Influenza A Virus Shedding and Infectivity in Households

Background. Viral shedding is often considered to correlate with the infectivity of influenza, but the evidence for this is limited. Methods. In a detailed study of influenza virus transmission within households in 2008-2012, index case patients with confirmed influenza were identified in outpatient...

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Veröffentlicht in:The Journal of infectious diseases 2015-11, Vol.212 (9), p.1420-1428
Hauptverfasser: Tsang, Tim K., Cowling, Benjamin J., Fang, Vicky J., Chan, Kwok-Hung, Ip, Dennis K. M., Leung, Gabriel M., Peiris, J. S. Malik, Cauchemez, Simon
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container_end_page 1428
container_issue 9
container_start_page 1420
container_title The Journal of infectious diseases
container_volume 212
creator Tsang, Tim K.
Cowling, Benjamin J.
Fang, Vicky J.
Chan, Kwok-Hung
Ip, Dennis K. M.
Leung, Gabriel M.
Peiris, J. S. Malik
Cauchemez, Simon
description Background. Viral shedding is often considered to correlate with the infectivity of influenza, but the evidence for this is limited. Methods. In a detailed study of influenza virus transmission within households in 2008-2012, index case patients with confirmed influenza were identified in outpatient clinics, and we collected nose and throat swab spec-, imens for testing by reverse-transcription polymerase chain reaction from all household members regardless of illness. We used individual-based hazard models to characterize the relationship between viral load (V) and infectivity. Results. Assuming that infectivity was proportional to viral load V gave the worst fit, because it strongly overestimated the proportion of transmission occurring at symptom onset. Alternative models assuming that infectivity was proportional to a various functions of V provided better fits, although they all overestimated the proportion of transmission occurring > 3 days after symptom onset. The best fitting model assumed that infectivity was proportion to Vγ, with estimates of γ = 0.136 and γ = 0.156 for seasonal influenza A(H1N1) and A(H3N2) respectively. Conclusions. All the models we considered that used viral loads to approximate infectivity of a case imperfectly explained the timing of influenza secondary infections in households. Identification of more accurate correlates of infectivity will be important to inform control policies and disease modeling.
doi_str_mv 10.1093/infdis/jiv225
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M. ; Leung, Gabriel M. ; Peiris, J. S. Malik ; Cauchemez, Simon</creator><creatorcontrib>Tsang, Tim K. ; Cowling, Benjamin J. ; Fang, Vicky J. ; Chan, Kwok-Hung ; Ip, Dennis K. M. ; Leung, Gabriel M. ; Peiris, J. S. Malik ; Cauchemez, Simon</creatorcontrib><description>Background. Viral shedding is often considered to correlate with the infectivity of influenza, but the evidence for this is limited. Methods. In a detailed study of influenza virus transmission within households in 2008-2012, index case patients with confirmed influenza were identified in outpatient clinics, and we collected nose and throat swab spec-, imens for testing by reverse-transcription polymerase chain reaction from all household members regardless of illness. We used individual-based hazard models to characterize the relationship between viral load (V) and infectivity. Results. Assuming that infectivity was proportional to viral load V gave the worst fit, because it strongly overestimated the proportion of transmission occurring at symptom onset. Alternative models assuming that infectivity was proportional to a various functions of V provided better fits, although they all overestimated the proportion of transmission occurring &gt; 3 days after symptom onset. The best fitting model assumed that infectivity was proportion to Vγ, with estimates of γ = 0.136 and γ = 0.156 for seasonal influenza A(H1N1) and A(H3N2) respectively. Conclusions. All the models we considered that used viral loads to approximate infectivity of a case imperfectly explained the timing of influenza secondary infections in households. Identification of more accurate correlates of infectivity will be important to inform control policies and disease modeling.