenza contemporaneously in the same villages in several seasons, and different variants were on one occasion found on successive days in bedfellows. The regular occurrence of epidemics in winter was often accompanied by the disappearance of the epidemic variants and their replacement, after a virus-free interval, by new variants.</p><p>These epidemiological findings seem best interpreted on the following tentative hypothesis. Influenza A sufferers do not transmit the virus during their illness; instead it rapidly becomes latent in their tissues so that they become symptomless carrier-hosts and develop specific immunity. Next season an extraneous seasonally mediated stimulus reactivates the latent virus residues so that the carrier-host becomes briefly infectious, though symptomless. Antigenic drift occurs because particles reconstituted to be identical with the progenitor virus cannot escape the specific immunity it has provoked in the carrier host. He can shed only mutants also determined by the progenitor virus. From the assortment of mutants shed by the carrier-host, his non-immune companions select that (those) which is best fitted to survive, and it rapidly causes influenzal illness. Epidemics consist largely or entirely of such persons sick with influenza caused by reactivated virus caught from symptomless carrier-hosts.</p></abstract><counts><page-count count="16"></page-count></counts><custom-meta-wrap><custom-meta><meta-name>pdf</meta-name><meta-value>S002217240002578Xa.pdf</meta-value></custom-meta></custom-meta-wrap></article-meta></front><back><ref-list><title>References</title><ref><citation id="ref001" citation-type="journal"><name><surname>Andrewes</surname><given-names>C. H.</given-names></name> (<year>1951</year>). <article-title>The epidemiology of influenza in the light of the 1951 outbreak</article-title>. <source>Proceedings of the Royal Society of Medicine</source> <volume>44</volume>, <fpage>803</fpage>.</citation></ref><ref><citation id="ref002" citation-type="journal"><name><surname>Andrewes</surname><given-names>C. 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A)</source>, <volume>233</volume>, <fpage>440</fpage>.</citation></ref></ref-list></back></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Epidemic mechanisms of Type A influenza</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Epidemic mechanisms of Type A influenza</title></titleInfo><name type="personal"><namePart type="given">R. E.</namePart><namePart type="family">Hope-simpson</namePart><affiliation>Epidemiological Research Unit, 86 Dyer Street, Cirencester, Gloucestershire, England</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>Cambridge University Press</publisher><place><placeTerm type="text">Cambridge, UK</placeTerm></place><dateIssued encoding="w3cdtf">1979-08</dateIssued><copyrightDate encoding="w3cdtf">1979</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract type="normal">The antigenic varieties of influenza A virus isolated from 1968 to 1976 in a surveillance of a small, rather remote population were similar to those from England and Wales as a whole, despite frequent antigenic changes during the period. Household studies in the first two H3N2 influenza A epidemics found low attack rates within households, a high proportion (70%) of affected households with only one case of influenza, similar distributions of affected households in the two epidemics by the number of cases of influenza and similar distributions of the influenza cases by the day of their onset in the household outbreak. No serial interval could be demonstrated by cumulating household outbreaks. More than one minor variant was causing influenza contemporaneously in the same villages in several seasons, and different variants were on one occasion found on successive days in bedfellows. The regular occurrence of epidemics in winter was often accompanied by the disappearance of the epidemic variants and their replacement, after a virus-free interval, by new variants. These epidemiological findings seem best interpreted on the following tentative hypothesis. Influenza A sufferers do not transmit the virus during their illness; instead it rapidly becomes latent in their tissues so that they become symptomless carrier-hosts and develop specific immunity. Next season an extraneous seasonally mediated stimulus reactivates the latent virus residues so that the carrier-host becomes briefly infectious, though symptomless. Antigenic drift occurs because particles reconstituted to be identical with the progenitor virus cannot escape the specific immunity it has provoked in the carrier host. He can shed only mutants also determined by the progenitor virus. From the assortment of mutants shed by the carrier-host, his non-immune companions select that (those) which is best fitted to survive, and it rapidly causes influenzal illness. Epidemics consist largely or entirely of such persons sick with influenza caused by reactivated virus caught from symptomless carrier-hosts.</abstract><relatedItem type="host"><titleInfo><title>Journal of Hygiene</title></titleInfo><titleInfo type="abbreviated"><title>J. Hyg.</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">0022-1724</identifier><identifier type="PublisherID">HYG</identifier><part><date>1979</date><detail type="volume"><caption>vol.</caption><number>83</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>11</start><end>26</end><total>16</total></extent></part></relatedItem><identifier type="istex">2105ADD361658E5FCDA3862C9BB3E414A99DDAE7</identifier><identifier type="ark">ark:/67375/6GQ-90WZ3G4R-C</identifier><identifier type="DOI">10.1017/S002217240002578X</identifier><identifier type="PII">S002217240002578X</identifier><identifier type="ArticleID">02578</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © Cambridge University Press 1979</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-G3RCRD03-V">cambridge</recordContentSource><recordOrigin>Copyright © Cambridge University Press 1979</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6GQ-90WZ3G4R-C/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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