Suppression of Human Immunodeficiency Virus Replication during Acute Measles
Identifieur interne : 003805 ( Istex/Corpus ); précédent : 003804; suivant : 003806Suppression of Human Immunodeficiency Virus Replication during Acute Measles
Auteurs : William J. Moss ; Judith J. Ryon ; Mwaka Monze ; Felicity Cutts ; Thomas C. Quinn ; Diane E. GriffinSource :
- The Journal of Infectious Diseases [ 0022-1899 ] ; 2002-04-15.
Abstract
To determine the effect of measles virus coinfection on plasma human immunodeficiency virus (HIV) RNA levels, a prospective study of hospitalized children with measles was conducted between January 1998 and October 2000 in Lusaka, Zambia. Plasma HIV RNA levels were measured during acute measles and 1 month after hospital discharge. The median plasma HIV RNA level in 33 children with measles who were followed longitudinally was 5339 copies/mL at study entry, 60,121 copies/mL at hospital discharge, and 387,148 copies/mL at 1-month follow-up. The median plasma HIV RNA level in children without acute illness was 228,454 copies/mL. Plasma levels of immune activation markers were elevated during the period of reduced plasma HIV RNA. Plasma levels of several potential HIV suppressive factors also were elevated during acute measles. HIV replication is transiently suppressed during acute measles at a time of intense immune activation.
Url:
DOI: 10.1086/340027
Links to Exploration step
ISTEX:AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Suppression of Human Immunodeficiency Virus Replication during Acute Measles</title><author><name sortKey="Moss, William J" sort="Moss, William J" uniqKey="Moss W" first="William J." last="Moss">William J. Moss</name><affiliation><mods:affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of International Health, Bloomberg School of Public Health, Bethesda, Maryland</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: wmoss@jhsph.edu</mods:affiliation></affiliation><affiliation><mods:affiliation>Reprints or correspondence: Dr. William J. Moss, W. Harry Feinstone Dept. of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 615 N. Wolfe St., Rm. E5132, Baltimore, MD 21205-2179</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: wmoss@jhsph.edu</mods:affiliation></affiliation></author><author><name sortKey="Ryon, Judith J" sort="Ryon, Judith J" uniqKey="Ryon J" first="Judith J." last="Ryon">Judith J. Ryon</name><affiliation><mods:affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Monze, Mwaka" sort="Monze, Mwaka" uniqKey="Monze M" first="Mwaka" last="Monze">Mwaka Monze</name><affiliation><mods:affiliation>Virology Laboratory, University Teaching Hospital, Lusaka, Zambia</mods:affiliation></affiliation></author><author><name sortKey="Cutts, Felicity" sort="Cutts, Felicity" uniqKey="Cutts F" first="Felicity" last="Cutts">Felicity Cutts</name><affiliation><mods:affiliation>Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Quinn, Thomas C" sort="Quinn, Thomas C" uniqKey="Quinn T" first="Thomas C." last="Quinn">Thomas C. Quinn</name><affiliation><mods:affiliation>Division of Infectious Diseases, School of Medicine, Johns Hopkins University, Baltimore, Bethesda, Maryland</mods:affiliation></affiliation><affiliation><mods:affiliation>National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Griffin, Diane E" sort="Griffin, Diane E" uniqKey="Griffin D" first="Diane E." last="Griffin">Diane E. Griffin</name><affiliation><mods:affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797</idno><date when="2002" year="2002">2002</date><idno type="doi">10.1086/340027</idno><idno type="url">https://api.istex.fr/document/AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">003805</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">003805</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Suppression of Human Immunodeficiency Virus Replication during Acute Measles</title><author><name sortKey="Moss, William J" sort="Moss, William J" uniqKey="Moss W" first="William J." last="Moss">William J. Moss</name><affiliation><mods:affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of International Health, Bloomberg School of Public Health, Bethesda, Maryland</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: wmoss@jhsph.edu</mods:affiliation></affiliation><affiliation><mods:affiliation>Reprints or correspondence: Dr. William J. Moss, W. Harry Feinstone Dept. of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 615 N. Wolfe St., Rm. E5132, Baltimore, MD 21205-2179</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: wmoss@jhsph.edu</mods:affiliation></affiliation></author><author><name sortKey="Ryon, Judith J" sort="Ryon, Judith J" uniqKey="Ryon J" first="Judith J." last="Ryon">Judith J. Ryon</name><affiliation><mods:affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Monze, Mwaka" sort="Monze, Mwaka" uniqKey="Monze M" first="Mwaka" last="Monze">Mwaka Monze</name><affiliation><mods:affiliation>Virology Laboratory, University Teaching Hospital, Lusaka, Zambia</mods:affiliation></affiliation></author><author><name sortKey="Cutts, Felicity" sort="Cutts, Felicity" uniqKey="Cutts F" first="Felicity" last="Cutts">Felicity Cutts</name><affiliation><mods:affiliation>Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Quinn, Thomas C" sort="Quinn, Thomas C" uniqKey="Quinn T" first="Thomas C." last="Quinn">Thomas C. Quinn</name><affiliation><mods:affiliation>Division of Infectious Diseases, School of Medicine, Johns Hopkins University, Baltimore, Bethesda, Maryland</mods:affiliation></affiliation><affiliation><mods:affiliation>National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland</mods:affiliation></affiliation></author><author><name sortKey="Griffin, Diane E" sort="Griffin, Diane E" uniqKey="Griffin D" first="Diane E." last="Griffin">Diane E. Griffin</name><affiliation><mods:affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">The Journal of Infectious Diseases</title><title level="j" type="abbrev">The Journal of Infectious Diseases</title><idno type="ISSN">0022-1899</idno><idno type="eISSN">1537-6613</idno><imprint><publisher>University of Chicago Press</publisher><date type="published" when="2002-04-15">2002-04-15</date><biblScope unit="volume">185</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1035">1035</biblScope><biblScope unit="page" to="1042">1042</biblScope></imprint><idno type="ISSN">0022-1899</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-1899</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">To determine the effect of measles virus coinfection on plasma human immunodeficiency virus (HIV) RNA levels, a prospective study of hospitalized children with measles was conducted between January 1998 and October 2000 in Lusaka, Zambia. Plasma HIV RNA levels were measured during acute measles and 1 month after hospital discharge. The median plasma HIV RNA level in 33 children with measles who were followed longitudinally was 5339 copies/mL at study entry, 60,121 copies/mL at hospital discharge, and 387,148 copies/mL at 1-month follow-up. The median plasma HIV RNA level in children without acute illness was 228,454 copies/mL. Plasma levels of immune activation markers were elevated during the period of reduced plasma HIV RNA. Plasma levels of several potential HIV suppressive factors also were elevated during acute measles. HIV replication is transiently suppressed during acute measles at a time of intense immune activation.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>William J. Moss</name><affiliations><json:string>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</json:string><json:string>Department of International Health, Bloomberg School of Public Health, Bethesda, Maryland</json:string><json:string>E-mail: wmoss@jhsph.edu</json:string></affiliations></json:item><json:item><name>Judith J. Ryon</name><affiliations><json:string>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</json:string></affiliations></json:item><json:item><name>Mwaka Monze</name><affiliations><json:string>Virology Laboratory, University Teaching Hospital, Lusaka, Zambia</json:string></affiliations></json:item><json:item><name>Felicity Cutts</name><affiliations><json:string>Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Thomas C. Quinn</name><affiliations><json:string>Division of Infectious Diseases, School of Medicine, Johns Hopkins University, Baltimore, Bethesda, Maryland</json:string><json:string>National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland</json:string></affiliations></json:item><json:item><name>Diane E. Griffin</name><affiliations><json:string>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</json:string></affiliations></json:item></author><language><json:string>unknown</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>To determine the effect of measles virus coinfection on plasma human immunodeficiency virus (HIV) RNA levels, a prospective study of hospitalized children with measles was conducted between January 1998 and October 2000 in Lusaka, Zambia. Plasma HIV RNA levels were measured during acute measles and 1 month after hospital discharge. The median plasma HIV RNA level in 33 children with measles who were followed longitudinally was 5339 copies/mL at study entry, 60,121 copies/mL at hospital discharge, and 387,148 copies/mL at 1-month follow-up. The median plasma HIV RNA level in children without acute illness was 228,454 copies/mL. Plasma levels of immune activation markers were elevated during the period of reduced plasma HIV RNA. Plasma levels of several potential HIV suppressive factors also were elevated during acute measles. HIV replication is transiently suppressed during acute measles at a time of intense immune activation.</abstract><qualityIndicators><score>8.692</score><pdfVersion>1.2</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>939</abstractCharCount><pdfWordCount>5822</pdfWordCount><pdfCharCount>37754</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>141</abstractWordCount></qualityIndicators><title>Suppression of Human Immunodeficiency Virus Replication during Acute Measles</title><genre><json:string>research-article</json:string></genre><host><title>The Journal of Infectious Diseases</title><language><json:string>unknown</json:string></language><issn><json:string>0022-1899</json:string></issn><eissn><json:string>1537-6613</json:string></eissn><publisherId><json:string>jid</json:string></publisherId><volume>185</volume><issue>8</issue><pages><first>1035</first><last>1042</last></pages><genre><json:string>journal</json:string></genre></host><categories><wos><json:string>science</json:string><json:string>microbiology</json:string><json:string>infectious diseases</json:string><json:string>immunology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>biomedical research</json:string><json:string>microbiology</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string><json:string>cardiologie. appareil circulatoire</json:string></inist></categories><publicationDate>2002</publicationDate><copyrightDate>2002</copyrightDate><doi><json:string>10.1086/340027</json:string></doi><id>AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Suppression of Human Immunodeficiency Virus Replication during Acute Measles</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://publisher-list.data.istex.fr">University of Chicago Press</publisher><availability><licence><p>© 2002 by the Infectious Diseases Society of America</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-GTWS0RDP-M">oup</p></availability><date>2002</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note><note>Presented in part: annual meeting of the Infectious Diseases Society of America, Philadelphia, 18–21 November 1999 (abstract 698).