Rapid and slow progressors differ by a single MHC class I haplotype in a family of MHC-defined rhesus macaques infected with SIV
Identifieur interne : 001774 ( Istex/Corpus ); précédent : 001773; suivant : 001775Rapid and slow progressors differ by a single MHC class I haplotype in a family of MHC-defined rhesus macaques infected with SIV
Auteurs : David T. Evans ; Leslie A. Knapp ; Peicheng Jing ; Jacque L. Mitchen ; Marta Dykhuizen ; David C. Montefiori ; C. David Pauza ; David I. WatkinsSource :
- Immunology Letters [ 0165-2478 ] ; 1999.
English descriptors
- KwdEn :
- Teeft :
- Aids virus, Allele, Allelic differences, Amino acid sequences, Antibody responses, Assay, Cdna, Cdna bands, Cell line, Ctls, Denaturing gradient, Disease progression, Elsevier science, Epitope, Fresh medium, Generic primers, Haplotype, Heparinized tubes, Heterogeneous virus stock, High neutralizing antibody titers, Immune responses, Immunology, Immunology letters, Important role, Infectious centers assay, Kaslow, Locus, Macaque, Neutralizing, Neutralizing antibody responses, Peptide, Plasma dilution, Plasma virus titers, Pmol primers, Polymorphic, Polymorphic region, Primary viremia, Primer, Progression, Progressors, Rapid progressors, Rhesus, Rhesus macaques, Room temperature, Second round, Sibling, Sibling macaques, Slow progressors, Stable transfectants, Urea gradient, Urea gradients, Variable rates, Viral loads, Viremia, Virus replication.
Abstract
Abstract: Highly polymorphic HLA class I molecules may influence rates of disease progression of HIV-infected individuals. Recent evidence suggests that individuals who mount vigorous CTL responses to multiple HIV-1 epitopes have reduced viral loads, and survive longer than individuals that make a less robust or less diverse CTL response. It has been difficult, however, to define associations between particular HLA class I alleles and rates of disease progression. This may be due, in part, to the uncontrolled variables associated with naturally acquired HIV infections. Studies using MHC-defined, non-human primates infected with well characterized viral stocks should help to clarify this relationship. To explore the possibility that MHC class I polymorphism can influence disease progression, we infected four Mamu-DRB-identical individuals from a family of MHC-defined rhesus macaques intravenously with 40 TCID50SIVmac239. Two of these macaques developed severe wasting and were euthanized within 80 days of infection, while the other two survived for more than 400 days without showing any symptoms of disease. Since all four of these macaques were Mamu-DRB-identical, we were able to exclude the MHC class II DRB loci as determinant of disease progression. Interestingly, both of the slow progressors made CTL responses to the same three SIV CTL epitopes, which were restricted by two molecules (Mamu-B*03 and B*04) encoded by their common maternal haplotype. The two rapid progressors did not share this haplotype with the slow progressors, and we were unable to detect CTL responses in these two siblings. These observations implicate products of the Mamu-B*03 and B*04 alleles in resistance to disease progression in this family of SIV-infected macaques, and provide additional evidence that certain MHC class I-restricted CTL responses may play a significant role in delaying the onset of AIDS.
Url:
DOI: 10.1016/S0165-2478(98)00151-5
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Rapid and slow progressors differ by a single MHC class I haplotype in a family of MHC-defined rhesus macaques infected with SIV</title><author><name sortKey="Evans, David T" sort="Evans, David T" uniqKey="Evans D" first="David T." last="Evans">David T. Evans</name><affiliation><mods:affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</mods:affiliation></affiliation></author><author><name sortKey="Knapp, Leslie A" sort="Knapp, Leslie A" uniqKey="Knapp L" first="Leslie A." last="Knapp">Leslie A. Knapp</name><affiliation><mods:affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</mods:affiliation></affiliation></author><author><name sortKey="Jing, Peicheng" sort="Jing, Peicheng" uniqKey="Jing P" first="Peicheng" last="Jing">Peicheng Jing</name><affiliation><mods:affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</mods:affiliation></affiliation></author><author><name sortKey="Mitchen, Jacque L" sort="Mitchen, Jacque L" uniqKey="Mitchen J" first="Jacque L." last="Mitchen">Jacque L. Mitchen</name><affiliation><mods:affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</mods:affiliation></affiliation></author><author><name sortKey="Dykhuizen, Marta" sort="Dykhuizen, Marta" uniqKey="Dykhuizen M" first="Marta" last="Dykhuizen">Marta Dykhuizen</name><affiliation><mods:affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</mods:affiliation></affiliation></author><author><name sortKey="Montefiori, David C" sort="Montefiori, David C" uniqKey="Montefiori D" first="David C." last="Montefiori">David C. Montefiori</name><affiliation><mods:affiliation>Department of Surgery, Duke University Medical Center, Center for AIDS Research, Durham NC 27710, USA</mods:affiliation></affiliation></author><author><name sortKey="Pauza, C David" sort="Pauza, C David" uniqKey="Pauza C" first="C. David" last="Pauza">C. 