HIV‐associated chronic immune activation
Identifieur interne : 000416 ( Istex/Corpus ); précédent : 000415; suivant : 000417HIV‐associated chronic immune activation
Auteurs : Mirko Paiardini ; Michaela Müller-TrutwinSource :
- Immunological Reviews [ 0105-2896 ] ; 2013-07.
English descriptors
- Teeft :
- Activation, Acute infection, Acute phase, Agms, Antiretroviral, Antiretroviral therapy, Cardiovascular disease, Ccr5, Ccr5 expression, Cell activation, Cell depletion, Central memory, Chronic, Chronic infection, Chronic phase, Clin, Coagulation, Cytokine, Dendritic, Disease progression, Epithelial, Gastrointestinal tract, Germinal centers, High levels, Hivinfected, Hivinfected individuals, Homeostasis, Homeostatic, Homeostatic proliferation, Human virus, Human virus infection, Human virus type, Immune, Immune activation, Immune cells, Immune responses, Immune system, Immunol, Immunologic, Immunological, Immunological reviews, Immunological reviews paiardini, Immunomodulatory, Infection, Interferon, Intestinal, John wiley sons, Lymph, Lymph nodes, Lymphocyte, Lymphoid, Lymphoid tissue, Macaque, Mangabey, Microbial, Microbial translocation, Monocyte, Mucosal, Mucosal integrity, Mucosal sites, Natural history, Natural hosts, Ndings, Node, Paiardini, Pathogenesis, Pathogenic, Peripheral blood, Personal communication, Plasma levels, Plasmacytoid, Plasmacytoid dendritic cells, Plo, Primary infection, Primate, Primates, Probiotic, Progression, Proliferation, Psoriatic arthritis, Rapa, Rapamycin, Recent studies, Recent study, Receptor, Relative contribution, Replication, Residual, Rhesus, Rhesus macaques, Simian, Simian virus, Simian virus infection, Sivagm, Sivmac, Sooty, Sooty mangabeys, Subset, Supplementation, Suppressive, Target cells, Translocation, Treg, Tregs, Unpublished data, Vicious cycle, Viral, Viral load, Viral replication, Viremia, Virol, Virus, Virus infection, Wiley.
Abstract
Systemic chronic immune activation is considered today as the driving force of CD4+ T‐cell depletion and acquired immunodeficiency syndrome (AIDS). A residual chronic immune activation persists even in HIV‐infected patients in which viral replication is successfully inhibited by anti‐retroviral therapy, with the extent of this residual immune activation being associated with CD4+ T‐cell loss. Unfortunately, the causal link between chronic immune activation and CD4+ T‐cell loss has not been formally established. This article provides first a brief historical overview on how the perception of the causative role of immune activation has changed over the years and lists the different kinds of immune activation characteristic of human immunodeficiency virus (HIV) infection. The mechanisms proposed to explain the chronic immune activation are multiple and are enumerated here, as well as the mechanisms proposed on how chronic immune activation could lead to AIDS. In addition, we summarize the lessons learned from natural hosts that know how to ‘show AIDS the door’, and discuss how these studies informed the design of novel immune modulatory interventions that are currently being tested. Finally, we review the current approaches aimed at targeting chronic immune activation and evoke future perspectives.
Url:
DOI: 10.1111/imr.12079
Links to Exploration step
ISTEX:1EB392A99746558E8CC569E249CF34D9DAF93AA2Le document en format XML
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In addition, we summarize the lessons learned from natural hosts that know how to ‘show AIDS the door’, and discuss how these studies informed the design of novel immune modulatory interventions that are currently being tested. 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(AIDS). A residual chronic immune activation persists even in HIV‐infected patients in which viral replication is successfully inhibited by anti‐retroviral therapy, with the extent of this residual immune activation being associated with CD4+ T‐cell loss. Unfortunately, the causal link between chronic immune activation and CD4+ T‐cell loss has not been formally established. This article provides first a brief historical overview on how the perception of the causative role of immune activation has changed over the years and lists the different kinds of immune activation characteristic of human immunodeficiency virus (HIV) infection. The mechanisms proposed to explain the chronic immune activation are multiple and are enumerated here, as well as the mechanisms proposed on how chronic immune activation could lead to AIDS. In addition, we summarize the lessons learned from natural hosts that know how to ‘show AIDS the door’, and discuss how these studies informed the design of novel immune modulatory interventions that are currently being tested. 