Initiation of antiretroviral therapy during chronic SIV infection leads to rapid reduction in viral loads and the level of T‐cell immune response
Identifieur interne : 001368 ( Istex/Corpus ); précédent : 001367; suivant : 001369Initiation of antiretroviral therapy during chronic SIV infection leads to rapid reduction in viral loads and the level of T‐cell immune response
Auteurs : Jean D. Boyer ; Sanjeev Kumar ; Tara Robinson ; Rose Parkinson ; Ling Wu ; Mark Lewis ; David I. Watkins ; David B. WeinerSource :
- Journal of Medical Primatology [ 0047-2565 ] ; 2006-08.
Abstract
In the present era of increasing resistance of human immunodeficiency virus (HIV) to antiviral drugs, exploration of adjunct therapies directed at immune responses in combination with antiretroviral drugs may be of value for the treatment of acquired immunodeficiency syndrome. In this study, we designed a model for immune therapy using SIVmac251 infection in rhesus macaques. We explored the outcomes of primary infection on viral loads and the resulting T‐cell immune responses in primates. The SIV‐infected rhesus macaque model exhibited features similar to those observed in HIV‐1 infection of humans. Major histocompatibility complex (MHC) segregation with viral loads were found to associate with viral containment and hence the duration of the disease‐free latency period. Thus a better understanding of the relative roles of MHC class I allele in control of viral replication may provide important information for prophylactic or therapeutic vaccine designs. Mamu‐A01 is significantly associated with higher immune response and control of viral replication. This allele is frequent in rhesus macaques of Indian origin (22%). Interestingly, Mamu‐B01 (26% animals) was associated with lower immune responses and higher viral loads. Another allele, A08 was also predominantly present in 37% of the animals in this study. We observed higher viral replication in individual SIV‐infected rhesus monkeys that did not demonstrate strong cellular immune responses. The results are important for understanding SIV disease progression in different MHC Mamu alleles and also for improving the interpretation and quality of pre‐clinical studies in rhesus monkeys.
Url:
DOI: 10.1111/j.1600-0684.2006.00179.x
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Another allele, A08 was also predominantly present in 37% of the animals in this study. We observed higher viral replication in individual SIV‐infected rhesus monkeys that did not demonstrate strong cellular immune responses. 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[27]</json:string><json:string>Boyer et al.</json:string><json:string>[27]</json:string><json:string>[26]</json:string><json:string>[1, 14]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-RL5MK2D3-R</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - zoology</json:string><json:string>2 - veterinary sciences</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 - Veterinary</json:string><json:string>3 - General Veterinary</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Agricultural and Biological Sciences</json:string><json:string>3 - Animal Science and Zoology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 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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>In the present era of increasing resistance of human immunodeficiency virus (HIV) to antiviral drugs, exploration of adjunct therapies directed at immune responses in combination with antiretroviral drugs may be of value for the treatment of acquired immunodeficiency syndrome. In this study, we designed a model for immune therapy using SIVmac251 infection in rhesus macaques. We explored the outcomes of primary infection on viral loads and the resulting T‐cell immune responses in primates. The SIV‐infected rhesus macaque model exhibited features similar to those observed in HIV‐1 infection of humans. Major histocompatibility complex (MHC) segregation with viral loads were found to associate with viral containment and hence the duration of the disease‐free latency period. Thus a better understanding of the relative roles of MHC class I allele in control of viral replication may provide important information for prophylactic or therapeutic vaccine designs. Mamu‐A01 is significantly associated with higher immune response and control of viral replication. This allele is frequent in rhesus macaques of Indian origin (22%). Interestingly, Mamu‐B01 (26% animals) was associated with lower immune responses and higher viral loads. Another allele, A08 was also predominantly present in 37% of the animals in this study. We observed higher viral replication in individual SIV‐infected rhesus monkeys that did not demonstrate strong cellular immune responses. The results are important for understanding SIV disease progression in different MHC Mamu alleles and also for improving the interpretation and quality of pre‐clinical studies in rhesus monkeys.