</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Suppression of Human Immunodeficiency Virus Replication during Acute Measles</title><author xml:id="author-0000" corresp="yes"><persName><forename type="first">William J.</forename><surname>Moss</surname></persName><email>wmoss@jhsph.edu</email><email>wmoss@jhsph.edu</email><affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</affiliation><affiliation>Department of International Health, Bloomberg School of Public Health, Bethesda, Maryland</affiliation><affiliation>Reprints or correspondence: Dr. William J. Moss, W. Harry Feinstone Dept. of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 615 N. Wolfe St., Rm. E5132, Baltimore, MD 21205-2179</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Judith J.</forename><surname>Ryon</surname></persName><affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Mwaka</forename><surname>Monze</surname></persName><affiliation>Virology Laboratory, University Teaching Hospital, Lusaka, Zambia</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Felicity</forename><surname>Cutts</surname></persName><note type="biography">a Present affiliation: Medical Research Council Laboratories, Fajara, Banjul, The Gambia.</note><affiliation>a Present affiliation: Medical Research Council Laboratories, Fajara, Banjul, The Gambia.</affiliation><affiliation>Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Thomas C.</forename><surname>Quinn</surname></persName><affiliation>Division of Infectious Diseases, School of Medicine, Johns Hopkins University, Baltimore, Bethesda, Maryland</affiliation><affiliation>National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Diane E.</forename><surname>Griffin</surname></persName><affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</affiliation></author><idno type="istex">AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797</idno><idno type="ark">ark:/67375/HXZ-MPBKPNH7-T</idno><idno type="DOI">10.1086/340027</idno></analytic><monogr><title level="j">The Journal of Infectious Diseases</title><title level="j" type="abbrev">The Journal of Infectious Diseases</title><idno type="pISSN">0022-1899</idno><idno type="eISSN">1537-6613</idno><idno type="publisher-id">jid</idno><idno type="PublisherID-hwp">jinfdis</idno><imprint><publisher>University of Chicago Press</publisher><date type="published" when="2002-04-15"></date><biblScope unit="volume">185</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1035">1035</biblScope><biblScope unit="page" to="1042">1042</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2002</date></creation><abstract><p>To determine the effect of measles virus coinfection on plasma human immunodeficiency virus (HIV) RNA levels, a prospective study of hospitalized children with measles was conducted between January 1998 and October 2000 in Lusaka, Zambia. Plasma HIV RNA levels were measured during acute measles and 1 month after hospital discharge. The median plasma HIV RNA level in 33 children with measles who were followed longitudinally was 5339 copies/mL at study entry, 60,121 copies/mL at hospital discharge, and 387,148 copies/mL at 1-month follow-up. The median plasma HIV RNA level in children without acute illness was 228,454 copies/mL. Plasma levels of immune activation markers were elevated during the period of reduced plasma HIV RNA. Plasma levels of several potential HIV suppressive factors also were elevated during acute measles. HIV replication is transiently suppressed during acute measles at a time of intense immune activation.</p></abstract></profileDesc><revisionDesc><change when="2002-04-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup, element #text not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article">
<front>
<journal-meta>
<journal-id journal-id-type="hwp">jinfdis</journal-id>
<journal-id journal-id-type="publisher-id">jid</journal-id>
<journal-title>The Journal of Infectious Diseases</journal-title>
<abbrev-journal-title>The Journal of Infectious Diseases</abbrev-journal-title>
<issn pub-type="ppub">0022-1899</issn>
<issn pub-type="epub">1537-6613</issn>
<publisher>
<publisher-name>University of Chicago Press</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="doi">10.1086/340027</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Major Articles</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Suppression of Human Immunodeficiency Virus Replication during Acute Measles</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" corresp="yes">
<name><surname>Moss</surname>
<given-names>William J.</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="aff" rid="aff2">2</xref>
<xref ref-type="corresp" rid="cor1"></xref>
</contrib>
<contrib contrib-type="author">
<name><surname>Ryon</surname>
<given-names>Judith J.</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
<contrib contrib-type="author">
<name><surname>Monze</surname>
<given-names>Mwaka</given-names>
</name>
<xref ref-type="aff" rid="aff5">5</xref>
</contrib>
<contrib contrib-type="author">
<name><surname>Cutts</surname>
<given-names>Felicity</given-names>
</name>
<xref ref-type="aff" rid="aff6">6</xref>
<xref ref-type="fn" rid="fn1">a</xref>
</contrib>
<contrib contrib-type="author">
<name><surname>Quinn</surname>
<given-names>Thomas C.</given-names>
</name>
<xref ref-type="aff" rid="aff3">3</xref>
<xref ref-type="aff" rid="aff4">4</xref>
</contrib>
<contrib contrib-type="author">
<name><surname>Griffin</surname>
<given-names>Diane E.</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
</contrib>
</contrib-group>
<aff id="aff1"><label>1</label><institution>W. Harry Feinstone Department of Molecular Microbiology and Immunology</institution>, <addr-line>Bethesda, Maryland</addr-line></aff>
<aff id="aff2"><label>2</label><institution>Department of International Health, Bloomberg School of Public Health</institution>, <addr-line>Bethesda, Maryland</addr-line></aff>
<aff id="aff3"><label>3</label><institution>Division of Infectious Diseases, School of Medicine, Johns Hopkins University, Baltimore</institution>, <addr-line>Bethesda, Maryland</addr-line></aff>
<aff id="aff4"><label>4</label><institution>National Institute of Allergy and Infectious Diseases, National Institutes of Health</institution>, <addr-line>Bethesda, Maryland</addr-line></aff>
<aff id="aff5"><label>5</label><institution>Virology Laboratory, University Teaching Hospital</institution>, <addr-line>Lusaka, Zambia</addr-line></aff>
<aff id="aff6"><label>6</label><institution>Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine</institution>, <addr-line>London, United Kingdom</addr-line></aff>
<author-notes>
<corresp id="cor1">Reprints or correspondence: Dr. William J. Moss, W. Harry Feinstone Dept. of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 615 N. Wolfe St., Rm. E5132, Baltimore, MD 21205-2179 (<email>wmoss@jhsph.edu</email>).</corresp>
<fn fn-type="presented-at">
<p>Presented in part: annual meeting of the Infectious Diseases Society of America, Philadelphia, 18–21 November 1999 (abstract 698).</p>
</fn>
<fn fn-type="other">
<p>Written informed consent was obtained from the parents or guardians of the children studied. The study protocol was reviewed and approved by institutional review boards at the Johns Hopkins University Bloomberg School of Public Health, the London School of Hygiene and Tropical Medicine, and the University Teaching Hospital, Lusaka, Zambia.</p>
</fn>
<fn fn-type="financial-disclosure">
<p>Financial support: National Institutes of Health (AI 23047); World Health Organization;Wyeth-Lederle Vaccines and Pediatrics Young Investigator Award in Vaccine Development of the Infectious Diseases Society of America (to W.J.M.).</p>
</fn>
<fn id="fn1" fn-type="current-aff">
<label>a</label>
<p>Present affiliation: Medical Research Council Laboratories, Fajara, Banjul, The Gambia.</p>
</fn>
</author-notes>
<pub-date pub-type="ppub">
<day>15</day>
<month>4</month>
<year>2002</year>
</pub-date>
<volume>185</volume>
<issue>8</issue>
<fpage>1035</fpage>
<lpage>1042</lpage>
<history>
<date date-type="received">
<day>9</day>
<month>10</month>
<year>2001</year>
</date>
<date date-type="rev-recd">
<day>18</day>
<month>12</month>
<year>2001</year>
</date>
</history>
<copyright-statement>© 2002 by the Infectious Diseases Society of America</copyright-statement>
<copyright-year>2002</copyright-year>
<abstract>
<p>To determine the effect of measles virus coinfection on plasma human immunodeficiency virus (HIV) RNA levels, a prospective study of hospitalized children with measles was conducted between January 1998 and October 2000 in Lusaka, Zambia. Plasma HIV RNA levels were measured during acute measles and 1 month after hospital discharge. The median plasma HIV RNA level in 33 children with measles who were followed longitudinally was 5339 copies/mL at study entry, 60,121 copies/mL at hospital discharge, and 387,148 copies/mL at 1-month follow-up. The median plasma HIV RNA level in children without acute illness was 228,454 copies/mL. Plasma levels of immune activation markers were elevated during the period of reduced plasma HIV RNA. Plasma levels of several potential HIV suppressive factors also were elevated during acute measles. HIV replication is transiently suppressed during acute measles at a time of intense immune activation.</p>
</abstract>
</article-meta>
</front>
<body>
<p>Increases in plasma human immunodeficiency virus (HIV) RNA levels occur in HIV-infected children and adults coinfected with a variety of pathogens [<xref ref-type="bibr" rid="R1">1</xref>–<xref ref-type="bibr" rid="R4">4</xref>] and after vaccination [<xref ref-type="bibr" rid="R5">5</xref>–<xref ref-type="bibr" rid="R12">12</xref>]. The mechanisms responsible for enhanced HIV replication are unclear but may be related to an increase in the number of activated CD4<sup>+</sup> T lymphocytes susceptible to HIV infection and an increase in proinflammatory cytokines capable of inducing HIV replication [<xref ref-type="bibr" rid="R13">13</xref>]. Elevated levels of immune activation markers have been associated with increases in plasma HIV RNA after opportunistic infection in HIV-infected adults [<xref ref-type="bibr" rid="R14">14</xref>]. Although increases in HIV RNA are often transient, chronic or recurrent infections may result in a sustained increase in plasma HIV RNA and accelerate HIV disease progression [<xref ref-type="bibr" rid="R15">15</xref>, <xref ref-type="bibr" rid="R15">16</xref>].</p>
<p>Several coinfections, however, have the potential to inhibit HIV replication. For instance, human herpesvirus 6 [<xref ref-type="bibr" rid="R17">17</xref>, <xref ref-type="bibr" rid="R18">18</xref>] and influenza virus [<xref ref-type="bibr" rid="R19">19</xref>] suppressed HIV replication in vitro when either virus or supernatant fluid from stimulated peripheral blood mononuclear cells (PBMC) was added to cultures of HIV-infected cells. Supernatant fluids from PBMC of healthy adults, but not HIV-infected adults, suppressed HIV replication in vitro after influenza vaccination [<xref ref-type="bibr" rid="R20">20</xref>]. Suppression of HIV replication in vivo has been described only in persons infected with <italic>Orientia tsutsugamushi</italic>, the etiologic agent of scrub typhus [<xref ref-type="bibr" rid="R21">21</xref>].</p>
<p>Measles continues to be a major cause of child morbidity and mortality, particularly in countries in sub-Saharan Africa [<xref ref-type="bibr" rid="R22">22</xref>]. In central and eastern Africa, many countries have a high prevalence of HIV infection and a high incidence of measles. Measles virus itself is highly immunosuppressive, and much of measles mortality is attributable to secondary infections that result from suppression of cellular immunity [<xref ref-type="bibr" rid="R23">23</xref>–<xref ref-type="bibr" rid="R25">25</xref>]. The effects of measles virus on the immune system are complex, however, and result not only in a state of immune suppression but also in a state of immune activation [<xref ref-type="bibr" rid="R26">26</xref>–<xref ref-type="bibr" rid="R28">28</xref>]. The immune dysregulation that accompanies measles might be expected to enhance HIV replication in coinfected children. This hypothesis was tested in a prospective study of HIV-infected children with measles in Zambia.</p>
