Quasispecies analysis of novel HIV‐1 recombinants of subtypes A and G reveals no similarity to the mosaic structure of CRF02_AG
Identifieur interne : 000649 ( Istex/Corpus ); précédent : 000648; suivant : 000650Quasispecies analysis of novel HIV‐1 recombinants of subtypes A and G reveals no similarity to the mosaic structure of CRF02_AG
Auteurs : Rebecca L. R. Powell ; Frank A. J. Konings ; Aubin Nanfack ; Sherri Burda ; Mateusz M. Urbanski ; D. Saa ; Phillipe N. NyambiSource :
- Journal of Medical Virology [ 0146-6615 ] ; 2007-09.
English descriptors
- KwdEn :
- Bootscanning, Bootstrap, Bootstrap plots, Bootstrap value, Breakpoint, Breakpoint analysis, Breakpoints, Burda, Cameroon, Clone, Dual infections, Genetic material, Grant sponsor, Human virus type, Hxb2, Hxb2 location, Konings, Nyambi, Parental subtypes, Phylogenetic, Phylogenetic analysis, Phylogenetic trees, Present study, Primer, Quasispecies, Recombinant, Recombinant form, Recombinant forms, Recombinant pattern, Recombinant patterns, Recombination, Recombination breakpoints, Reference sequences, Replicative, Study subjects, Subsequent breakpoint analysis, Subtype, Subtypes, Tness, Urfs, Viral, Viral forms, Virol, Virus, Virus culture, Virus type, York university school, Zhong.
- Teeft :
- Bootscanning, Bootstrap, Bootstrap plots, Bootstrap value, Breakpoint, Breakpoint analysis, Breakpoints, Burda, Cameroon, Clone, Dual infections, Genetic material, Grant sponsor, Human virus type, Hxb2, Hxb2 location, Konings, Nyambi, Parental subtypes, Phylogenetic, Phylogenetic analysis, Phylogenetic trees, Present study, Primer, Quasispecies, Recombinant, Recombinant form, Recombinant forms, Recombinant pattern, Recombinant patterns, Recombination, Recombination breakpoints, Reference sequences, Replicative, Study subjects, Subsequent breakpoint analysis, Subtype, Subtypes, Tness, Urfs, Viral, Viral forms, Virol, Virus, Virus culture, Virus type, York university school, Zhong.
Abstract
HIV‐1 circulating recombinant form (CRF) 02_AG is responsible for greater than 65% of HIV‐1 infections in Cameroon and is widespread across West and West‐Central Africa. The parental subtypes A1 and G cocirculate in this part of Africa, and high rates of infection predispose to the generation of AG unique recombinant forms (URFs). Little is known as to whether A1 and G can recombine and thrive in vivo with breakpoints other than those characteristic of CRF02_AG. In this study, six unique recombinant viruses of subtypes A1 and G were identified in two individuals in Cameroon. A 1.5 kb fragment of the reverse transcriptase (RT) region of pol (HXB2 location 2,612–4,159) and the entire env gene (HXB2 location 6,202–9,096) were evaluated by phylogenetic and breakpoint analyses. Each URF was found to have breakpoints different than CRF02_AG, indicating that A and G gene segments are functionally compatible with more than one pattern of recombination. Furthermore, contemporaneous, cultured viruses from these individuals were analyzed, revealing different proportions of URFs compared to those found in plasma, possibly indicating compart mentalization and/or phenotypic variation among the URFs. CRF02_AG emerged from West‐Central Africa to become a highly successful viral strain. As such, monitoring the spread of newly emerging AG recombinants is critical not only for understanding the epidemiology of HIV‐1, but also in the design of future therapeutics and vaccines appropriate to this part of Africa, and globally. J. Med. Virol. 79:1270–1285, 2007. © Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jmv.20937
Links to Exploration step
ISTEX:EB49E7B8174AF945CCC0CBF0C7A881B69BC77A77Le document en format XML
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R. Powell</name><affiliation><mods:affiliation>Department of Microbiology, New York University School of Medicine, New York, New York</mods:affiliation></affiliation></author><author><name sortKey="Konings, Frank A J" sort="Konings, Frank A J" uniqKey="Konings F" first="Frank A. J." last="Konings">Frank A. J. 