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">SIV</term><term xml:id="k2">ART</term><term xml:id="k3">FTC PMPA</term><term xml:id="k4">CD4 T cells</term><term xml:id="k5">IFN‐γ</term></keywords><keywords rend="tocHeading1"><term>Original 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-RL5MK2D3-R/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>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-0684</doi><issn type="print">0047-2565</issn><issn type="electronic">1600-0684</issn><idGroup><id type="product" value="JMP"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="JOURNAL OF MEDICAL PRIMATOLOGY">Journal of Medical Primatology</title></titleGroup></publicationMeta><publicationMeta level="part" position="08004"><doi origin="wiley">10.1111/jmp.2006.35.issue-4-5</doi><numberingGroup><numbering type="journalVolume" number="35">35</numbering><numbering type="journalIssue">4‐5</numbering></numberingGroup><coverDate startDate="2006-08">August 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="4" status="forIssue"><doi origin="wiley">10.1111/j.1600-0684.2006.00179.x</doi><idGroup><id type="unit" value="JMP179"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><eventGroup><event type="firstOnline" date="2006-07-11"></event><event type="publishedOnlineFinalForm" date="2006-07-11"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-07"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-31"></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" number="202">202</numbering><numbering type="pageLast" number="209">209</numbering></numberingGroup><correspondenceTo> Jean D. Boyer, PhD, Department of Pathology and Laboratory Medicine, 505 SCL, 422 Curie Blvd. Philadelphia, PA 19104, USA.
Tel.: 215 662 2382;
fax: 215 573 9436;
e‐mail: <email>boyerj@mail.med.upenn.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JMP.JMP179.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted May 1, 2006.</unparsedEditorialHistory><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="1"></count></countGroup><titleGroup><title type="main">Initiation of antiretroviral therapy during chronic SIV infection leads to rapid reduction in viral loads and the level of T‐cell immune response</title><title type="shortAuthors">Boyer et al.</title><title type="short">SIV chronic infection model</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Jean D.</givenNames><familyName>Boyer</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Sanjeev</givenNames><familyName>Kumar</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Tara</givenNames><familyName>Robinson</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Rose</givenNames><familyName>Parkinson</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>Ling</givenNames><familyName>Wu</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a2"><personName><givenNames>Mark</givenNames><familyName>Lewis</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a3"><personName><givenNames>David I.</givenNames><familyName>Watkins</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a1"><personName><givenNames>David B.</givenNames><familyName>Weiner</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation> Bioqual, Frederick, MD, USA</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="US"><unparsedAffiliation> Wisconsin National Primate Research Center and Department of Pathology and Laboratory Medicine, University of Wisconsin, Madison, WI, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">SIV</keyword><keyword xml:id="k2">ART</keyword><keyword xml:id="k3">FTC PMPA</keyword><keyword xml:id="k4">CD4 T cells</keyword><keyword xml:id="k5">IFN‐γ</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>In the present era of increasing resistance of human immunodeficiency virus (HIV) to antiviral drugs, exploration of adjunct therapies directed at immune responses in combination with antiretroviral drugs may be of value for the treatment of acquired immunodeficiency syndrome. In this study, we designed a model for immune therapy using SIVmac251 infection in rhesus macaques. We explored the outcomes of primary infection on viral loads and the resulting T‐cell immune responses in primates. The SIV‐infected rhesus macaque model exhibited features similar to those observed in HIV‐1 infection of humans. Major histocompatibility complex (MHC) segregation with viral loads were found to associate with viral containment and hence the duration of the disease‐free latency period. Thus a better understanding of the relative roles of MHC class I allele in control of viral replication may provide important information for prophylactic or therapeutic vaccine designs. Mamu‐A01 is significantly associated with higher immune response and control of viral replication. This allele is frequent in rhesus macaques of Indian origin (22%). Interestingly, Mamu‐B01 (26% animals) was associated with lower immune responses and higher viral loads. Another allele, A08 was also predominantly present in 37% of the animals in this study. We observed higher viral replication in individual SIV‐infected rhesus monkeys that did not demonstrate strong cellular immune responses. The results are important for understanding SIV disease progression in different MHC Mamu alleles and also for improving the interpretation and quality of pre‐clinical studies in rhesus monkeys.