Analyses of human papillomavirus genotypes and viral loads in anogenital warts
Identifieur interne : 000617 ( Istex/Corpus ); précédent : 000616; suivant : 000618Analyses of human papillomavirus genotypes and viral loads in anogenital warts
Auteurs : Siolian L. R. Ball ; David M. Winder ; Katie Vaughan ; Nashat Hanna ; Jonathan Levy ; Jane C. Sterling ; Margaret A. Stanley ; Peter K. C. GoonSource :
- Journal of Medical Virology [ 0146-6615 ] ; 2011-08.
English descriptors
- Teeft :
- Anogenital, Anogenital warts, Assay, Bakkers jmje, Cervical, Clin, Condyloma, Condylomata acuminata, Copy number, Genital, Genital wart samples, Genital warts, Genotyping test, High risk, High risk hpvs, Hpvs, Human papillomavirus, Human papillomavirus infection, Human papillomavirus types, Lesion, Lesion causality, Linear array, Linear array assay, Linear array results, Massuger lfag, Methods section, Mrna, Mrna analysis, Mrna levels, Multiple infections, Oncogenic hpvs, Other hpvs, Papillomavirus, Primer, Qpcr, Relative mrna levels, Risk hpvs, Standard curves, Strain prevalence, Supplementary table, Taqmantm qpcr, Threshold value, Vaccine, Vaccine failure, Viral, Viral load, Viral loads, Virol, Wart tissue, Young women.
Abstract
Condylomata acuminata (genital warts) are the most common sexually transmitted viral diseases. These lesions are caused by infection with mucosal human papillomaviruses (HPVs). However, there is limited information on HPV strain distribution involved in the molecular pathogenesis of these lesions. To address this, the strain prevalence and the frequency of multiple HPV infections were determined in wart tissue obtained from 31 patients attending a wart clinic. These lesions were bisected and subjected to parallel DNA and mRNA extractions. HPV‐type prevalence and incidence of multiple infections were determined by the Roche Linear Array assay. qPCR compared HPV 6, 11, 16, and 18 viral loads and RT‐qPCR measured HPV 6 and 11 E6 genomic expression levels. Seventy‐one percent of these samples were infected with multiple HPVs. Only one sample was negative for HPV 6 or 11 DNA. Forty‐eight percent of samples were positive for a high risk (oncogenic) HPV. The results show that multiple infections in tissue are frequent and the subsequent analysis of HPV 6 and 11 E6 DNA viral loads suggested that other HPVs could be causing lesions. Further analysis of HPV 6/11 E6 mRNA levels showed that there was no discernable relationship between HPV 6 E6 DNA viral load and relative HPV 6 or 11 E6 mRNA levels thereby questioning the relevance of viral load to lesion causality. J. Med. Virol. 83:1345–1350, 2011. © 2011 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jmv.22111
Links to Exploration step
ISTEX:4D122193585FC84E1D55726EC916A2AC11A358EFLe document en format XML
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Goon</name><affiliation><mods:affiliation>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Medical Virology</title><title level="j" type="alt">JOURNAL OF MEDICAL VIROLOGY</title><idno type="ISSN">0146-6615</idno><idno type="eISSN">1096-9071</idno><imprint><biblScope unit="vol">83</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1345">1345</biblScope><biblScope unit="page" to="1350">1350</biblScope><biblScope unit="page-count">6</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2011-08">2011-08</date></imprint><idno type="ISSN">0146-6615</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0146-6615</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Anogenital</term><term>Anogenital warts</term><term>Assay</term><term>Bakkers jmje</term><term>Cervical</term><term>Clin</term><term>Condyloma</term><term>Condylomata acuminata</term><term>Copy number</term><term>Genital</term><term>Genital wart samples</term><term>Genital warts</term><term>Genotyping test</term><term>High risk</term><term>High risk hpvs</term><term>Hpvs</term><term>Human papillomavirus</term><term>Human papillomavirus infection</term><term>Human papillomavirus types</term><term>Lesion</term><term>Lesion causality</term><term>Linear array</term><term>Linear array assay</term><term>Linear array results</term><term>Massuger lfag</term><term>Methods section</term><term>Mrna</term><term>Mrna analysis</term><term>Mrna levels</term><term>Multiple infections</term><term>Oncogenic hpvs</term><term>Other hpvs</term><term>Papillomavirus</term><term>Primer</term><term>Qpcr</term><term>Relative mrna levels</term><term>Risk hpvs</term><term>Standard curves</term><term>Strain prevalence</term><term>Supplementary table</term><term>Taqmantm qpcr</term><term>Threshold value</term><term>Vaccine</term><term>Vaccine failure</term><term>Viral</term><term>Viral load</term><term>Viral loads</term><term>Virol</term><term>Wart tissue</term><term>Young women</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Condylomata acuminata (genital warts) are the most common sexually transmitted viral diseases. These lesions are caused by infection with mucosal human papillomaviruses (HPVs). However, there is limited information on HPV strain distribution involved in the molecular pathogenesis of these lesions. To address this, the strain prevalence and the frequency of multiple HPV infections were determined in wart tissue obtained from 31 patients attending a wart clinic. These lesions were