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Urbanski</name><affiliation><mods:affiliation>Department of Pathology, New York University School of Medicine, New York, New York</mods:affiliation></affiliation></author><author><name sortKey="Saa, D" sort="Saa, D" uniqKey="Saa D" first="D." last="Saa">D. Saa</name><affiliation><mods:affiliation>Ministry of Public Health, Yaoundé, Cameroon</mods:affiliation></affiliation></author><author><name sortKey="Nyambi, Phillipe N" sort="Nyambi, Phillipe N" uniqKey="Nyambi P" first="Phillipe N." last="Nyambi">Phillipe N. Nyambi</name><affiliation><mods:affiliation>Department of Pathology, New York University School of Medicine, New York, New York</mods:affiliation></affiliation><affiliation><mods:affiliation>Veterans Affairs New York Harbor Healthcare Systems, New York, New York</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Pathology, New York University School of Medicine, c/o V.A. Medical Center, 423 East 23rd street, Room 18124N, New York, NY 10010.===</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">79</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1270">1270</biblScope><biblScope unit="page" to="1285">1285</biblScope><biblScope unit="page-count">16</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-09">2007-09</date></imprint><idno type="ISSN">0146-6615</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0146-6615</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Bootscanning</term><term>Bootstrap</term><term>Bootstrap plots</term><term>Bootstrap value</term><term>Breakpoint</term><term>Breakpoint analysis</term><term>Breakpoints</term><term>Burda</term><term>Cameroon</term><term>Clone</term><term>Dual infections</term><term>Genetic material</term><term>Grant sponsor</term><term>Human virus type</term><term>Hxb2</term><term>Hxb2 location</term><term>Konings</term><term>Nyambi</term><term>Parental subtypes</term><term>Phylogenetic</term><term>Phylogenetic analysis</term><term>Phylogenetic trees</term><term>Present study</term><term>Primer</term><term>Quasispecies</term><term>Recombinant</term><term>Recombinant form</term><term>Recombinant forms</term><term>Recombinant pattern</term><term>Recombinant patterns</term><term>Recombination</term><term>Recombination breakpoints</term><term>Reference sequences</term><term>Replicative</term><term>Study subjects</term><term>Subsequent breakpoint analysis</term><term>Subtype</term><term>Subtypes</term><term>Tness</term><term>Urfs</term><term>Viral</term><term>Viral forms</term><term>Virol</term><term>Virus</term><term>Virus culture</term><term>Virus type</term><term>York university school</term><term>Zhong</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Bootscanning</term><term>Bootstrap</term><term>Bootstrap plots</term><term>Bootstrap value</term><term>Breakpoint</term><term>Breakpoint analysis</term><term>Breakpoints</term><term>Burda</term><term>Cameroon</term><term>Clone</term><term>Dual infections</term><term>Genetic material</term><term>Grant sponsor</term><term>Human virus type</term><term>Hxb2</term><term>Hxb2 location</term><term>Konings</term><term>Nyambi</term><term>Parental subtypes</term><term>Phylogenetic</term><term>Phylogenetic analysis</term><term>Phylogenetic trees</term><term>Present study</term><term>Primer</term><term>Quasispecies</term><term>Recombinant</term><term>Recombinant form</term><term>Recombinant forms</term><term>Recombinant pattern</term><term>Recombinant patterns</term><term>Recombination</term><term>Recombination breakpoints</term><term>Reference sequences</term><term>Replicative</term><term>Study subjects</term><term>Subsequent breakpoint analysis</term><term>Subtype</term><term>Subtypes</term><term>Tness</term><term>Urfs</term><term>Viral</term><term>Viral forms</term><term>Virol</term><term>Virus</term><term>Virus culture</term><term>Virus type</term><term>York university school</term><term>Zhong</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">HIV‐1 circulating recombinant form (CRF) 02_AG is responsible for greater than 65% of HIV‐1 infections in Cameroon and is widespread across West and West‐Central Africa. The parental subtypes A1 and G cocirculate in this part of Africa, and high rates of infection predispose to the generation of AG unique recombinant forms (URFs). Little is known as to whether A1 and G can recombine and thrive in vivo with breakpoints other than those characteristic of CRF02_AG. In this study, six unique recombinant viruses of subtypes A1 and G were identified in two individuals in Cameroon. A 1.5 kb fragment of the reverse transcriptase (RT) region of pol (HXB2 location 2,612–4,159) and the entire env gene (HXB2 location 6,202–9,096) were evaluated by phylogenetic and breakpoint analyses. Each URF was found to have breakpoints different than CRF02_AG, indicating that A and G gene segments are functionally compatible with more than one pattern of recombination. Furthermore, contemporaneous, cultured viruses from these individuals were analyzed, revealing different proportions of URFs compared to those found in plasma, possibly indicating compart mentalization and/or phenotypic variation among the URFs. CRF02_AG emerged from West‐Central Africa to become a highly successful viral strain. As such, monitoring the spread of newly emerging AG recombinants is critical not only for understanding the epidemiology of HIV‐1, but also in the design of future therapeutics and vaccines appropriate to this part of Africa, and globally. J. Med. Virol. 