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Initiation of antiretroviral therapy during chronic SIV infection leads to rapid reduction in viral loads and the level of T‐cell immune response</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>SIV chronic infection model</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Initiation of antiretroviral therapy during chronic SIV infection leads to rapid reduction in viral loads and the level of T‐cell immune response</title></titleInfo><name type="personal"><namePart type="given">Jean D.</namePart><namePart type="family">Boyer</namePart><affiliation> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sanjeev</namePart><namePart type="family">Kumar</namePart><affiliation> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tara</namePart><namePart type="family">Robinson</namePart><affiliation> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rose</namePart><namePart type="family">Parkinson</namePart><affiliation> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ling</namePart><namePart type="family">Wu</namePart><affiliation> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mark</namePart><namePart type="family">Lewis</namePart><affiliation> Bioqual, Frederick, MD, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David I.</namePart><namePart type="family">Watkins</namePart><affiliation> Wisconsin National Primate Research Center and Department of Pathology and Laboratory Medicine, University of Wisconsin, Madison, WI, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David B.</namePart><namePart type="family">Weiner</namePart><affiliation> Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA, USA</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>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2006-08</dateIssued><edition>Accepted May 1, 2006.</edition><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">3</extent><extent unit="tables">1</extent></physicalDescription><abstract lang="en">In the present era of increasing resistance of human immunodeficiency virus (HIV) to antiviral drugs, exploration of adjunct therapies directed at immune responses in combination with antiretroviral drugs may be of value for the treatment of acquired immunodeficiency syndrome. In this study, we designed a model for immune therapy using SIVmac251 infection in rhesus macaques. We explored the outcomes of primary infection on viral loads and the resulting T‐cell immune responses in primates. The SIV‐infected rhesus macaque model exhibited features similar to those observed in HIV‐1 infection of humans. Major histocompatibility complex (MHC) segregation with viral loads were found to associate with viral containment and hence the duration of the disease‐free latency period. Thus a better understanding of the relative roles of MHC class I allele in control of viral replication may provide important information for prophylactic or therapeutic vaccine designs. Mamu‐A01 is significantly associated with higher immune response and control of viral replication. This allele is frequent in rhesus macaques of Indian origin (22%). Interestingly, Mamu‐B01 (26% animals) was associated with lower immune responses and higher viral loads. Another allele, A08 was also predominantly present in 37% of the animals in this study. We observed higher viral replication in individual SIV‐infected rhesus monkeys that did not demonstrate strong cellular immune responses. The results are important for understanding SIV disease progression in different MHC Mamu alleles and also for improving the interpretation and quality of pre‐clinical studies in rhesus monkeys.</abstract><subject lang="en"><genre>keywords</genre><topic>SIV</topic><topic>ART</topic><topic>FTC PMPA</topic><topic>CD4 T cells</topic><topic>IFN‐γ</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Medical Primatology</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">0047-2565</identifier><identifier type="eISSN">1600-0684</identifier><identifier type="DOI">10.1111/(ISSN)1600-0684</identifier><identifier type="PublisherID">JMP</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>35</number></detail><detail type="issue"><caption>no.</caption><number>4‐5</number></detail><extent unit="pages"><start>202</start><end>209</end><total>8</total></extent></part></relatedItem><relatedItem type="references" displayLabel="cit1"><titleInfo><title>The cost of HIV treatment and care: a global review</title></titleInfo><name type="personal"><namePart type="given">EJ</namePart><namePart type="family">Beck</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AH</namePart><namePart type="family">Miners</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Tolley</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Beck EJ, Miners AH, Tolley K: The cost of HIV treatment and care: a global review. 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