bisected and subjected to parallel DNA and mRNA extractions. HPV‐type prevalence and incidence of multiple infections were determined by the Roche Linear Array assay. qPCR compared HPV 6, 11, 16, and 18 viral loads and RT‐qPCR measured HPV 6 and 11 E6 genomic expression levels. Seventy‐one percent of these samples were infected with multiple HPVs. Only one sample was negative for HPV 6 or 11 DNA. Forty‐eight percent of samples were positive for a high risk (oncogenic) HPV. The results show that multiple infections in tissue are frequent and the subsequent analysis of HPV 6 and 11 E6 DNA viral loads suggested that other HPVs could be causing lesions. Further analysis of HPV 6/11 E6 mRNA levels showed that there was no discernable relationship between HPV 6 E6 DNA viral load and relative HPV 6 or 11 E6 mRNA levels thereby questioning the relevance of viral load to lesion causality. J. Med. 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Ball</name><affiliations><json:string>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</json:string><json:string>E-mail: slrb2@cam.ac.uk</json:string><json:string>Correspondence address: Division of Virology, Department of Pathology, University of Cambridge, Level 5 Laboratories Block, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK.===</json:string></affiliations></json:item><json:item><name>David M. Winder</name><affiliations><json:string>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</json:string></affiliations></json:item><json:item><name>Katie Vaughan</name><affiliations><json:string>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</json:string></affiliations></json:item><json:item><name>Nashat Hanna</name><affiliations><json:string>Department of GU/HIV Medicine, St. Mary's Hospital, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Jonathan Levy</name><affiliations><json:string>Paris Diderot University, ERAMUS Scholar 2007, Paris, France</json:string></affiliations></json:item><json:item><name>Jane C. Sterling</name><affiliations><json:string>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</json:string></affiliations></json:item><json:item><name>Margaret A. Stanley</name><affiliations><json:string>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</json:string></affiliations></json:item><json:item><name>Peter K.C. Goon</name><affiliations><json:string>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>HPV</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>genital warts</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>E6 DNA viral loads</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>E6 mRNA</value></json:item></subject><articleId><json:string>JMV22111</json:string></articleId><arkIstex>ark:/67375/WNG-PJRJLHR6-H</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Condylomata acuminata (genital warts) are the most common sexually transmitted viral diseases. These lesions are caused by infection with mucosal human papillomaviruses (HPVs). However, there is limited information on HPV strain distribution involved in the molecular pathogenesis of these lesions. To address this, the strain prevalence and the frequency of multiple HPV infections were determined in wart tissue obtained from 31 patients attending a wart clinic. These lesions were bisected and subjected to parallel DNA and mRNA extractions. HPV‐type prevalence and incidence of multiple infections were determined by the Roche Linear Array assay. qPCR compared HPV 6, 11, 16, and 18 viral loads and RT‐qPCR measured HPV 6 and 11 E6 genomic expression levels. Seventy‐one percent of these samples were infected with multiple HPVs. Only one sample was negative for HPV 6 or 11 DNA. Forty‐eight percent of samples were positive for a high risk (oncogenic) HPV. The results show that multiple infections in tissue are frequent and the subsequent analysis of HPV 6 and 11 E6 DNA viral loads suggested that other HPVs could be causing lesions. Further analysis of HPV 6/11 E6 mRNA levels showed that there was no discernable relationship between HPV 6 E6 DNA viral load and relative HPV 6 or 11 E6 mRNA levels thereby questioning the relevance of viral load to lesion causality. J. Med. Virol. 83:1345–1350, 2011. © 2011 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>9.01</score><pdfWordCount>4274</pdfWordCount><pdfCharCount>25240</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>6</pdfPageCount><pdfPageSize>594 x 792 pts</pdfPageSize><pdfWordsPerPage>712</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>228</abstractWordCount><abstractCharCount>1435</abstractCharCount><keywordCount>4</keywordCount></qualityIndicators><title>Analyses of human papillomavirus genotypes and viral loads in anogenital warts</title><pmid><json:string>21678438</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Journal of Medical Virology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1002/(ISSN)1096-9071</json:string></doi><issn><json:string>0146-6615</json:string></issn><eissn><json:string>1096-9071</json:string></eissn><publisherId><json:string>JMV</json:string></publisherId><volume>83</volume><issue>8</issue><pages><first>1345</first><last>1350</last><total>6</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Research Article</value></json:item><json:item><value>Research Articles</value></json:item></subject></host><namedEntities><unitex><date><json:string>2011</json:string><json:string>2007</json:string></date><geogName></geogName><orgName><json:string>Merck Research Laboratories, Westpoint, USA, and GSK Biologicals, Rixensart, Belgium</json:string><json:string>Addenbrooke’s Hospital, Hills Road, Cambridge CB</json:string><json:string>Roche Diagnostics Ltd.