79:1270–1285, 2007. © Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>clone</json:string><json:string>recombinant</json:string><json:string>virol</json:string><json:string>urfs</json:string><json:string>recombination</json:string><json:string>breakpoint</json:string><json:string>breakpoints</json:string><json:string>phylogenetic</json:string><json:string>quasispecies</json:string><json:string>bootstrap</json:string><json:string>cameroon</json:string><json:string>subtypes</json:string><json:string>viral</json:string><json:string>nyambi</json:string><json:string>konings</json:string><json:string>bootstrap value</json:string><json:string>zhong</json:string><json:string>human virus type</json:string><json:string>hxb2</json:string><json:string>phylogenetic analysis</json:string><json:string>replicative</json:string><json:string>hxb2 location</json:string><json:string>burda</json:string><json:string>study subjects</json:string><json:string>tness</json:string><json:string>primer</json:string><json:string>bootscanning</json:string><json:string>virus culture</json:string><json:string>recombinant form</json:string><json:string>subtype</json:string><json:string>reference sequences</json:string><json:string>phylogenetic trees</json:string><json:string>breakpoint analysis</json:string><json:string>parental subtypes</json:string><json:string>recombinant forms</json:string><json:string>grant sponsor</json:string><json:string>present study</json:string><json:string>viral forms</json:string><json:string>bootstrap plots</json:string><json:string>dual infections</json:string><json:string>genetic material</json:string><json:string>subsequent breakpoint analysis</json:string><json:string>york university school</json:string><json:string>recombinant patterns</json:string><json:string>recombinant pattern</json:string><json:string>recombination breakpoints</json:string><json:string>virus type</json:string><json:string>virus</json:string></teeft></keywords><author><json:item><name>Rebecca L.R. Powell</name><affiliations><json:string>Department of Microbiology, New York University School of Medicine, New York, New York</json:string></affiliations></json:item><json:item><name>Frank A.J. Konings</name><affiliations><json:string>Department of Microbiology, New York University School of Medicine, New York, New York</json:string></affiliations></json:item><json:item><name>Aubin Nanfack</name><affiliations><json:string>Laboratoire de Santé Hygiène Mobile, Yaoundé, Cameroon</json:string></affiliations></json:item><json:item><name>Sherri Burda</name><affiliations><json:string>Department of Pathology, New York University School of Medicine, New York, New York</json:string></affiliations></json:item><json:item><name>Mateusz M. Urbanski</name><affiliations><json:string>Department of Pathology, New York University School of Medicine, New York, New York</json:string></affiliations></json:item><json:item><name>D. Saa</name><affiliations><json:string>Ministry of Public Health, Yaoundé, Cameroon</json:string></affiliations></json:item><json:item><name>Phillipe N. Nyambi</name><affiliations><json:string>Department of Pathology, New York University School of Medicine, New York, New York</json:string><json:string>Veterans Affairs New York Harbor Healthcare Systems, New York, New York</json:string><json:string>Department of Pathology, New York University School of Medicine, c/o V.A. Medical Center, 423 East 23rd street, Room 18124N, New York, NY 10010.