<sec sec-type="subjects|methods">
<title>Subjects and Methods</title>
<p><italic>Subjects</italic>. We studied children hospitalized with the clinical diagnosis of measles (fever and maculopapularrash with conjunctivitis, rhinorrhea, or cough) at the University Teaching Hospital, Lusaka, Zambia, between January 1998 and October 2000. Children who were severely ill or who died within hours of admission were less likely to be enrolled. In addition, the number of children enrolled per day was limited by the capacity to process specimens in the laboratory. Parents or guardians were requested to return with each child 1 month after discharge, but active tracing of children who failed to return was not performed. As of August 1999, parents or guardians also were requested to return with the child 3 months after hospital discharge. A blood specimen and clinical information were collected at hospital admission, discharge, and follow-up visits. Laboratory values for HIV-infected children with measles were compared with those of HIV-uninfected children with measles and 2 groups of children without acute illness: a group of HIV-infected children and a group of HIV-uninfected children. Plasma HIV RNA levels in HIV-infected children with measles were compared with those in HIV-infected children without acute illness, who were recruited at a well-child clinic, at a local school, or during a measles mass immunization campaign. All other measurements in HIV-infected children with measles were compared with those of HIV-uninfected children with measles and a group of HIV-uninfected children without acute illness, who were recruited from a well-child clinic or local school.</p>
<p><italic>Specimen collection and processing</italic>. Blood specimens were collected in a sterile tube that contained EDTA and were transported to the laboratory. Aliquots of whole blood were removed for white blood cell count and monoclonal antibody staining for flow cytometry. White blood cell counts and differential white blood cell counts were performed manually. Plasma was separated and was stored in aliquots at - 70°C for later measurement of antibodies to measles virus and HIV, plasma HIV RNA levels, and levels of immune activation markers, cytokines, and β-chemokines.</p>
<p><italic>Measles virus IgM antibody detection</italic>. Measles was confirmed by detection of measles virus-specific IgM in plasma by EIA (Wampole Laboratories). Children were classified as having measles if measles virus-specific IgM was detected at any time point.</p>
<p><italic>Detection of HIV RNA</italic>. Plasma was tested for antibody to HIV by EIA (Organon Technika). Plasma samples from children with a positive EIA for antibody to HIV were assayed for HIV RNA by reverse-transcriptase-polymerase chain reaction (Amplicor HIV-1 Monitor version 1.5; Roche Molecular Systems). Children were classified as HIV-infected if HIV RNA was detected in a plasma sample obtained at any time point. Values below the limit of detection of 400 copies/mL were assigned a value of 399 copies/mL for analysis. All laboratory assays were performed without knowledge of HIV-infection status.</p>
<p><italic>Flow cytometry</italic>. Whole blood was stained with directly labeled monoclonal antibodies to CD3, CD4, and CD8 antigens. After red blood cell lysis, flow cytometry was performed on a FACScan flow cytometer that used Cell Quest software (Becton Dickinson).</p>
<p><italic>Plasma markers of immune activation</italic>. Plasma levels of immune activation markers were quantified by use of EIA and RIA on stored plasma samples. EIA kits were used to measure soluble CD4 (sCD4), soluble CD8 (sCD8), soluble interleukin-2 receptor (sIL-2R; Endogen), and soluble tumor necrosis factor receptor II (sTNF-RII; Quantikine; R&D Systems). An RIA was used for the quantitative determination of β<sub>2</sub>-microglobulin (Pharmacia & Upjohn). Values below the limit of detection (21, 56, 346, and 7.8 U/ mL for sCD4, sCD8, sIL-2R, and sTNF-RII, respectively; 0.2 mg/ mL for β<sub>2</sub>-microglobulin) were assigned values midway between 0 and the lower limit of detection for the purpose of analysis.</p>
<p><italic>Plasma chemokine and cytokine levels</italic>. Plasma levels of the β-chemokines RANTES, macrophage inflammatory protein (MIP)1α, and MIP-1β were measured on stored plasma samples by use of EIA kits (Quantikine; R&D Systems). Plasma levels of IL-10 were quantified by EIA that used primary and secondary antibody pairs (Pharmingen), according to the manufacturer's instructions. Avidin-horseradish peroxidase was used to detect biotin-labeled secondary antibodies, and dilutions of recombinant human IL-10 (Pharmingen) were used as standards. Plasma levels of IL-16 were measured by EIA (BioSource International). Optical density readings were interpreted with SOFTmax PRO software (Molecular Devices). Values below the limit of detection (31.2 ng/mL for RANTES; 31.2 pg/mL for MIP-lα, MIP-β, and IL-10; 23.4 pg/ mL for IL-16) were assigned values midway between 0 and the lower limit of detection for the purpose of analysis.</p>
<p><italic>Statistical analysis</italic>. The Kruskal-Wallis test was used to determine whether measurements among HIV-infected children with measles differed from those among HIV-uninfected children with measles or control children. The Wilcoxon signed-rank test was used to determine whether measurements changed from entry to discharge or follow-up. Differences in sex distribution between study groups were compared by the χ<sup>2</sup> test, and differences in median age between study groups were compared by the Kruskal-Wallis test. No formal adjustment was made for multiple testing. Data analysis was performed with Stata Statistical Software Release 6.0 (Stata).</p>
</sec>
<sec sec-type="results">
<title>Results</title>
<p><italic>Characteristics of the study children</italic>. Between January 1998 and October 2000, we enrolled 655 children hospitalized due to suspected measles; they made up 27% of all children hospitalized due to suspected measles at the University Teaching Hospital between those time points. Of 584 children for whom sufficient information was available to ascertain both measles and HIV infection status, 546 (93%) had measles, as confirmed by IgM EIA. Ninety-three children with measles (17%) were coinfected with HIV. The median age of the HIV-infected children with measles was 11 months, and 59% were boys (<xref ref-type="fig" rid="F2">table 1</xref>). Blood specimens were available from 89 coinfected children at study entry, from 66 at hospital discharge, from 39 at 1-month follow-up, and from 10 at 3-month follow-up.</p>
<p>Plasma HIV RNA levels were measured in 22 HIV-infected children without evidence of acute illness in a well-child clinic, at school, or during a measles mass immunization campaign. For the 13 children enrolled in the measles immunization campaign, blood was obtained prior to vaccination. Their median age was 26 months, and 57% were boys (<xref ref-type="fig" rid="F2">table 1</xref>). Insufficient plasma was available for additional assays on this group of children.</p>
<p>For comparison with children coinfected with measles and HIV, percentages and cell counts of CD4<sup>+</sup> and CD8<sup>+</sup> T lymphocytes and levels of plasma immune activation markers (IL-10, IL-16, and β-chemokines) were measured in a subset of 367 HIV-uninfected children with measles and 164 HIV-uninfected children without evidence of acute illness (<xref ref-type="fig" rid="F2">table 1</xref>). There was no statistically significant association between sex and study group (<italic>P</italic> = .4), but HIV-infected children with measles were significantly younger than the other groups of children (<italic>P</italic> = .01).</p>
<p><italic>HIV RNA levels</italic>. The median plasma HIV RNA level in all HIV-infected children with measles was 8216 copies/mL at study entry (range, 399–72,477,000 copies/mL) and increased to 107,567 copies/mL at hospital discharge (range, 399–13,812,850 copies/mL) and 373,748 copies/mL at 1-month follow-up (range, 872-3,210,000 copies/mL; <xref ref-type="fig" rid="F1">figure 1</xref>). Plasma HIV RNA levels were not measured in all children at all time points. The median plasma HIV RNA level was lower at entry than at hospital discharge (<italic>P</italic> = .0002) and 1-month follow-up (<italic>P</italic> = .0002). The median plasma HIV RNA level in 22 children without acute illness was 228,454 copies/mL (range, 474–1,339,027 copies/mL). This value was significantly higher than that in HIV-infected children with measles at study entry (<italic>P</italic> = .002) but was not significantly different from that in children with measles at either discharge or follow-up (<italic>P</italic> = .07 and .2, respectively).</p>
<p>Plasma HIV RNA levels were measured at all 3 time points (study entry, hospital discharge, and 1-month follow-up) in 33 HIV-infected children with measles. In addition, HIV RNA levels were measured in 10 of these children 3 months after hospital discharge. In this subset of children, the median plasma HIV RNA level was 5339 copies/mL at study entry (range, 399–18,074,200 copies/mL) and had increased to 60,121 copies/mL at hospital discharge (range, 399–13,812,850 copies/mL) and 387,148 copies/mL at 1-month follow-up (range, 872–3,210,000 copies/mL). In 10 coinfected children, the median plasma HIV RNA level at the 3-month follow-up visit was 177,300 copies/ mL (range, 916–357,000 copies/mL).</p>
<p>Eight HIV-infected children with measles had plasma HIV RNA levels below the limit of detection (400 copies/mL) at entry but had developed detectable levels by the time of hospital discharge or follow-up. Extremely high plasma HIV RNA levels (> 1 million copies/mL) were found in 20 coinfected children. Five of these children had plasma HIV RNA levels > 10 million copies/mL. Eight children had plasma HIV RNA levels > 1 million copies/mL at the time of study entry. The maximum plasma HIV RNA level was 72,477,000 copies/mL and was detected at study entry.</p>
<p><italic>T cell studies</italic>. CD4<sup>+</sup> and CD8<sup>+</sup> T lymphocyte subsets were measured in 52 HIV-infected children with measles at study entry, of whom 21 were also assessed at the 1-month follow-up. The median percentage of CD4<sup>+</sup> T lymphocytes did not change significantly from study entry to follow-up in these 21 children (18% and 17%, respectively; <italic>P</italic> = .6). As expected, the median percentage of CD4<sup>+</sup> T lymphocytes was lower in HIV-infected children than in HIV-uninfected children with measles (<xref ref-type="fig" rid="F3">table 2</xref>). The number of CD4<sup>+</sup> T lymphocytes was similar between HIV-infected and uninfected children during acute measles but had increased markedly only in the HIV-uninfected children by the time of 1-month follow-up. Both the median CD4<sup>+</sup> T lymphocyte cell count and the median percentage in HIV-infected children with measles at entry and at 1-month follow-up were approximately half those in HIV-uninfected children without measles (<xref ref-type="fig" rid="F3">table 2</xref>).</p>