</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1093/infdis/jiv225</identifier><identifier>PMID: 25883385</identifier><language>eng</language><publisher>United States: Oxford University Press</publisher><subject>Adolescent ; Adult ; Family Characteristics ; Female ; Humans ; Influenza A virus ; Influenza A Virus, H1N1 Subtype - isolation &amp; purification ; Influenza A Virus, H3N2 Subtype - isolation &amp; purification ; Influenza, Human - transmission ; Influenza, Human - virology ; Linear Models ; Major and Brief Reports ; Male ; Middle Aged ; Nose - virology ; Oseltamivir - therapeutic use ; Pharynx - virology ; Prospective Studies ; Specimen Handling ; Viral Load ; Virus Shedding ; VIRUSES ; Young Adult</subject><ispartof>The Journal of infectious diseases, 2015-11, Vol.212 (9), p.1420-1428</ispartof><rights>Copyright © 2015 Oxford University Press on behalf of the Infectious Diseases Society of America</rights><rights>The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.</rights><rights>The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: . 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-b8f7314dbe6028d49448b0c2c3276dd6f010680a2089b489381afe90d3ccd68e3</citedby><cites>FETCH-LOGICAL-c442t-b8f7314dbe6028d49448b0c2c3276dd6f010680a2089b489381afe90d3ccd68e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/43709384$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/43709384$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,780,784,803,885,27924,27925,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25883385$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsang, Tim K.</creatorcontrib><creatorcontrib>Cowling, Benjamin J.</creatorcontrib><creatorcontrib>Fang, Vicky J.</creatorcontrib><creatorcontrib>Chan, Kwok-Hung</creatorcontrib><creatorcontrib>Ip, Dennis K. 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Assuming that infectivity was proportional to viral load V gave the worst fit, because it strongly overestimated the proportion of transmission occurring at symptom onset. Alternative models assuming that infectivity was proportional to a various functions of V provided better fits, although they all overestimated the proportion of transmission occurring &gt; 3 days after symptom onset. The best fitting model assumed that infectivity was proportion to Vγ, with estimates of γ = 0.136 and γ = 0.156 for seasonal influenza A(H1N1) and A(H3N2) respectively. Conclusions. All the models we considered that used viral loads to approximate infectivity of a case imperfectly explained the timing of influenza secondary infections in households. 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M.</au><au>Leung, Gabriel M.</au><au>Peiris, J. S. Malik</au><au>Cauchemez, Simon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Influenza A Virus Shedding and Infectivity in Households</atitle><jtitle>The Journal of infectious diseases</jtitle><addtitle>J Infect Dis</addtitle><date>2015-11-01</date><risdate>2015</risdate><volume>212</volume><issue>9</issue><spage>1420</spage><epage>1428</epage><pages>1420-1428</pages><issn>0022-1899</issn><eissn>1537-6613</eissn><abstract>Background. Viral shedding is often considered to correlate with the infectivity of influenza, but the evidence for this is limited. Methods. In a detailed study of influenza virus transmission within households in 2008-2012, index case patients with confirmed influenza were identified in outpatient clinics, and we collected nose and throat swab spec-, imens for testing by reverse-transcription polymerase chain reaction from all household members regardless of illness. We used individual-based hazard models to characterize the relationship between viral load (V) and infectivity. Results. Assuming that infectivity was proportional to viral load V gave the worst fit, because it strongly overestimated the proportion of transmission occurring at symptom onset. Alternative models assuming that infectivity was proportional to a various functions of V provided better fits, although they all overestimated the proportion of transmission occurring &gt; 3 days after symptom onset. The best fitting model assumed that infectivity was proportion to Vγ, with estimates of γ = 0.136 and γ = 0.156 for seasonal influenza A(H1N1) and A(H3N2) respectively. Conclusions. All the models we considered that used viral loads to approximate infectivity of a case imperfectly explained the timing of influenza secondary infections in households. 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subjects Adolescent
Adult
Family Characteristics
Female
Humans
Influenza A virus
Influenza A Virus, H1N1 Subtype - isolation & purification
Influenza A Virus, H3N2 Subtype - isolation & purification
Influenza, Human - transmission
Influenza, Human - virology
Linear Models
Major and Brief Reports
Male
Middle Aged
Nose - virology
Oseltamivir - therapeutic use
Pharynx - virology
Prospective Studies
Specimen Handling
Viral Load
Virus Shedding
VIRUSES
Young Adult
title Influenza A Virus Shedding and Infectivity in Households
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