===</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>HIV‐1 CRF02_AG</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cameroon</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>HIV‐1 recombination</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>evolution</value></json:item></subject><articleId><json:string>JMV20937</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>HIV‐1 circulating recombinant form (CRF) 02_AG is responsible for greater than 65% of HIV‐1 infections in Cameroon and is widespread across West and West‐Central Africa. The parental subtypes A1 and G cocirculate in this part of Africa, and high rates of infection predispose to the generation of AG unique recombinant forms (URFs). Little is known as to whether A1 and G can recombine and thrive in vivo with breakpoints other than those characteristic of CRF02_AG. In this study, six unique recombinant viruses of subtypes A1 and G were identified in two individuals in Cameroon. A 1.5 kb fragment of the reverse transcriptase (RT) region of pol (HXB2 location 2,612–4,159) and the entire env gene (HXB2 location 6,202–9,096) were evaluated by phylogenetic and breakpoint analyses. Each URF was found to have breakpoints different than CRF02_AG, indicating that A and G gene segments are functionally compatible with more than one pattern of recombination. Furthermore, contemporaneous, cultured viruses from these individuals were analyzed, revealing different proportions of URFs compared to those found in plasma, possibly indicating compart mentalization and/or phenotypic variation among the URFs. CRF02_AG emerged from West‐Central Africa to become a highly successful viral strain. As such, monitoring the spread of newly emerging AG recombinants is critical not only for understanding the epidemiology of HIV‐1, but also in the design of future therapeutics and vaccines appropriate to this part of Africa, and globally. J. Med. Virol. 79:1270–1285, 2007. © Wiley‐Liss, Inc.</abstract><qualityIndicators><score>7.868</score><pdfVersion>1.3</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1584</abstractCharCount><pdfWordCount>5858</pdfWordCount><pdfCharCount>36221</pdfCharCount><pdfPageCount>16</pdfPageCount><abstractWordCount>239</abstractWordCount></qualityIndicators><title>Quasispecies analysis of novel HIV‐1 recombinants of subtypes A and G reveals no similarity to the mosaic structure of CRF02_AG</title><genre><json:string>article</json:string></genre><host><title>Journal of Medical 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xml:id="author-0000"><persName><forename type="first">Rebecca L.R.</forename><surname>Powell</surname></persName><affiliation>Department of Microbiology, New York University School of Medicine, New York, New York<address><country key="US"></country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Frank A.J.</forename><surname>Konings</surname></persName><affiliation>Department of Microbiology, New York University School of Medicine, New York, New York<address><country key="US"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Aubin</forename><surname>Nanfack</surname></persName><affiliation>Laboratoire de Santé Hygiène Mobile, Yaoundé, Cameroon<address><country key="US"></country></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Sherri</forename><surname>Burda</surname></persName><affiliation>Department of Pathology, New York University School of Medicine, New York, New York<address><country key="US"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Mateusz M.</forename><surname>Urbanski</surname></persName><affiliation>Department of Pathology, New York University School of Medicine, New York, New York<address><country key="US"></country></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">D.</forename><surname>Saa</surname></persName><affiliation>Ministry of Public Health, Yaoundé, Cameroon<address><country key="US"></country></address></affiliation></author><author xml:id="author-0006" role="corresp"><persName><forename type="first">Phillipe N.</forename><surname>Nyambi</surname></persName><email>phillipe.nyambi@med.nyu.edu</email><affiliation>Department of Pathology, New York University School of Medicine, New York, New York<address><country key="US"></country></address></affiliation><affiliation>Veterans Affairs New York Harbor Healthcare Systems, New York, New York<address><country key="US"></country></address></affiliation><affiliation>Department of Pathology, New York University School of Medicine, c/o V.A. Medical Center, 423 East 23rd street, Room 18124N, New York, NY 10010.