<p>The median percentage of CD8+ T lymphocytes increased from 38% at entry to 44% at follow-up in the 21 HIV-infected children with measles studied at both time points (<italic>P</italic> = .02). In contrast to the median number of CD4<sup>+</sup> T lymphocytes, the median number of CD8<italic>+</italic> T lymphocytes increased 2-fold from 1169 cells/mm<sup>3</sup> at entry to 2477 cells/mm<sup>3</sup> at follow-up in these 21 coinfected children (<italic>P</italic> = .002). The median percentage and number of CD8<sup>+</sup> T lymphocytes in coinfected children were approximately double those in HIV-uninfected children with measles and HIV-uninfected control children (<xref ref-type="fig" rid="F3">table 2</xref>).</p>
<p><italic>Plasma markers of immune activation</italic>. There were trends toward rising sCD4 and β<sub>2</sub>-microglobulin and declining sCD8, sIL-2R, and sTNF-RU levels after acute measles in HIV-infected children (<xref ref-type="fig" rid="F4">table 3</xref>); however, since we had very low numbers of subjects at follow-up, we had low power to determine whether differences were significant. Both HIV-infected and -uninfected children had elevations of sIL-2R and sTNR-RH during acute measles that had declined toward levels in HIV-uninfected control children by the time of 1-month follow-up. However, HIV-infected children had persistently elevated levels of sCD4, sCD8, and β<sub>2</sub>-microglobulin at 1-month follow-up, compared with those in HIV-uninfected children with measles. Levels of sCD8, β<sub>2</sub>-microglobulin, sIL-2R, and sTNF-RII at study entry in HIVinfected children with measles were significantly higher than values in HIV-uninfected control children, and levels of sCD8 and β<sub>2</sub>-microglobulin among HIV-infected children with measles remained significantly higher than those among HIV-uninfected control children at the time of 1-month follow-up.</p>
<p><italic>Potential HNsuppressive factors</italic>. Plasma levels of several potential HIV suppressive factors were measured in a subset of children (<xref ref-type="fig" rid="F5">table 4</xref>). Median plasma levels of IL-10 were elevated in HIV-infected and -uninfected children with measles at both entry and 1-month follow-up, compared with those in control children, and remained elevated at 1-month follow-up in 2 HIVinfected children with measles. Median plasma levels of IL-16 at entry were similar in children with measles and control children but had decreased in children with measles at the 1-month follow-up (<italic>P</italic> =.02 for comparison of entry and 1-month followup values in HIV-uninfected children with measles). Median plasma levels of RANTES at entry were elevated in children with measles compared with those of HIV-uninfected control children and remained high at follow-up. Children coinfected with measles and HIV had significantly higher median plasma levels of RANTES at entry than HIV-uninfected children with measles. Median plasma levels of MIP-1α were generally below the limit of detection but had increased at follow-up in HIV-infected children with measles (<italic>P</italic> = .03 for comparison of entry and 1-month follow-up values in HIV-infected children with measles). Median plasma levels of MIP-1β in HIV-infected children with measles were similar to levels in HIV-uninfected children at entry but had increased in 5 children by the time of 1-month follow-up.</p>
</sec>
<sec sec-type="discussion">
<title>Discussion</title>
<p>The low median plasma HIV RNA level at study entry strongly suggests that HIV replication is transiently suppressed early in the course of measles. Although we were unable to measure plasma HIV RNA levels prior to measles, several factors support the hypothesis that HIV replication was suppressed during acute measles virus infection. First, plasma HIV RNA levels at ∼1 month after onset of measles rash were similar to levels in HIV-infected children without acute measles virus infection. Second, plasma HIV levels from cohorts of children with perinatally acquired HIV infection in developed countries are reported to be in the range of 50,000–200,000 copies/mL during the first few years of life [<xref ref-type="bibr" rid="R29">29</xref>–<xref ref-type="bibr" rid="R31">31</xref>]. One cohort study in the United States showed that plasma HIV RNA levels did not decrease to steady-state levels of 50,000–100,000 copies/mL until age ∼6 years [<xref ref-type="bibr" rid="R32">32</xref>]. Few studies have examined plasma HIV RNA levels in children born in Africa, but there are some data to suggest that levels are higher than those in industrialized countries. Median HIV RNA levels in children in Malawi reached 355,000 copies/ mL at age 8 weeks, declined to 200,000 copies/mL at age 1 year [<xref ref-type="bibr" rid="R33">33</xref>], and remained high through the second year of life [<xref ref-type="bibr" rid="R34">34</xref>]. Data on plasma HIV RNA levels in older children in Africa have not been published. Third, 8 children developed detectable plasma levels of HIV RNA only ≥8 days after the onset of measles rash. This supports suppression of replication early in the illness, although an alternative explanation would be that the immune response of these children was able to control HIV replication until it was perturbed by measles virus coinfection.</p>
<p>This study is limited by potential selection bias, because we were unable to enroll HIV-infected children without characteristic clinical manifestations of measles or children who died shortly after hospitalization. In addition, a large proportion of children did not return for follow-up. Nevertheless, the dramatic changes in plasma HIV RNA levels in the 33 coinfected children with measurements at hospital admission, discharge, and 1-month follow-up strongly suggest suppression of HIV replication during acute measles in some children at a time when several plasma markers of immune activation were markedly elevated.</p>
<p>Several potential mechanisms could explain the transient suppression of HIV replication early during the course of measles. Measles virus infection results in lymphopenia, with reductions in CD4<sup>+</sup> T lymphocyte percentage and number. The nadir of the lymphopenia precedes the onset of rash [<xref ref-type="bibr" rid="R35">35</xref>], and values usually return to normal by 1 month after the onset of the rash [<xref ref-type="bibr" rid="R36">36</xref>–<xref ref-type="bibr" rid="R39">39</xref>]. This early reduction in CD4<sup>+</sup> T lymphocytes could decrease the number of target cells for HIV replication. An alternative explanation is that measles virus infection stimulates the production of soluble factor(s) capable of suppressing HIV replication. Several classes of factors with this ability have been identified, including the β-chemokines [<xref ref-type="bibr" rid="R40">40</xref>], CD8<sup>+</sup> cell antiviral factor [<xref ref-type="bibr" rid="R41">41</xref>, <xref ref-type="bibr" rid="R42">42</xref>], and the cytokines IL-10 [<xref ref-type="bibr" rid="R43">43</xref>] and IL-16 [<xref ref-type="bibr" rid="R44">44</xref>, <xref ref-type="bibr" rid="R45">45</xref>]. However, a relationship between serum β-chemokine levels and HIV disease progression has not been clearly demonstrated [<xref ref-type="bibr" rid="R46">46</xref>–<xref ref-type="bibr" rid="R48">48</xref>], and we did not find temporal changes in plasma β-chemokine levels that were consistent with a suppressive effect on HIV replication during measles virus infection. Nevertheless, median plasma levels of RANTES were highest in HIV-infected children with measles. Although they were not significantly higher than those in control children, plasma levels of IL-16 were significantly higher at entry than at 1-month follow-up in children with measles, inversely related to the changes in plasma HIV RNA levels. IL-16 has been shown to inhibit the transcription of the HIV long terminal repeat [<xref ref-type="bibr" rid="R49">49</xref>–<xref ref-type="bibr" rid="R51">51</xref>], and decreased plasma IL-16 levels are associated with HIV disease progression [<xref ref-type="bibr" rid="R44">44</xref>, <xref ref-type="bibr" rid="R52">52</xref>].</p>
<p>The only previous demonstration of suppression of HIV replication in humans, to our knowledge, was after coinfection with <italic>O. tsutsugamushi</italic>, the cause of scrub typhus [<xref ref-type="bibr" rid="R21">21</xref>]. Three days after hospitalization, median HIV-1 RNA levels were lower in 10 patients with scrub typhus than in 5 patients who had other acute infections. Threefold or greater reductions in HIV-1 RNA levels were observed in 4 patients during acute infection with scrub typhus. Scrub typhus was speculated to lower plasma HIV RNA levels by favoring replication of non- syncytia-inducing HIV variants, although there was no direct evidence for this hypothesis. In macaques infected with simian immunodeficiency virus (SIV), inoculation with both <italic>Mycobacterium bovis</italic> bacille Calmette-Guérin and staphylococcal enterotoxin B resulted in a several-log decrease in plasma SIV RNA levels [<xref ref-type="bibr" rid="R53">53</xref>]. However, the mechanisms responsible for this reduction in plasma viremia are not known.</p>
<p>Whether the rebound increase in HIV replication during the 1–2 months after measles results in accelerated HIV disease progression or merely signifies a return to steady state remains unclear. Plasma HIV RNA levels and CD4 lymphocyte percentages early in life are independently predictive of prognosis in children [<xref ref-type="bibr" rid="R32">32</xref>, <xref ref-type="bibr" rid="R54">54</xref>–<xref ref-type="bibr" rid="R57">57</xref>]. In HIV-infected children with measles, the percentage of CD4<sup>+</sup> T lymphocytes remained low for ≥6 weeks after rash onset. Reflecting the resolution of the measles-induced lymphopenia, the number of CD4<sup>+</sup> T lymphocytes increased at follow-up but was still much lower than that in HIV-uninfected children with measles. Concurrently, the number of CD8<sup>+</sup> T lymphocytes increased. This increase may represent an expansion of CD8<sup>+</sup> T lymphocytes in response to enhanced HIV replication but may also occur in response to measles virus [<xref ref-type="bibr" rid="R36">36</xref>].</p>
<p>Plasma markers of immune activation also are independent predictors of disease progression in HIV-infected children [<xref ref-type="bibr" rid="R58">58</xref>, <xref ref-type="bibr" rid="R59">59</xref>] and adults [<xref ref-type="bibr" rid="R60">60</xref>–<xref ref-type="bibr" rid="R64">64</xref>]. Those with the strongest predictive value include sTNF-RH, β<sub>2</sub>-microglobulin, neopterin, sIL-2R, and sCD8. In children without HIV infection, plasma levels of sCD8 rise at the time of measles rash but decline sharply as the rash resolves [<xref ref-type="bibr" rid="R65">65</xref>]. The sustained elevation in sCD8 that we observed in HIV-infected children indicates increased activation as well as expansion of the pool of CD8<sup>+</sup> T lymphocytes, which suggests accelerated HIV disease progression after measles [<xref ref-type="bibr" rid="R66">66</xref>]. The unexpectedly low levels of sCD4 early during the course of measles in HIV-infected children may reflect the low number of CD4<sup>+</sup> T lymphocytes during the period of measles-induced lymphopenia.</p>
<p>In summary, we report the first in vivo evidence of the suppression of HIV replication by a viral coinfection. The mechanisms by which measles virus coinfection suppresses HIV replication concurrent with intense immune activation remain unknown but may provide clues to understanding both HIV pathogenesis and immunity. Further work is needed to clarify whether the changes in T cell subsets and the increases in activation markers at follow-up indicate enhanced HIV progression after measles.</p>
</sec>
</body>
<back>
<ack>
<title>Acknowledgments</title>