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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract style="main" xml:id="imr12079-abs-0001"><head>Summary</head><p>Systemic chronic immune activation is considered today as the driving force of <hi rend="fc">CD</hi>4<hi rend="superscript">+</hi> T‐cell depletion and acquired immunodeficiency syndrome (<hi rend="fc">AIDS</hi>). A residual chronic immune activation persists even in <hi rend="fc">HIV</hi>‐infected patients in which viral replication is successfully inhibited by anti‐retroviral therapy, with the extent of this residual immune activation being associated with <hi rend="fc">CD</hi>4<hi rend="superscript">+</hi> T‐cell loss. Unfortunately, the causal link between chronic immune activation and <hi rend="fc">CD</hi>4<hi rend="superscript">+</hi> T‐cell loss has not been formally established. This article provides first a brief historical overview on how the perception of the causative role of immune activation has changed over the years and lists the different kinds of immune activation characteristic of human immunodeficiency virus (<hi rend="fc">HIV</hi>) infection. The mechanisms proposed to explain the chronic immune activation are multiple and are enumerated here, as well as the mechanisms proposed on how chronic immune activation could lead to <hi rend="fc">AIDS</hi>. In addition, we summarize the lessons learned from natural hosts that know how to ‘show <hi rend="fc">AIDS</hi> the door’, and discuss how these studies informed the design of novel immune modulatory interventions that are currently being tested. Finally, we review the current approaches aimed at targeting chronic immune activation and evoke future perspectives.</p></abstract><textClass><keywords><term xml:id="imr12079-kwd-0001">HIV</term><term xml:id="imr12079-kwd-0002">SIV</term><term xml:id="imr12079-kwd-0003">pathogenesis</term><term xml:id="imr12079-kwd-0004">immune activation</term><term xml:id="imr12079-kwd-0005">inflammation</term><term xml:id="imr12079-kwd-0006">natural hosts</term></keywords><keywords rend="articleCategory"><term>Invited Review</term></keywords><keywords rend="tocHeading1"><term>Invited Reviews</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-ZM9VZ2LK-T/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 type="serialArticle" version="2.0" xml:id="imr12079" xml:lang="en"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-065X</doi><issn type="print">0105-2896</issn><issn type="electronic">1600-065X</issn><idGroup><id type="product" value="IMR"></id></idGroup><titleGroup><title sort="IMMUNOLOGICAL REVIEWS" type="main">Immunological Reviews</title><title type="short">Immunol Rev</title></titleGroup></publicationMeta><publicationMeta level="part" position="10"><doi origin="wiley">10.1111/imr.2013.254.issue-1</doi><titleGroup><title type="specialIssueTitle">HIV Immunology</title></titleGroup><copyright ownership="publisher">© 2013 John Wiley & Sons A/S</copyright><numberingGroup><numbering number="254" type="journalVolume">254</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2013-07">July 2013</coverDate></publicationMeta><publicationMeta level="unit" position="60" status="forIssue" type="reviewArticle"><doi>10.1111/imr.12079</doi><idGroup><id type="unit" value="IMR12079"></id></idGroup><countGroup><count number="24" type="pageTotal"></count></countGroup><titleGroup><title type="articleCategory">Invited Review</title><title type="tocHeading1">Invited Reviews</title></titleGroup><copyright ownership="publisher">© 2013 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</copyright><eventGroup><event agent="SPS" date="2013-04-25" type="xmlCreated"></event><event agent="SPS" date="2013-07-19" type="xmlCorrected"></event><event type="publishedOnlineFinalForm" date="2013-06-16"></event><event type="firstOnline" date="2013-06-16"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-13"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.6.4 mode:FullText" date="2015-10-04"></event></eventGroup><numberingGroup><numbering type="pageFirst">78</numbering><numbering type="pageLast">101</numbering></numberingGroup><correspondenceTo><lineatedText><line>Correspondence to:</line><line><i>Mirko Paiardini</i></line><line>Division of Microbiology and Immunology</line><line>Yerkes National Primate Research Center</line><line>Department of Pathology and Laboratory Medicine</line><line>Emory University School of Medicine</line><line>954 Gatewood Road</line><line>Atlanta, GA 30329, USA</line><line>Tel.: +1 404 727 9840</line><line>Fax: +1 404 727 7768</line><line>e‐mail: <email>mirko.paiardini@emory.edu</email></line></lineatedText></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:IMR.IMR12079.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main"><fc>HIV</fc>‐associated chronic immune activation</title><title type="shortAuthors">Paiardini & Müller‐Trutwin</title></titleGroup><creators><creator affiliationRef="#imr12079-aff-0001" corresponding="yes" creatorRole="author" xml:id="imr12079-cr-0001"><personName><givenNames>Mirko</givenNames> <familyName>Paiardini</familyName></personName></creator><creator affiliationRef="#imr12079-aff-0002" creatorRole="author" xml:id="imr12079-cr-0002"><personName><givenNames>Michaela</givenNames> <familyName>Müller‐Trutwin</familyName></personName></creator></creators><affiliationGroup><affiliation countryCode="US" type="organization" xml:id="imr12079-aff-0001"><orgDiv>Division of Microbiology and Immunology</orgDiv> <orgDiv>Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine</orgDiv> <orgName>Emory