===</affiliation></author><idno type="istex">EB49E7B8174AF945CCC0CBF0C7A881B69BC77A77</idno><idno type="DOI">10.1002/jmv.20937</idno><idno type="unit">JMV20937</idno><idno type="toTypesetVersion">file:JMV.JMV20937.pdf</idno></analytic><monogr><title level="j" type="main">Journal of Medical Virology</title><title level="j" type="alt">JOURNAL OF MEDICAL VIROLOGY</title><idno type="pISSN">0146-6615</idno><idno type="eISSN">1096-9071</idno><idno type="book-DOI">10.1002/(ISSN)1096-9071</idno><idno type="book-part-DOI">10.1002/jmv.v79:9</idno><idno type="product">JMV</idno><imprint><biblScope unit="vol">79</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="1270">1270</biblScope><biblScope unit="page" to="1285">1285</biblScope><biblScope unit="page-count">16</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007-09"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><head>Abstract</head><p>HIV‐1 circulating recombinant form (CRF) 02_AG is responsible for greater than 65% of HIV‐1 infections in Cameroon and is widespread across West and West‐Central Africa. The parental subtypes A1 and G cocirculate in this part of Africa, and high rates of infection predispose to the generation of AG unique recombinant forms (URFs). Little is known as to whether A1 and G can recombine and thrive in vivo with breakpoints other than those characteristic of CRF02_AG. In this study, six unique recombinant viruses of subtypes A1 and G were identified in two individuals in Cameroon. A 1.5 kb fragment of the reverse transcriptase (RT) region of <hi rend="italic">pol</hi> (HXB2 location 2,612–4,159) and the entire <hi rend="italic">env</hi> gene (HXB2 location 6,202–9,096) were evaluated by phylogenetic and breakpoint analyses. Each URF was found to have breakpoints different than CRF02_AG, indicating that A and G gene segments are functionally compatible with more than one pattern of recombination. Furthermore, contemporaneous, cultured viruses from these individuals were analyzed, revealing different proportions of URFs compared to those found in plasma, possibly indicating compart mentalization and/or phenotypic variation among the URFs. CRF02_AG emerged from West‐Central Africa to become a highly successful viral strain. As such, monitoring the spread of newly emerging AG recombinants is critical not only for understanding the epidemiology of HIV‐1, but also in the design of future therapeutics and vaccines appropriate to this part of Africa, and globally. J. Med. Virol. 79:1270–1285, 2007. © Wiley‐Liss, Inc.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="kwd1">HIV‐1 CRF02_AG</term><term xml:id="kwd2">Cameroon</term><term xml:id="kwd3">HIV‐1 recombination</term><term xml:id="kwd4">evolution</term></keywords><classCode scheme="articleCategory">Research Article</classCode></textClass><langUsage><language ident="EN"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/EB49E7B8174AF945CCC0CBF0C7A881B69BC77A77/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. Med. Virol.</title></titleGroup></publicationMeta><publicationMeta level="part" position="90"><doi origin="wiley" registered="yes">10.1002/jmv.v79:9</doi><numberingGroup><numbering type="journalVolume" number="79">79</numbering><numbering type="journalIssue">9</numbering></numberingGroup><coverDate startDate="2007-09">September 2007</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="40" status="forIssue"><doi origin="wiley" registered="yes">10.1002/jmv.20937</doi><idGroup><id type="unit" value="JMV20937"></id></idGroup><countGroup><count type="pageTotal" number="16"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title></titleGroup><copyright ownership="publisher">Copyright © 2007 Wiley‐Liss, Inc.</copyright><eventGroup><event type="manuscriptAccepted" date="2007-05-24"></event><event type="firstOnline" date="2007-07-02"></event><event type="publishedOnlineFinalForm" date="2007-07-02"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-15"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-20"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-30"></event></eventGroup><numberingGroup><numbering type="pageFirst">1270</numbering><numbering type="pageLast">1285</numbering></numberingGroup><correspondenceTo>Department of Pathology, New York University School of Medicine, c/o V.A. Medical Center, 423 East 23rd street, Room 18124N, New York, NY 10010.===</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JMV.JMV20937.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="7"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="43"></count><count type="wordTotal" number="1626"></count></countGroup><titleGroup><title type="main" xml:lang="en">Quasispecies analysis of novel HIV‐1 recombinants of subtypes A and G reveals no similarity to the mosaic structure of CRF02_AG<link href="#fn1"></link></title><title type="short" xml:lang="en">Emerging Unique Recombinant Forms of HIV‐1 Subtypes A and G</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Rebecca L.R.