<p>We thank Christopher L. Karp (Children's Hospital Research Foundation, Cincinnati) for providing insightful comments and suggestions in the early development of this project and Elizabeth Johnson (Bloomberg School of Public Health, Johns Hopkins University, Baltimore) for assistance with statistical analyses. We thank N. P. Luo, L. Munkonkange, E. M. Chomba, Evans Mpabalwani, Gina Mulundu, and Francis Kasolo for facilitating research at the Virology Laboratory and University Teaching Hospital in Zambia; the laboratory and nursing staff in Zambia for work with patient recruitment and sample processing; and the Japan International Cooperation Agency for generously allowing the use of laboratory facilities.</p>
</ack>
<ref-list>
<title>References</title>
<ref id="R1"><label>1.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Marchisio</surname><given-names>P</given-names></name><name><surname>Esposito</surname><given-names>S</given-names></name><name><surname>Zanchetta</surname><given-names>N</given-names></name><name><surname>Tornaghi</surname><given-names>R</given-names></name><name><surname>Gismondo</surname><given-names>MR</given-names></name><name><surname>Principi</surname><given-names>N</given-names></name></person-group><article-title>Effect of superimposed infections on viral replication in human immunodeficiency virus type 1-infected children</article-title><source>Pediatr Infect Dis J</source><year>1998</year><volume>17</volume><fpage>755</fpage><lpage>7</lpage></nlm-citation></ref>
<ref id="R2"><label>2.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Mole</surname><given-names>L</given-names></name><name><surname>Ripich</surname><given-names>S</given-names></name><name><surname>Margolis</surname><given-names>D</given-names></name><name><surname>Holodniy</surname><given-names>M</given-names></name></person-group><article-title>The impact of active herpes simplex virus infection on human immunodeficiency virus load</article-title><source>J Infect Dis</source><year>1997</year><volume>176</volume><fpage>766</fpage><lpage>70</lpage></nlm-citation></ref>
<ref id="R3"><label>3.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Donovan</surname><given-names>RM</given-names></name><name><surname>Bush</surname><given-names>CE</given-names></name><name><surname>Markowitz</surname><given-names>NP</given-names></name><name><surname>Baxa</surname><given-names>DM</given-names></name><name><surname>Saravolatz</surname><given-names>LD</given-names></name></person-group><article-title>Changes in virus load markers during AIDS-associated opportunistic diseases in human immunodeficiency virus-infected persons</article-title><source>J Infect Dis</source><year>1996</year><volume>174</volume><fpage>401</fpage><lpage>3</lpage></nlm-citation></ref>
<ref id="R4"><label>4.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Golletti</surname><given-names>D</given-names></name><name><surname>Weissman</surname><given-names>D</given-names></name><name><surname>Jackson</surname><given-names>RW</given-names></name><etal></etal></person-group><article-title>Effect of <italic>Mycobacterium tuberculosis</italic> on HIV replication: role of immune activation</article-title><source>J Immunol</source><year>1996</year><volume>157</volume><fpage>1271</fpage><lpage>8</lpage></nlm-citation></ref>
<ref id="R5"><label>5.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Tasker</surname><given-names>SA</given-names></name><name><surname>O'Brien</surname><given-names>WA</given-names></name><name><surname>Treanor</surname><given-names>JJ</given-names></name><etal></etal></person-group><article-title>Effects of influenza vaccination in HIV-infected adults: a double-blind, placebo-controlled trial</article-title><source>Vaccine</source><year>1998</year><volume>16</volume><fpage>1039</fpage><lpage>42</lpage></nlm-citation></ref>
<ref id="R6"><label>6.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Stanley</surname><given-names>SK</given-names></name><name><surname>Ostrowski</surname><given-names>MA</given-names></name><name><surname>Justement</surname><given-names>IS</given-names></name><etal></etal></person-group><article-title>Effect of immunization with a common recall antigen on viral expression in patients infected with human immunodeficiency virus type 1</article-title><source>N Engl J Med</source><year>1996</year><volume>334</volume><fpage>1222</fpage><lpage>30</lpage></nlm-citation></ref>
<ref id="R7"><label>7.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Brichacek</surname><given-names>B</given-names></name><name><surname>Swindells</surname><given-names>S</given-names></name><name><surname>Janoff</surname><given-names>EN</given-names></name><name><surname>Pirruccello</surname><given-names>S</given-names></name><name><surname>Stevenson</surname><given-names>M</given-names></name></person-group><article-title>Increased plasma human immunodeficiency virus type 1 burden following antigenic challenge with pneumococcal vaccine</article-title><source>J Infect Dis</source><year>1996</year><volume>174</volume><fpage>1191</fpage><lpage>9</lpage></nlm-citation></ref>
<ref id="R8"><label>8.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Cheeseman</surname><given-names>SH</given-names></name><name><surname>Davaro</surname><given-names>RE</given-names></name><name><surname>Ellision</surname><given-names>RT</given-names></name></person-group><article-title>Hepatitis B vaccination and plasma HIV-1 RNA</article-title><source>N Engl J Med</source><year>1996</year><volume>334</volume><fpage>1272</fpage></nlm-citation></ref>
<ref id="R9"><label>9.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Ramilo</surname><given-names>O</given-names></name><name><surname>Hicks</surname><given-names>PJ</given-names></name><name><surname>Borvak</surname><given-names>J</given-names></name><etal></etal></person-group><article-title>T cell activation and human immunodeficiency virus replication after influenza immunization of infected children</article-title><source>Pediatr Infect Dis J</source><year>1996</year><volume>15</volume><fpage>197</fpage><lpage>203</lpage></nlm-citation></ref>
<ref id="R10"><label>10.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Staprans</surname><given-names>SI</given-names></name><name><surname>Hamiltion</surname><given-names>BL</given-names></name><name><surname>Follansbee</surname><given-names>SE</given-names></name><etal></etal></person-group><article-title>Activation of virus replication after vaccination of HIV-1-infected individuals</article-title><source>J Exp Med</source><year>1995</year><volume>182</volume><fpage>1727</fpage><lpage>37</lpage></nlm-citation></ref>
<ref id="R11"><label>11.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>O'Brien</surname><given-names>WA</given-names></name><name><surname>Grovit-Ferbas</surname><given-names>K</given-names></name><name><surname>Namazi</surname><given-names>A</given-names></name><etal></etal></person-group><article-title>Human immunodeficiency virus-type 1 replication can be increased in peripheral blood of seropositive patients after influenza vaccination</article-title><source>Blood</source><year>1995</year><volume>86</volume><fpage>1082</fpage><lpage>9</lpage></nlm-citation></ref>
<ref id="R12"><label>12.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Ho</surname><given-names>DD</given-names></name></person-group><article-title>HIV-1 viraemia and influenza</article-title><source>Lancet</source><year>1992</year><volume>339</volume><fpage>1549</fpage></nlm-citation></ref>
<ref id="R13"><label>13.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Ostrowski</surname><given-names>MA</given-names></name><name><surname>Krakauer</surname><given-names>DC</given-names></name><name><surname>Li</surname><given-names>Y</given-names></name><etal></etal></person-group><article-title>Effect of immune activation on the dynamics of human immunodeficiency virus replication and on the distribution of viral quasispecies</article-title><source>J Virol</source><year>1998</year><volume>72</volume><fpage>7772</fpage><lpage>84</lpage></nlm-citation></ref>
<ref id="R14"><label>14.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Sulkowski</surname><given-names>MS</given-names></name><name><surname>Chaisson</surname><given-names>RE</given-names></name><name><surname>Karp</surname><given-names>CL</given-names></name><name><surname>Moore</surname><given-names>RD</given-names></name><name><surname>Margolick</surname><given-names>JB</given-names></name><name><surname>Quinn</surname><given-names>TC</given-names></name></person-group><article-title>The effect of acute infectious illnesses on plasma human immunodeficiency virus (HIV) type 1 load and the expression of serologic mar kers of immune activation among HIV-infected adults</article-title><source>J Infect Dis</source><year>1998</year><volume>178</volume><fpage>1642</fpage><lpage>8</lpage></nlm-citation></ref>
<ref id="R15"><label>15.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Chaisson</surname><given-names>RE</given-names></name><name><surname>Gallant</surname><given-names>JE</given-names></name><name><surname>Keruly</surname><given-names>JC</given-names></name><name><surname>Moore</surname><given-names>RD</given-names></name></person-group><article-title>Impact of opportunistic diseases on survival in patients with HIV disease</article-title><source>AIDS</source><year>1998</year><volume>12</volume><fpage>29</fpage><lpage>33</lpage></nlm-citation></ref>
<ref id="R16"><label>16.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Whalen</surname><given-names>C</given-names></name><name><surname>Horsburgh</surname><given-names>CR</given-names></name><name><surname>Hom</surname><given-names>D</given-names></name><name><surname>Lahart</surname><given-names>C</given-names></name><name><surname>Simberkoff</surname><given-names>M</given-names></name><name><surname>Ellner</surname><given-names>J</given-names></name></person-group><article-title>Accelerated course of human immunodeficiency virus infection after tuberculosis</article-title><source>Am J Respir Crit Care Med</source><year>1995</year><volume>151</volume><fpage>129</fpage><lpage>35</lpage></nlm-citation></ref>
<ref id="R17"><label>17.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Levy</surname><given-names>JA</given-names></name><name><surname>Landay</surname><given-names>A</given-names></name><name><surname>Lennette</surname><given-names>ET</given-names></name></person-group><article-title>Human herpesvirus 6 inhibits human immunodeficiency virus type 1 replication in cell culture</article-title><source>J Clin Microbiol</source><year>1990</year><volume>28</volume><fpage>2362</fpage><lpage>4</lpage></nlm-citation></ref>
<ref id="R18"><label>18.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Asada</surname><given-names>H</given-names></name><name><surname>Klaus-Kovtun</surname><given-names>V</given-names></name><name><surname>Golding</surname><given-names>H</given-names></name><name><surname>Katz</surname><given-names>SI</given-names></name><name><surname>Blauvelt</surname><given-names>A</given-names></name></person-group><article-title>Human herpesvirus 6 infects dendritic cells and suppresses human immunodeficiency virus type 1 replication in coinfected cultures</article-title><source>J Virol</source><year>1999</year><volume>73</volume><fpage>4019</fpage><lpage>28</lpage></nlm-citation></ref>
<ref id="R19"><label>19.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Pinto</surname><given-names>LA</given-names></name><name><surname>Blazevic</surname><given-names>V</given-names></name><name><surname>Patterson</surname><given-names>BK</given-names></name><name><surname>Trubey</surname><given-names>CM</given-names></name><name><surname>Dolan</surname><given-names>MJ</given-names></name><name><surname>Shearer</surname><given-names>GM</given-names></name></person-group><article-title>Inhibition of human immunodeficiency virus type 1 replication prior to reverse transcription by influenza virus stimulation</article-title><source>J Virol</source><year>2000</year><volume>74</volume><fpage>4505</fpage><lpage>11</lpage></nlm-citation></ref>