</json:string><json:string>Department of Pathology, University of Cambridge, Level</json:string><json:string>Mary’s Hospital, London, UK</json:string><json:string>Department of GU/HIV Medicine, St</json:string><json:string>Division of Virology</json:string><json:string>Mary’s Hospital, London, United Kingdom</json:string><json:string>Wiley-Liss, Inc</json:string><json:string>Research Ethics Committee</json:string><json:string>Paris Diderot University</json:string><json:string>LISS, INC.</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Viral Load</json:string><json:string>David M. 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Goon</json:string></persName><placeName><json:string>UK</json:string><json:string>London</json:string><json:string>Paisley</json:string><json:string>France</json:string><json:string>Lyon</json:string></placeName><ref_url><json:string>http://www.cstl.nist.gov/div</json:string></ref_url><ref_bibl><json:string>Fairley et al., 2009</json:string><json:string>Woo et al., 2007</json:string><json:string>Brown et al., 1999</json:string><json:string>Sanclemente et al., 2007</json:string><json:string>Muller et al., 2010</json:string><json:string>Molden et al., 1349</json:string><json:string>Coleman et al., 2008</json:string><json:string>Chan et al., 2009</json:string><json:string>de Boer et al., 2007</json:string><json:string>Aubin et al., 2008</json:string><json:string>Ohl et al. [2006]</json:string><json:string>Nielson et al., 2009</json:string><json:string>Viera and Garrett, 2005</json:string><json:string>Qian et al. 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[2005]</json:string><json:string>Potocnik et al., 2007</json:string><json:string>Ball et al.</json:string><json:string>van Hamont et al., 2006</json:string><json:string>Halfon et al., 2010</json:string><json:string>Cattani et al., 2009</json:string><json:string>van Ham et al., 2005</json:string><json:string>Tucker et al., 2001</json:string><json:string>Schmitt et al., 2010</json:string><json:string>Giuliano et al., 2008</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-PJRJLHR6-H</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - virology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - virology</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Infectious Diseases</json:string><json:string>1 - Life 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type="main">Analyses of human papillomavirus genotypes and viral loads in anogenital warts</title><title level="a" type="short" xml:lang="en">HPV Genotypes and Viral Loads in Anogenital Warts</title><author xml:id="author-0000" role="corresp"><persName><forename type="first">Siolian L.R.</forename><surname>Ball</surname></persName><email>slrb2@cam.ac.uk</email><affiliation><orgName type="department">Department of Pathology</orgName><orgName type="institution">University of Cambridge</orgName><address><addrLine>Cambridge</addrLine><addrLine>United Kingdom</addrLine><country key="GB" xml:lang="en">UNITED KINGDOM</country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">David M.</forename><surname>Winder</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><orgName type="institution">University of Cambridge</orgName><address><addrLine>Cambridge</addrLine><addrLine>United Kingdom</addrLine><country key="GB" xml:lang="en">UNITED KINGDOM</country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Katie</forename><surname>Vaughan</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><orgName type="institution">University of Cambridge</orgName><address><addrLine>Cambridge</addrLine><addrLine>United Kingdom</addrLine><country key="GB" xml:lang="en">UNITED KINGDOM</country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Nashat</forename><surname>Hanna</surname></persName><affiliation><orgName type="division">Department of GU/HIV Medicine</orgName><orgName type="institution">St. Mary's Hospital</orgName><address><addrLine>London</addrLine><addrLine>United Kingdom</addrLine><country key="GB" xml:lang="en">UNITED KINGDOM</country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Jonathan</forename><surname>Levy</surname></persName><affiliation><orgName type="institution">Paris Diderot University</orgName><address><addrLine>ERAMUS Scholar 2007</addrLine><addrLine>Paris, France</addrLine><country key="FR" xml:lang="en">FRANCE</country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Jane C.</forename><surname>Sterling</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><orgName type="institution">University of Cambridge</orgName><address><addrLine>Cambridge</addrLine><addrLine>United Kingdom</addrLine><country key="GB" xml:lang="en">UNITED KINGDOM</country></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Margaret A.