</givenNames><familyName>Powell</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Frank A.J.</givenNames><familyName>Konings</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Aubin</givenNames><familyName>Nanfack</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Sherri</givenNames><familyName>Burda</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Mateusz M.</givenNames><familyName>Urbanski</familyName></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af4"><personName><givenNames>D.</givenNames><familyName>Saa</familyName></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af3 #af5" corresponding="yes"><personName><givenNames>Phillipe N.</givenNames><familyName>Nyambi</familyName></personName><contactDetails><email>phillipe.nyambi@med.nyu.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Microbiology, New York University School of Medicine, New York, New York</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Laboratoire de Santé Hygiène Mobile, Yaoundé, Cameroon</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Pathology, New York University School of Medicine, New York, New York</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Ministry of Public Health, Yaoundé, Cameroon</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Veterans Affairs New York Harbor Healthcare Systems, New York, New York</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">HIV‐1 CRF02_AG</keyword><keyword xml:id="kwd2">Cameroon</keyword><keyword xml:id="kwd3">HIV‐1 recombination</keyword><keyword xml:id="kwd4">evolution</keyword></keywordGroup><fundingInfo><fundingAgency>The National Institute of Allergy and Infectious Diseases (NIAID)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>National Institutes of Health (NIH)</fundingAgency><fundingNumber>AI47053</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Fogarty International Center</fundingAgency><fundingNumber>TW01254</fundingNumber><fundingNumber>TW01409</fundingNumber></fundingInfo><fundingInfo><fundingAgency>NYU Center for AIDS Research</fundingAgency><fundingNumber>AI027742‐17</fundingNumber></fundingInfo><fundingInfo><fundingAgency>The Department of Veterans Affairs (Merit Review Award and the Research Enhancement Program)</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>HIV‐1 circulating recombinant form (CRF) 02_AG is responsible for greater than 65% of HIV‐1 infections in Cameroon and is widespread across West and West‐Central Africa. The parental subtypes A1 and G cocirculate in this part of Africa, and high rates of infection predispose to the generation of AG unique recombinant forms (URFs). Little is known as to whether A1 and G can recombine and thrive in vivo with breakpoints other than those characteristic of CRF02_AG. In this study, six unique recombinant viruses of subtypes A1 and G were identified in two individuals in Cameroon. A 1.5 kb fragment of the reverse transcriptase (RT) region of <i>pol</i> (HXB2 location 2,612–4,159) and the entire <i>env</i> gene (HXB2 location 6,202–9,096) were evaluated by phylogenetic and breakpoint analyses. Each URF was found to have breakpoints different than CRF02_AG, indicating that A and G gene segments are functionally compatible with more than one pattern of recombination. Furthermore, contemporaneous, cultured viruses from these individuals were analyzed, revealing different proportions of URFs compared to those found in plasma, possibly indicating compart mentalization and/or phenotypic variation among the URFs. CRF02_AG emerged from West‐Central Africa to become a highly successful viral strain. As such, monitoring the spread of newly emerging AG recombinants is critical not only for understanding the epidemiology of HIV‐1, but also in the design of future therapeutics and vaccines appropriate to this part of Africa, and globally. J. Med. Virol. 79:1270–1285, 2007. © Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Data presented in part at the AIDS Vaccine 2006 Conference, Amsterdam, 08/29/06–09/01/06.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Quasispecies analysis of novel HIV‐1 recombinants of subtypes A and G reveals no similarity to the mosaic structure of CRF02_AG</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Emerging Unique Recombinant Forms of HIV‐1 Subtypes A and G</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Quasispecies analysis of novel HIV‐1 recombinants of subtypes A and G reveals no similarity to the mosaic structure of CRF02_AG</title></titleInfo><name type="personal"><namePart type="given">Rebecca L.R.