<ref id="R20"><label>20.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Pinto</surname><given-names>LA</given-names></name><name><surname>Blazevic</surname><given-names>V</given-names></name><name><surname>Anderson</surname><given-names>SA</given-names></name><etal></etal></person-group><article-title>Influenza virus-stimulated generation of anti-human immunodeficiency virus (HIV) activity after influenza vaccination in HIV-infected individuals and healthy control subjects</article-title><source>J Infect Dis</source><year>2001</year><volume>183</volume><fpage>1000</fpage><lpage>8</lpage></nlm-citation></ref>
<ref id="R21"><label>21.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Watt</surname><given-names>G</given-names></name><name><surname>Kantipong</surname><given-names>P</given-names></name><name><surname>de Souza</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>HIV-1 suppression during acute scrub-typhus infection</article-title><source>Lancet</source><year>2000</year><volume>356</volume><fpage>475</fpage><lpage>9</lpage></nlm-citation></ref>
<ref id="R22"><label>22.</label><nlm-citation citation-type="journal"><article-title>Centers for Disease Control and Prevention. Global measles control and regional elimination, 1998–1999</article-title><source>MMWR Moth Mortal Wkly Rep</source><year>1999</year><volume>48</volume><fpage>1124</fpage><lpage>30</lpage></nlm-citation></ref>
<ref id="R23"><label>23.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Morley</surname><given-names>D</given-names></name></person-group><article-title>Severe measles in the tropics. I</article-title><source>BMJ</source><year>1969</year><volume>1</volume><fpage>297</fpage><lpage>300</lpage></nlm-citation></ref>
<ref id="R24"><label>24.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Whittle</surname><given-names>HC</given-names></name><name><surname>Dossetor</surname><given-names>J</given-names></name><name><surname>Oduloju</surname><given-names>A</given-names></name><name><surname>Bryceson</surname><given-names>ADM</given-names></name><name><surname>Greenwood</surname><given-names>BM</given-names></name></person-group><article-title>Cell-mediated immunity during natural measles infection</article-title><source>J Clin Invest</source><year>1978</year><volume>62</volume><fpage>678</fpage><lpage>84</lpage></nlm-citation></ref>
<ref id="R25"><label>25.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Akramuzzaman</surname><given-names>SM</given-names></name><name><surname>Cutts</surname><given-names>FT</given-names></name><name><surname>Wheeler</surname><given-names>JG</given-names></name><name><surname>Hossain</surname><given-names>MI</given-names></name></person-group><article-title>Increased childhood morbidity after measles is short-term in urban Bangladesh</article-title><source>Am J Epidemiol</source><year>2000</year><volume>151</volume><fpage>723</fpage><lpage>35</lpage></nlm-citation></ref>
<ref id="R26"><label>26.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Griffin</surname><given-names>DE</given-names></name><name><surname>Ward</surname><given-names>BJ</given-names></name><name><surname>Jauregui</surname><given-names>E</given-names></name><name><surname>Johnson</surname><given-names>RT</given-names></name><name><surname>Vaisberg</surname><given-names>A</given-names></name></person-group><article-title>Immune activation in measles</article-title><source>N Engl J Med</source><year>1989</year><volume>320</volume><fpage>1667</fpage><lpage>72</lpage></nlm-citation></ref>
<ref id="R27"><label>27.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Griffin</surname><given-names>DE</given-names></name><name><surname>Ward</surname><given-names>BJ</given-names></name><name><surname>Jauregui</surname><given-names>E</given-names></name><name><surname>Johnson</surname><given-names>RT</given-names></name><name><surname>Vaisberg</surname><given-names>A</given-names></name></person-group><article-title>Immune activation during measles: interferon-γ and neopterin in plasma cerebrospinal fluid in complicated and uncomplicated disease</article-title><source>J Infect Dis</source><year>1990</year><volume>161</volume><fpage>449</fpage><lpage>53</lpage></nlm-citation></ref>
<ref id="R28"><label>28.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Griffin</surname><given-names>DE</given-names></name><name><surname>Ward</surname><given-names>BJ</given-names></name><name><surname>Jauregui</surname><given-names>E</given-names></name><name><surname>Johnson</surname><given-names>RT</given-names></name><name><surname>Vaisberg</surname><given-names>A</given-names></name></person-group><article-title>Immune activation during measles: β<sub>2</sub> microglobulin in plasma and cerebrospinal fluid in complicated and uncomplicated disease</article-title><source>J Infect Dis</source><year>1992</year><volume>166</volume><fpage>1170</fpage><lpage>3</lpage></nlm-citation></ref>
<ref id="R29"><label>29.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>De Rossi</surname><given-names>A</given-names></name><name><surname>Masiero</surname><given-names>S</given-names></name><name><surname>Giaquinto</surname><given-names>C</given-names></name><etal></etal></person-group><article-title>Dynamics of viral replication in infants with vertically acquired human immunodeficiency virus type 1 infection</article-title><source>J Clin Invest</source><year>1996</year><volume>97</volume><fpage>323</fpage><lpage>30</lpage></nlm-citation></ref>
<ref id="R30"><label>30.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>McIntosh</surname><given-names>K</given-names></name><name><surname>Shevitz</surname><given-names>A</given-names></name><name><surname>Zaknun</surname><given-names>D</given-names></name><etal></etal></person-group><article-title>Age- and time-related changes in extracellular viral load in children vertically infected by human immunodeficiency virus</article-title><source>Pediatr Infect Dis J</source><year>1996</year><volume>15</volume><fpage>1087</fpage><lpage>91</lpage></nlm-citation></ref>
<ref id="R31"><label>31.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Dickover</surname><given-names>RE</given-names></name><name><surname>Dillon</surname><given-names>M</given-names></name><name><surname>Gillette</surname><given-names>SG</given-names></name><etal></etal></person-group><article-title>Rapid increases in load of human immunodeficiency virus correlate with early disease progression and loss of CD4 cells in vertically infected infants</article-title><source>J Infect Dis</source><year>1994</year><volume>170</volume><fpage>1279</fpage><lpage>84</lpage></nlm-citation></ref>
<ref id="R32"><label>32.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Palumbo</surname><given-names>PE</given-names></name><name><surname>Raskino</surname><given-names>C</given-names></name><name><surname>Fiscus</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>Predictive value of quantitative plasma HIV RNA and CD4<sup>+</sup> lymphocyte count in HIV-infected infants and children</article-title><source>JAMA</source><year>1998</year><volume>279</volume><fpage>756</fpage><lpage>61</lpage></nlm-citation></ref>
<ref id="R33"><label>33.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Biggar</surname><given-names>RJ</given-names></name><name><surname>Janes</surname><given-names>M</given-names></name><name><surname>Pilon</surname><given-names>R</given-names></name><etal></etal></person-group><article-title>Virus levels in untreated African infants infected with human immunodeficiency virus type 1</article-title><source>J Infect Dis</source><year>1999</year><volume>180</volume><fpage>1838</fpage><lpage>43</lpage></nlm-citation></ref>
<ref id="R34"><label>34.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Taha</surname><given-names>TE</given-names></name><name><surname>Kumwenda</surname><given-names>NI</given-names></name><name><surname>Hoover</surname><given-names>DR</given-names></name><etal></etal></person-group><article-title>Association of HIV-1 load and CD4 lymphocyte count with mortality among untreated African children over one year of age</article-title><source>AIDS</source><year>2000</year><volume>14</volume><fpage>453</fpage><lpage>9</lpage></nlm-citation></ref>
<ref id="R35"><label>35.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Auwaerter</surname><given-names>PG</given-names></name><name><surname>Rota</surname><given-names>PA</given-names></name><name><surname>Elkins</surname><given-names>WR</given-names></name><etal></etal></person-group><article-title>Measles virus infection in rhesus macaques: altered immune responses and comparison of the virulence of six different virus strains</article-title><source>J Infect Dis</source><year>1999</year><volume>180</volume><fpage>950</fpage><lpage>8</lpage></nlm-citation></ref>
<ref id="R36"><label>36.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Lisse</surname><given-names>I</given-names></name><name><surname>Samb</surname><given-names>B</given-names></name><name><surname>Whittle</surname><given-names>H</given-names></name><etal></etal></person-group><article-title>Acute and long-term changes in Tlymphocyte subsets in response to clinical and subclinical measles. A community study from rural Senegal</article-title><source>Scand J Infect Dis</source><year>1998</year><volume>30</volume><fpage>17</fpage><lpage>21</lpage></nlm-citation></ref>
<ref id="R37"><label>37.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Griffin</surname><given-names>DE</given-names></name><name><surname>Ward</surname><given-names>BJ</given-names></name></person-group><article-title>Differential CD4 T cell activation in measles</article-title><source>J Infect Dis</source><year>1993</year><volume>168</volume><fpage>275</fpage><lpage>81</lpage></nlm-citation></ref>
<ref id="R38"><label>38.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Dagan</surname><given-names>R</given-names></name><name><surname>Phillip</surname><given-names>M</given-names></name><name><surname>Sarov</surname><given-names>I</given-names></name><name><surname>Skibin</surname><given-names>A</given-names></name><name><surname>Epstein</surname><given-names>S</given-names></name><name><surname>Kuperman</surname><given-names>O</given-names></name></person-group><article-title>Cellular immunity and T-lymphocyte subsets in young children with acute measles</article-title><source>J Med Virol</source><year>1987</year><volume>22</volume><fpage>175</fpage><lpage>82</lpage></nlm-citation></ref>
<ref id="R39"><label>39.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Kiepeila</surname><given-names>P</given-names></name><name><surname>Coovadia</surname><given-names>HM</given-names></name><name><surname>Coward</surname><given-names>P</given-names></name></person-group><article-title>T helper cell defect related to severity in measles</article-title><source>Scand J Infect Dis</source><year>1987</year><volume>19</volume><fpage>185</fpage><lpage>92</lpage></nlm-citation></ref>
<ref id="R40"><label>40.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Cocchi</surname><given-names>F</given-names></name><name><surname>De Vico</surname><given-names>AL</given-names></name><name><surname>Garzino-Demo</surname><given-names>A</given-names></name><name><surname>Arya</surname><given-names>SK</given-names></name><name><surname>Gallo</surname><given-names>RC</given-names></name><name><surname>Lusso</surname><given-names>P</given-names></name></person-group><article-title>Identification of RANTES, MIP-1α, and MIP-α as the major HIV-suppressive factors produced by CD8<sup>+</sup> T cells</article-title><source>Science</source><year>1995</year><volume>270</volume><fpage>1811</fpage><lpage>5</lpage></nlm-citation></ref>