</forename><surname>Stanley</surname></persName><affiliation><orgName type="department">Department of Pathology</orgName><orgName type="institution">University of 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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><p><hi rend="italic">Condylomata acuminata</hi> (genital warts) are the most common sexually transmitted viral diseases. These lesions are caused by infection with mucosal human papillomaviruses (HPVs). However, there is limited information on HPV strain distribution involved in the molecular pathogenesis of these lesions. To address this, the strain prevalence and the frequency of multiple HPV infections were determined in wart tissue obtained from 31 patients attending a wart clinic. These lesions were bisected and subjected to parallel DNA and mRNA extractions. HPV‐type prevalence and incidence of multiple infections were determined by the Roche Linear Array assay. qPCR compared HPV 6, 11, 16, and 18 viral loads and RT‐qPCR measured HPV 6 and 11 E6 genomic expression levels. Seventy‐one percent of these samples were infected with multiple HPVs. Only one sample was negative for HPV 6 or 11 DNA. Forty‐eight percent of samples were positive for a high risk (oncogenic) HPV. The results show that multiple infections in tissue are frequent and the subsequent analysis of HPV 6 and 11 E6 DNA viral loads suggested that other HPVs could be causing lesions. Further analysis of HPV 6/11 E6 mRNA levels showed that there was no discernable relationship between HPV 6 E6 DNA viral load and relative HPV 6 or 11 E6 mRNA levels thereby questioning the relevance of viral load to lesion causality. J. Med. Virol. 83:1345–1350, 2011. © 2011 Wiley‐Liss, Inc.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="kwd1">HPV</term><term xml:id="kwd2">genital warts</term><term xml:id="kwd3">E6 DNA viral loads</term><term xml:id="kwd4">E6 mRNA</term></keywords><keywords rend="articleCategory"><term>Research Article</term></keywords><keywords rend="tocHeading1"><term>Research Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-PJRJLHR6-H/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1096-9071</doi><issn type="print">0146-6615</issn><issn type="electronic">1096-9071</issn><idGroup><id type="product" value="JMV"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="JOURNAL OF MEDICAL VIROLOGY">Journal of Medical Virology</title><title type="short">J. 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Additional supporting information may be found in the online version of this article.
</p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:01466615:media:jmv22111:jmv_22111_sm_SuppTabS1"></mediaResource><caption>Supplemental Table S1</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:01466615:media:jmv22111:jmv_22111_sm_SuppTabS2"></mediaResource><caption>Supplemental Table S2</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p><i>Condylomata acuminata</i> (genital warts) are the most common sexually transmitted viral diseases. These lesions are caused by infection with mucosal human papillomaviruses (HPVs). However, there is limited information on HPV strain distribution involved in the molecular pathogenesis of these lesions. To address this, the strain prevalence and the frequency of multiple HPV infections were determined in wart tissue obtained from 31 patients attending a wart clinic. These lesions were bisected and subjected to parallel DNA and mRNA extractions. HPV‐type prevalence and incidence of multiple infections were determined by the Roche Linear Array assay. qPCR compared HPV 6, 11, 16, and 18 viral loads and RT‐qPCR measured HPV 6 and 11 E6 genomic expression levels. Seventy‐one percent of these samples were infected with multiple HPVs. Only one sample was negative for HPV 6 or 11 DNA. Forty‐eight percent of samples were positive for a high risk (oncogenic) HPV. The results show that multiple infections in tissue are frequent and the subsequent analysis of HPV 6 and 11 E6 DNA viral loads suggested that other HPVs could be causing lesions. Further analysis of HPV 6/11 E6 mRNA levels showed that there was no discernable relationship between HPV 6 E6 DNA viral load and relative HPV 6 or 11 E6 mRNA levels thereby questioning the relevance of viral load to lesion causality. J. Med. Virol. 83:1345–1350, 2011. © 2011 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Conflicts of interest: PKCG and MAS act as consultants to Sanofi Pasteur‐MSD, Lyon, France and are in receipt of an unrestricted educational grant. MAS also acts as consultant to Merck Research Laboratories, Westpoint, USA, and GSK Biologicals, Rixensart, Belgium.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Analyses of human papillomavirus genotypes and viral loads in anogenital warts</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>HPV Genotypes and Viral Loads in Anogenital Warts</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Analyses of human papillomavirus genotypes and viral loads in anogenital warts</title></titleInfo><name type="personal"><namePart type="given">Siolian L.R.</namePart><namePart type="family">Ball</namePart><affiliation>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</affiliation><affiliation>E-mail: slrb2@cam.ac.uk</affiliation><affiliation>Correspondence address: Division of Virology, Department of Pathology, University of Cambridge, Level 5 Laboratories Block, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK.===</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David M.