</namePart><namePart type="family">Powell</namePart><affiliation>Department of Microbiology, New York University School of Medicine, New York, New York</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Frank A.J.</namePart><namePart type="family">Konings</namePart><affiliation>Department of Microbiology, New York University School of Medicine, New York, New York</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Aubin</namePart><namePart type="family">Nanfack</namePart><affiliation>Laboratoire de Santé Hygiène Mobile, Yaoundé, Cameroon</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sherri</namePart><namePart type="family">Burda</namePart><affiliation>Department of Pathology, New York University School of Medicine, New York, New York</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mateusz M.</namePart><namePart type="family">Urbanski</namePart><affiliation>Department of Pathology, New York University School of Medicine, New York, New York</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Saa</namePart><affiliation>Ministry of Public Health, Yaoundé, Cameroon</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Phillipe N.</namePart><namePart type="family">Nyambi</namePart><affiliation>Department of Pathology, New York University School of Medicine, New York, New York</affiliation><affiliation>Veterans Affairs New York Harbor Healthcare Systems, New York, New York</affiliation><affiliation>Department of Pathology, New York University School of Medicine, c/o V.A. Medical Center, 423 East 23rd street, Room 18124N, New York, NY 10010.===</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2007-09</dateIssued><dateValid encoding="w3cdtf">2007-05-24</dateValid><copyrightDate encoding="w3cdtf">2007</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">7</extent><extent unit="references">43</extent><extent unit="words">1626</extent></physicalDescription><abstract lang="en">HIV‐1 circulating recombinant form (CRF) 02_AG is responsible for greater than 65% of HIV‐1 infections in Cameroon and is widespread across West and West‐Central Africa. The parental subtypes A1 and G cocirculate in this part of Africa, and high rates of infection predispose to the generation of AG unique recombinant forms (URFs). Little is known as to whether A1 and G can recombine and thrive in vivo with breakpoints other than those characteristic of CRF02_AG. In this study, six unique recombinant viruses of subtypes A1 and G were identified in two individuals in Cameroon. A 1.5 kb fragment of the reverse transcriptase (RT) region of pol (HXB2 location 2,612–4,159) and the entire env gene (HXB2 location 6,202–9,096) were evaluated by phylogenetic and breakpoint analyses. Each URF was found to have breakpoints different than CRF02_AG, indicating that A and G gene segments are functionally compatible with more than one pattern of recombination. Furthermore, contemporaneous, cultured viruses from these individuals were analyzed, revealing different proportions of URFs compared to those found in plasma, possibly indicating compart mentalization and/or phenotypic variation among the URFs. CRF02_AG emerged from West‐Central Africa to become a highly successful viral strain. As such, monitoring the spread of newly emerging AG recombinants is critical not only for understanding the epidemiology of HIV‐1, but also in the design of future therapeutics and vaccines appropriate to this part of Africa, and globally. J. Med. Virol. 79:1270–1285, 2007. © Wiley‐Liss, Inc.</abstract><note type="content">*Data presented in part at the AIDS Vaccine 2006 Conference, Amsterdam, 08/29/06–09/01/06.</note><note type="funding">The National Institute of Allergy and Infectious Diseases (NIAID)</note><note type="funding">National Institutes of Health (NIH) - No. AI47053; </note><note type="funding">Fogarty International Center - No. TW01254; No. TW01409; </note><note type="funding">NYU Center for AIDS Research - No. AI027742‐17; </note><note type="funding">The Department of Veterans Affairs (Merit Review Award and the Research Enhancement Program)</note><subject lang="en"><genre>keywords</genre><topic>HIV‐1 CRF02_AG</topic><topic>Cameroon</topic><topic>HIV‐1 recombination</topic><topic>evolution</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Medical Virology</title></titleInfo><titleInfo type="abbreviated"><title>J. Med. 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