<ref id="R41"><label>41.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Walker</surname><given-names>CM</given-names></name><name><surname>Moody</surname><given-names>DJ</given-names></name><name><surname>Stites</surname><given-names>DP</given-names></name><name><surname>Levy</surname><given-names>JA</given-names></name></person-group><article-title>CD8<sup>+</sup> lymphocytes can control HIV infection in vitro by suppressing virus replication</article-title><source>Science</source><year>1986</year><volume>234</volume><fpage>1563</fpage><lpage>6</lpage></nlm-citation></ref>
<ref id="R42"><label>42.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Levy</surname><given-names>JA</given-names></name><name><surname>Mackewicz</surname><given-names>CE</given-names></name><name><surname>Barker</surname><given-names>E</given-names></name></person-group><article-title>Controlling HIV pathogenesis: the role of the noncytotoxic anti-HIV response of CD8+ T cells</article-title><source>Immunol Today</source><year>1996</year><volume>17</volume><fpage>217</fpage><lpage>24</lpage></nlm-citation></ref>
<ref id="R43"><label>43.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Akridge</surname><given-names>RE</given-names></name><name><surname>Oyafuso</surname><given-names>LKM</given-names></name><name><surname>Reed</surname><given-names>SG</given-names></name></person-group><article-title>IL-10 is induced during HIV-1 infection and is capable of decreasing viral replication in human macrophages</article-title><source>J Immunol</source><year>1994</year><volume>153</volume><fpage>5782</fpage><lpage>9</lpage></nlm-citation></ref>
<ref id="R44"><label>44.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Amiel</surname><given-names>C</given-names></name><name><surname>Darcissac</surname><given-names>E</given-names></name><name><surname>Truong</surname><given-names>ML</given-names></name><etal></etal></person-group><article-title>Interleukin-16 (IL-16) inhibits human immunodeficiency virus replication in cells from infected subjects, and serum IL-16 levels drop with disease progression</article-title><source>J Infect Dis</source><year>1999</year><volume>179</volume><fpage>83</fpage><lpage>91</lpage></nlm-citation></ref>
<ref id="R45"><label>45.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Center</surname><given-names>DM</given-names></name><name><surname>Kornfeld</surname><given-names>H</given-names></name><name><surname>Ryan</surname><given-names>TC</given-names></name><name><surname>Cruikshank</surname><given-names>WW</given-names></name></person-group><article-title>Interleukin 16: implications for CD4 functions and HIV-1 progression</article-title><source>Immunol Today</source><year>2000</year><volume>21</volume><fpage>273</fpage><lpage>80</lpage></nlm-citation></ref>
<ref id="R46"><label>46.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>MacKenzie</surname><given-names>SW</given-names></name><name><surname>Dallalio</surname><given-names>G</given-names></name><name><surname>North</surname><given-names>M</given-names></name><name><surname>Frame</surname><given-names>P</given-names></name><name><surname>Means</surname><given-names>RT</given-names><suffix>Jr</suffix></name></person-group><article-title>Serum chemokine levels in patients with non-progressing HIV infection</article-title><source>AIDS</source><year>1996</year><volume>10</volume><fpage>F29</fpage><lpage>33</lpage></nlm-citation></ref>
<ref id="R47"><label>47.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zanussi</surname><given-names>S</given-names></name><name><surname>D'Andrea</surname><given-names>M</given-names></name><name><surname>Simonelli</surname><given-names>C</given-names></name><name><surname>Tirelli</surname><given-names>U</given-names></name><name><surname>De Paoli</surname><given-names>P</given-names></name></person-group><article-title>Serum levels of RANTES and MIP-1α in HIV-positive long-term survivors and progressor patients</article-title><source>AIDS</source><year>1996</year><volume>10</volume><fpage>1431</fpage><lpage>2</lpage></nlm-citation></ref>
<ref id="R48"><label>48.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Clerici</surname><given-names>M</given-names></name><name><surname>Balotta</surname><given-names>C</given-names></name><name><surname>Trabattoni</surname><given-names>D</given-names></name><etal></etal></person-group><article-title>Chemokine production in HIVseropositive long-term asymptomatic individuals</article-title><source>AIDS</source><year>1996</year><volume>10</volume><fpage>1432</fpage><lpage>3</lpage></nlm-citation></ref>
<ref id="R49"><label>49.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Baler</surname><given-names>M</given-names></name><name><surname>Wenner</surname><given-names>A</given-names></name><name><surname>Bannert</surname><given-names>N</given-names></name><name><surname>Metzner</surname><given-names>K</given-names></name><name><surname>Kurth</surname><given-names>R</given-names></name></person-group><article-title>HIV suppression by interleukin-16</article-title><source>Nature</source><year>1995</year><volume>378</volume><fpage>563</fpage></nlm-citation></ref>
<ref id="R50"><label>50.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Maciaszek</surname><given-names>JW</given-names></name><name><surname>Parada</surname><given-names>NA</given-names></name><name><surname>Cruikshank</surname><given-names>WW</given-names></name><name><surname>Center</surname><given-names>DM</given-names></name><name><surname>Kornfeld</surname><given-names>H</given-names></name><name><surname>Viglianti</surname><given-names>GA</given-names></name></person-group><article-title>IL-16 represses HIV-1 promoter activity</article-title><source>J Immunol</source><year>1997</year><volume>158</volume><fpage>5</fpage><lpage>8</lpage></nlm-citation></ref>
<ref id="R51"><label>51.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zhou</surname><given-names>P</given-names></name><name><surname>Goldstein</surname><given-names>S</given-names></name><name><surname>Devadas</surname><given-names>K</given-names></name><name><surname>Tewari</surname><given-names>D</given-names></name><name><surname>Notkins</surname><given-names>AL</given-names></name></person-group><article-title>Human CD4+ cells transfected with IL-16 cDNA are resistant to HIV-1 infection: inhibition of mRNA expression</article-title><source>Nat Med</source><year>1997</year><volume>3</volume><fpage>659</fpage><lpage>64</lpage></nlm-citation></ref>
<ref id="R52"><label>52.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Scala</surname><given-names>E</given-names></name><name><surname>D'Offizi</surname><given-names>G</given-names></name><name><surname>Rosso</surname><given-names>R</given-names></name><etal></etal></person-group><article-title>C-C chemokines, IL-16, and soluble antiviral factor activity are increased in cloned T cells from subjects with longterm nonprogressive HIV infection</article-title><source>J Immunol</source><year>1997</year><volume>158</volume><fpage>4485</fpage><lpage>92</lpage></nlm-citation></ref>
<ref id="R53"><label>53.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Chen</surname><given-names>ZW</given-names></name><name><surname>Shen</surname><given-names>Y</given-names></name><name><surname>Zhou</surname><given-names>D</given-names></name><etal></etal></person-group><article-title>In vivo T-lymphocyte activation and transient reduction of viral replication in macaques infected with simian immunodeficiency virus</article-title><source>J Virol</source><year>2001</year><volume>75</volume><fpage>4713</fpage><lpage>20</lpage></nlm-citation></ref>
<ref id="R54"><label>54.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Dickover</surname><given-names>RE</given-names></name><name><surname>Dillon</surname><given-names>M</given-names></name><name><surname>Leung</surname><given-names>KM</given-names></name><etal></etal></person-group><article-title>Early prognostic indicators in primary perinatal human immunodeficiency virus type 1 infection: importance of viral RNA and the timing of transmission on long-term outcome</article-title><source>J Infect Dis</source><year>1998</year><volume>178</volume><fpage>375</fpage><lpage>87</lpage></nlm-citation></ref>
<ref id="R55"><label>55.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Abrams</surname><given-names>EJ</given-names></name><name><surname>Weedon</surname><given-names>J</given-names></name><name><surname>Steketee</surname><given-names>RW</given-names></name><etal></etal></person-group><article-title>Association of human immunodeficiency virus (HIV) load early in life with disease progression among HIV-infected infants. New York City Perinatal HIV Transmission Collaborative Study Group</article-title><source>J Infect Dis</source><year>1998</year><volume>178</volume><fpage>101</fpage><lpage>8</lpage></nlm-citation></ref>
<ref id="R56"><label>56.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Shearer</surname><given-names>WT</given-names></name><name><surname>Quinn</surname><given-names>TC</given-names></name><name><surname>LaRussa</surname><given-names>P</given-names></name><etal></etal></person-group><article-title>Viral load and disease progression in infants infected with human immunodeficiency virus type 1</article-title><source>N Engl J Med</source><year>1997</year><volume>336</volume><fpage>1337</fpage><lpage>42</lpage></nlm-citation></ref>
<ref id="R57"><label>57.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Mofenson</surname><given-names>L</given-names></name><name><surname>Korelitz</surname><given-names>J</given-names></name><name><surname>Meyer</surname><given-names>WA</given-names><suffix>III</suffix></name><etal></etal></person-group><article-title>The relationship between serum human immunodeficiency virus type 1 (HIV-1) RNA level, CD4 lymphocyte percent, and long-term mortality risk in HIV-1-infected children. National Institute of Child Health and Human Development Intravenous Immunoglobulin Clinical Trial Study Group</article-title><source>J Infect Dis</source><year>1997</year><volume>175</volume><fpage>1029</fpage><lpage>38</lpage></nlm-citation></ref>
<ref id="R58"><label>58.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Weiss</surname><given-names>M</given-names></name><name><surname>Martignoni</surname><given-names>M</given-names></name><name><surname>Petropoulou</surname><given-names>T</given-names></name><name><surname>Solder</surname><given-names>B</given-names></name><name><surname>Belohradsky</surname><given-names>BH</given-names></name></person-group><article-title>Increased serum levels of soluble tumor necrosis factor receptors (sTNF-Rs) in children and adolescents with vertically and horizontally transmitted HIV infection</article-title><source>Infection</source><year>1996</year><volume>24</volume><fpage>301</fpage><lpage>8</lpage></nlm-citation></ref>
<ref id="R59"><label>59.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Siller</surname><given-names>L</given-names></name><name><surname>Martin</surname><given-names>NL</given-names></name><name><surname>Kostuchenko</surname><given-names>P</given-names></name><etal></etal></person-group><article-title>Serum levels of soluble CD8, neopterin, β<sub>2</sub>-microglobulin and p24 antigen as indicators of disease progression in children with AIDS on zidovudine therapy</article-title><source>AIDS</source><year>1993</year><volume>7</volume><fpage>369</fpage><lpage>73</lpage></nlm-citation></ref>