</namePart><namePart type="family">Winder</namePart><affiliation>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Katie</namePart><namePart type="family">Vaughan</namePart><affiliation>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nashat</namePart><namePart type="family">Hanna</namePart><affiliation>Department of GU/HIV Medicine, St. Mary's Hospital, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jonathan</namePart><namePart type="family">Levy</namePart><affiliation>Paris Diderot University, ERAMUS Scholar 2007, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jane C.</namePart><namePart type="family">Sterling</namePart><affiliation>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Margaret A.</namePart><namePart type="family">Stanley</namePart><affiliation>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter K.C.</namePart><namePart type="family">Goon</namePart><affiliation>Department of Pathology, University of Cambridge, Cambridge, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-08</dateIssued><dateValid encoding="w3cdtf">2011-03-09</dateValid><copyrightDate encoding="w3cdtf">2011</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">1</extent><extent unit="tables">3</extent><extent unit="references">33</extent><extent unit="words">5298</extent></physicalDescription><abstract lang="en">Condylomata acuminata (genital warts) are the most common sexually transmitted viral diseases. These lesions are caused by infection with mucosal human papillomaviruses (HPVs). However, there is limited information on HPV strain distribution involved in the molecular pathogenesis of these lesions. To address this, the strain prevalence and the frequency of multiple HPV infections were determined in wart tissue obtained from 31 patients attending a wart clinic. These lesions were bisected and subjected to parallel DNA and mRNA extractions. HPV‐type prevalence and incidence of multiple infections were determined by the Roche Linear Array assay. qPCR compared HPV 6, 11, 16, and 18 viral loads and RT‐qPCR measured HPV 6 and 11 E6 genomic expression levels. Seventy‐one percent of these samples were infected with multiple HPVs. Only one sample was negative for HPV 6 or 11 DNA. Forty‐eight percent of samples were positive for a high risk (oncogenic) HPV. The results show that multiple infections in tissue are frequent and the subsequent analysis of HPV 6 and 11 E6 DNA viral loads suggested that other HPVs could be causing lesions. Further analysis of HPV 6/11 E6 mRNA levels showed that there was no discernable relationship between HPV 6 E6 DNA viral load and relative HPV 6 or 11 E6 mRNA levels thereby questioning the relevance of viral load to lesion causality. J. Med. Virol. 83:1345–1350, 2011. © 2011 Wiley‐Liss, Inc.</abstract><note type="content">*Conflicts of interest: PKCG and MAS act as consultants to Sanofi Pasteur‐MSD, Lyon, France and are in receipt of an unrestricted educational grant. MAS also acts as consultant to Merck Research Laboratories, Westpoint, USA, and GSK Biologicals, Rixensart, Belgium.</note><note type="funding">British Skin Foundation and Cancer Research UK (to P.K.C.G.)</note><subject lang="en"><genre>keywords</genre><topic>HPV</topic><topic>genital warts</topic><topic>E6 DNA viral loads</topic><topic>E6 mRNA</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Medical Virology</title></titleInfo><titleInfo type="abbreviated"><title>J. Med. Virol.</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><note type="content"> Additional supporting information may be found in the online version of this article.Supporting Info Item: Supplemental Table S1 - Supplemental Table S2 - </note><subject><genre>article-category</genre><topic>Research Article</topic><topic>Research Articles</topic></subject><identifier type="ISSN">0146-6615</identifier><identifier type="eISSN">1096-9071</identifier><identifier type="DOI">10.1002/(ISSN)1096-9071</identifier><identifier type="PublisherID">JMV</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>83</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>1345</start><end>1350</end><total>6</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>Human papillomavirus genotype distribution in external acuminata condylomata: A large French national study (EDiTH IV)</title></titleInfo><name type="personal"><namePart type="given">F</namePart><namePart type="family">Aubin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Prétet</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AC</namePart><namePart type="family">Jacquard</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Saunier</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">X</namePart><namePart type="family">Carcopino</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Jaroud</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Pradat</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Soubeyrand</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Leocmach</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Mougin</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Riethmuller</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Aubin F, Prétet JL, Jacquard AC, Saunier M, Carcopino X, Jaroud F, Pradat P, Soubeyrand B, Leocmach Y, Mougin C, Riethmuller D. 2008. 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