University</orgName> <address><city>Atlanta</city> <countryPart>GA</countryPart> <country>USA</country></address></affiliation><affiliation countryCode="FR" type="organization" xml:id="imr12079-aff-0002"><orgDiv>Regulation of Retroviral infections Unit</orgDiv> <orgName>Institut Pasteur</orgName> <address><city>Paris</city> <country>France</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="imr12079-kwd-0001">HIV</keyword><keyword xml:id="imr12079-kwd-0002">SIV</keyword><keyword xml:id="imr12079-kwd-0003">pathogenesis</keyword><keyword xml:id="imr12079-kwd-0004">immune activation</keyword><keyword xml:id="imr12079-kwd-0005">inflammation</keyword><keyword xml:id="imr12079-kwd-0006">natural hosts</keyword></keywordGroup><fundingInfo><fundingAgency>NIH</fundingAgency><fundingNumber>R01‐AI084836</fundingNumber><fundingNumber>R56‐AI087186</fundingNumber><fundingNumber>P51OD011132</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Yerkes National Primate Research Center</fundingAgency></fundingInfo><fundingInfo><fundingAgency>AREVA foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Sidaction</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:id="imr12079-abs-0001"><title type="main">Summary</title><p>Systemic chronic immune activation is considered today as the driving force of <fc>CD</fc>4<sup>+</sup> T‐cell depletion and acquired immunodeficiency syndrome (<fc>AIDS</fc>). A residual chronic immune activation persists even in <fc>HIV</fc>‐infected patients in which viral replication is successfully inhibited by anti‐retroviral therapy, with the extent of this residual immune activation being associated with <fc>CD</fc>4<sup>+</sup> T‐cell loss. Unfortunately, the causal link between chronic immune activation and <fc>CD</fc>4<sup>+</sup> T‐cell loss has not been formally established. This article provides first a brief historical overview on how the perception of the causative role of immune activation has changed over the years and lists the different kinds of immune activation characteristic of human immunodeficiency virus (<fc>HIV</fc>) infection. The mechanisms proposed to explain the chronic immune activation are multiple and are enumerated here, as well as the mechanisms proposed on how chronic immune activation could lead to <fc>AIDS</fc>. In addition, we summarize the lessons learned from natural hosts that know how to ‘show <fc>AIDS</fc> the door’, and discuss how these studies informed the design of novel immune modulatory interventions that are currently being tested. Finally, we review the current approaches aimed at targeting chronic immune activation and evoke future perspectives.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>HIV‐associated chronic immune activation</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>HIV‐associated chronic immune activation</title></titleInfo><name type="personal"><namePart type="given">Mirko</namePart><namePart type="family">Paiardini</namePart><affiliation>Division of Microbiology and Immunology, Yerkes National Primate Research Center, and Department of Pathology and Laboratory Medicine, Emory University, GA, Atlanta, USA</affiliation><affiliation>Correspondence to:Division of Microbiology and ImmunologyYerkes National Primate Research CenterDepartment of Pathology and Laboratory MedicineEmory University School of Medicine954 Gatewood RoadAtlanta, GA 30329, USATel.: +1 404 727 9840Fax: +1 404 727 7768e‐mail:</affiliation><affiliation>E-mail: mirko.paiardini@emory.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michaela</namePart><namePart type="family">Müller‐Trutwin</namePart><affiliation>Regulation of Retroviral infections Unit, Institut Pasteur, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2013-07</dateIssued><dateCreated encoding="w3cdtf">2013-04-25</dateCreated><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>Systemic chronic immune activation is considered today as the driving force of CD4+ T‐cell depletion and acquired immunodeficiency syndrome (AIDS). A residual chronic immune activation persists even in HIV‐infected patients in which viral replication is successfully inhibited by anti‐retroviral therapy, with the extent of this residual immune activation being associated with CD4+ T‐cell loss. Unfortunately, the causal link between chronic immune activation and CD4+ T‐cell loss has not been formally established. This article provides first a brief historical overview on how the perception of the causative role of immune activation has changed over the years and lists the different kinds of immune activation characteristic of human immunodeficiency virus (HIV) infection. The mechanisms proposed to explain the chronic immune activation are multiple and are enumerated here, as well as the mechanisms proposed on how chronic immune activation could lead to AIDS. In addition, we summarize the lessons learned from natural hosts that know how to ‘show AIDS the door’, and discuss how these studies informed the design of novel immune modulatory interventions that are currently being tested. 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