<ref id="R60"><label>60.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Plaeger</surname><given-names>S</given-names></name><name><surname>Bass</surname><given-names>HZ</given-names></name><name><surname>Nishanian</surname><given-names>P</given-names></name><etal></etal></person-group><article-title>The prognostic significance in HIV infection of immune activation represented by cell surface antigen and plasma activation marker changes</article-title><source>Clin Immunol</source><year>1999</year><volume>90</volume><fpage>238</fpage><lpage>46</lpage></nlm-citation></ref>
<ref id="R61"><label>61.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Salazar-Gonzalez</surname><given-names>IF</given-names></name><name><surname>Martinez-Maza</surname><given-names>O</given-names></name><name><surname>Nishanian</surname><given-names>P</given-names></name><etal></etal></person-group><article-title>Increased immune activation precedes the inflection point of CD4 T cells and the increased serum virus load in human immunodeficiency virus infection</article-title><source>J Infect Dis</source><year>1998</year><volume>178</volume><fpage>423</fpage><lpage>30</lpage></nlm-citation></ref>
<ref id="R62"><label>62.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Fahey</surname><given-names>JL</given-names></name><name><surname>Taylor</surname><given-names>JMG</given-names></name><name><surname>Manna</surname><given-names>B</given-names></name><etal></etal></person-group><article-title>Prognostic significance of plasma markers of immune activation, HIV viral load and CD4 T-cell measurements</article-title><source>AIDS</source><year>1998</year><volume>12</volume><fpage>1581</fpage><lpage>90</lpage></nlm-citation></ref>
<ref id="R63"><label>63.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Stein</surname><given-names>DS</given-names></name><name><surname>Lyles</surname><given-names>RH</given-names></name><name><surname>Graham</surname><given-names>NMH</given-names></name><etal></etal></person-group><article-title>Predicting clinical progression or death in subjects with early-stage human immunodeficiency virus (HIV) infection: a comparative analysis of quantification of HIV RNA, soluble tumor necrosis factor type II receptors, neopterin, and β<sub>2</sub>-microglobulin</article-title><source>J Infect Dis</source><year>1997</year><volume>176</volume><fpage>1161</fpage><lpage>7</lpage></nlm-citation></ref>
<ref id="R64"><label>64.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Fahey</surname><given-names>JL</given-names></name><name><surname>Taylor</surname><given-names>JM</given-names></name><name><surname>Detels</surname><given-names>R</given-names></name><etal></etal></person-group><article-title>The prognostic value of cellular and serologic markers in infection with human immunodeficiency virus type 1</article-title><source>N Engl J Med</source><year>1990</year><volume>322</volume><fpage>166</fpage><lpage>72</lpage></nlm-citation></ref>
<ref id="R65"><label>65.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Griffin</surname><given-names>DE</given-names></name><name><surname>Ward</surname><given-names>BJ</given-names></name><name><surname>Esolen</surname><given-names>LM</given-names></name></person-group><article-title>Pathogenesis of measles virus infection: an hypothesis for altered immune responses</article-title><source>J Infect Dis</source><year>1994</year><volume>170</volume><issue>Suppl 1</issue><fpage>S24</fpage><lpage>31</lpage></nlm-citation></ref>
<ref id="R66"><label>66.</label><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Kvale</surname><given-names>D</given-names></name><name><surname>Aukrust</surname><given-names>P</given-names></name><name><surname>Osnes</surname><given-names>K</given-names></name><name><surname>Muller</surname><given-names>F</given-names></name><name><surname>Froland</surname><given-names>SS</given-names></name></person-group><article-title>CD4 + and CD8 + lymphocytes and HIV RNA in HIV infection: high baseline counts and in particular rapid decrease of CD8 + lymphocytes predict AIDS</article-title><source>AIDS</source><year>1999</year><volume>13</volume><fpage>195</fpage><lpage>201</lpage></nlm-citation></ref>
</ref-list>
<sec sec-type="display-objects">
<title>Figures and Tables</title>
<fig id="F1" position="float">
<label><bold>Figure 1.</bold></label>
<caption>
<p>Plasma human immunodeficiency virus (HIV) RNA levels in children with measles (<italic>first 4 columns</italic>) and control children (<italic>fifth column</italic>). <italic>n</italic>, no. of children studied.
</p>
</caption>
<graphic mimetype="image" xlink:href="185-8-1035-fig001.tif"></graphic>
</fig>
<fig id="F2" position="float">
<label><bold>Table 1.</bold></label>
<caption>
<p>Characteristics of human immunodeficiency virus (HIV)-infected children with measles, HIV-uninfected children with measles, HIV-infected control children, and HIV-uninfected control children at study entry and at 1-month follow-up.
</p>
</caption>
<graphic mimetype="image" xlink:href="185-8-1035-fig002.tif"></graphic>
</fig>
<fig id="F3" position="float">
<label><bold>Table 2.</bold></label>
<caption>
<p>CD4<sup>+</sup> and CD8<sup>+</sup> T lymphocyte subsets in human immunodeficiency virus (HIV)-infected children with measles, HIV-uninfected children with measles, and HIV-uninfected control children at study entry and at 1-month follow-up.
</p>
</caption>
<graphic mimetype="image" xlink:href="185-8-1035-fig003.tif"></graphic>
</fig>
<fig id="F4" position="float">
<label><bold>Table 3.</bold></label>
<caption>
<p>Plasma immune activation markers in human immunodeficiency virus (HIV)-infected children with measles, HIV-uninfected children with measles, and HIV-uninfected control children at study entry and at 1-month follow-up.
</p>
</caption>
<graphic mimetype="image" xlink:href="185-8-1035-fig004.tif"></graphic>
</fig>
<fig id="F5" position="float">
<label><bold>Table 4.</bold></label>
<caption>
<p>Plasma levels of potential human immunodeficiency virus (HIV) suppressive factors in HIV-infected children with measles, HIV-uninfected children with measles, and HIV-uninfected control children at study entry and at 1-month follow-up.
</p>
</caption>
<graphic mimetype="image" xlink:href="185-8-1035-fig005.tif"></graphic>
</fig>
</sec>
</back>
</article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Suppression of Human Immunodeficiency Virus Replication during Acute Measles</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Suppression of Human Immunodeficiency Virus Replication during Acute Measles</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">William J.</namePart><namePart type="family">Moss</namePart><affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</affiliation><affiliation>Department of International Health, Bloomberg School of Public Health, Bethesda, Maryland</affiliation><affiliation>E-mail: wmoss@jhsph.edu</affiliation><affiliation>Reprints or correspondence: Dr. William J. Moss, W. Harry Feinstone Dept. of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, 615 N. Wolfe St., Rm. E5132, Baltimore, MD 21205-2179</affiliation><affiliation>E-mail: wmoss@jhsph.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Judith J.</namePart><namePart type="family">Ryon</namePart><affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mwaka</namePart><namePart type="family">Monze</namePart><affiliation>Virology Laboratory, University Teaching Hospital, Lusaka, Zambia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Felicity</namePart><namePart type="family">Cutts</namePart><affiliation>Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom</affiliation><description>a Present affiliation: Medical Research Council Laboratories, Fajara, Banjul, The Gambia.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas C.</namePart><namePart type="family">Quinn</namePart><affiliation>Division of Infectious Diseases, School of Medicine, Johns Hopkins University, Baltimore, Bethesda, Maryland</affiliation><affiliation>National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Diane E.</namePart><namePart type="family">Griffin</namePart><affiliation>W. Harry Feinstone Department of Molecular Microbiology and Immunology, Bethesda, Maryland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="research-article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>University of Chicago Press</publisher><dateIssued encoding="w3cdtf">2002-04-15</dateIssued><copyrightDate encoding="w3cdtf">2002</copyrightDate></originInfo><abstract>To determine the effect of measles virus coinfection on plasma human immunodeficiency virus (HIV) RNA levels, a prospective study of hospitalized children with measles was conducted between January 1998 and October 2000 in Lusaka, Zambia. Plasma HIV RNA levels were measured during acute measles and 1 month after hospital discharge. The median plasma HIV RNA level in 33 children with measles who were followed longitudinally was 5339 copies/mL at study entry, 60,121 copies/mL at hospital discharge, and 387,148 copies/mL at 1-month follow-up. The median plasma HIV RNA level in children without acute illness was 228,454 copies/mL. Plasma levels of immune activation markers were elevated during the period of reduced plasma HIV RNA. Plasma levels of several potential HIV suppressive factors also were elevated during acute measles. HIV replication is transiently suppressed during acute measles at a time of intense immune activation.</abstract><note type="footnotes">Presented in part: annual meeting of the Infectious Diseases Society of America, Philadelphia, 18–21 November 1999 (abstract 698).</note><relatedItem type="host"><titleInfo><title>The Journal of Infectious Diseases</title></titleInfo><titleInfo type="abbreviated"><title>The Journal of Infectious Diseases</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">0022-1899</identifier><identifier type="eISSN">1537-6613</identifier><identifier type="PublisherID">jid</identifier><identifier type="PublisherID-hwp">jinfdis</identifier><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>185</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>1035</start><end>1042</end></extent></part></relatedItem><identifier type="istex">AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797</identifier><identifier type="DOI">10.1086/340027</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2002 by the Infectious Diseases Society of America</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-GTWS0RDP-M">oup</recordContentSource><recordOrigin>© 2002 by the Infectious Diseases Society of America</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797/metadata/json</uri></json:item></metadata><covers><json:item><extension>tiff</extension><original>true</original><mimetype>image/tiff</mimetype><uri>https://api.istex.fr/document/AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797/covers/tiff</uri></json:item></covers><annexes><json:item><extension>jpeg</extension><original>true</original><mimetype>image/jpeg</mimetype><uri>https://api.istex.fr/document/AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797/annexes/jpeg</uri></json:item><json:item><extension>gif</extension><original>true</original><mimetype>image/gif</mimetype><uri>https://api.istex.fr/document/AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797/annexes/gif</uri></json:item><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797/annexes/pdf</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/SidaSubSaharaV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003805 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 003805 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= SidaSubSaharaV1
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:AAD9AB3DCF6ECF8EA0A29E62DEC74E7FDE363797
|texte= Suppression of Human Immunodeficiency Virus Replication during Acute Measles
}}
| This area was generated with Dilib version V0.6.32. |  |