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Evans</name><affiliation><mods:affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</mods:affiliation></affiliation></author><author><name sortKey="Knapp, Leslie A" sort="Knapp, Leslie A" uniqKey="Knapp L" first="Leslie A." last="Knapp">Leslie A. Knapp</name><affiliation><mods:affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</mods:affiliation></affiliation></author><author><name sortKey="Jing, Peicheng" sort="Jing, Peicheng" uniqKey="Jing P" first="Peicheng" last="Jing">Peicheng Jing</name><affiliation><mods:affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</mods:affiliation></affiliation></author><author><name sortKey="Mitchen, Jacque L" sort="Mitchen, Jacque L" uniqKey="Mitchen J" first="Jacque L." last="Mitchen">Jacque L. Mitchen</name><affiliation><mods:affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</mods:affiliation></affiliation></author><author><name sortKey="Dykhuizen, Marta" sort="Dykhuizen, Marta" uniqKey="Dykhuizen M" first="Marta" last="Dykhuizen">Marta Dykhuizen</name><affiliation><mods:affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</mods:affiliation></affiliation></author><author><name sortKey="Montefiori, David C" sort="Montefiori, David C" uniqKey="Montefiori D" first="David C." last="Montefiori">David C. Montefiori</name><affiliation><mods:affiliation>Department of Surgery, Duke University Medical Center, Center for AIDS Research, Durham NC 27710, USA</mods:affiliation></affiliation></author><author><name sortKey="Pauza, C David" sort="Pauza, C David" uniqKey="Pauza C" first="C. David" last="Pauza">C. David Pauza</name><affiliation><mods:affiliation>Department of Pathology and Laboratory, Medicine University of Wisconsin, Madison, WI 53715, USA</mods:affiliation></affiliation></author><author><name sortKey="Watkins, David I" sort="Watkins, David I" uniqKey="Watkins D" first="David I." last="Watkins">David I. Watkins</name><affiliation><mods:affiliation>E-mail: watkins@primate.wisc.edu</mods:affiliation></affiliation><affiliation><mods:affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Immunology Letters</title><title level="j" type="abbrev">IMLET</title><idno type="ISSN">0165-2478</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1999">1999</date><biblScope unit="volume">66</biblScope><biblScope unit="issue">1–3</biblScope><biblScope unit="page" from="53">53</biblScope><biblScope unit="page" to="59">59</biblScope></imprint><idno type="ISSN">0165-2478</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0165-2478</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>CTL</term><term>MHC</term><term>Non-human primate</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Aids virus</term><term>Allele</term><term>Allelic differences</term><term>Amino acid sequences</term><term>Antibody responses</term><term>Assay</term><term>Cdna</term><term>Cdna bands</term><term>Cell line</term><term>Ctls</term><term>Denaturing gradient</term><term>Disease progression</term><term>Elsevier science</term><term>Epitope</term><term>Fresh medium</term><term>Generic primers</term><term>Haplotype</term><term>Heparinized tubes</term><term>Heterogeneous virus stock</term><term>High neutralizing antibody titers</term><term>Immune responses</term><term>Immunology</term><term>Immunology letters</term><term>Important role</term><term>Infectious centers assay</term><term>Kaslow</term><term>Locus</term><term>Macaque</term><term>Neutralizing</term><term>Neutralizing antibody responses</term><term>Peptide</term><term>Plasma dilution</term><term>Plasma virus titers</term><term>Pmol primers</term><term>Polymorphic</term><term>Polymorphic region</term><term>Primary viremia</term><term>Primer</term><term>Progression</term><term>Progressors</term><term>Rapid progressors</term><term>Rhesus</term><term>Rhesus macaques</term><term>Room temperature</term><term>Second round</term><term>Sibling</term><term>Sibling macaques</term><term>Slow progressors</term><term>Stable transfectants</term><term>Urea gradient</term><term>Urea gradients</term><term>Variable rates</term><term>Viral loads</term><term>Viremia</term><term>Virus replication</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Highly polymorphic HLA class I molecules may influence rates of disease progression of HIV-infected individuals. Recent evidence suggests that individuals who mount vigorous CTL responses to multiple HIV-1 epitopes have reduced viral loads, and survive longer than individuals that make a less robust or less diverse CTL response. It has been difficult, however, to define associations between particular HLA class I alleles and rates of disease progression. This may be due, in part, to the uncontrolled variables associated with naturally acquired HIV infections. Studies using MHC-defined, non-human primates infected with well characterized viral stocks should help to clarify this relationship. To explore the possibility that MHC class I polymorphism can influence disease progression, we infected four Mamu-DRB-identical individuals from a family of MHC-defined rhesus macaques intravenously with 40 TCID50SIVmac239. Two of these macaques developed severe wasting and were euthanized within 80 days of infection, while the other two survived for more than 400 days without showing any symptoms of disease. Since all four of these macaques were Mamu-DRB-identical, we were able to exclude the MHC class II DRB loci as determinant of disease progression. Interestingly, both of the slow progressors made CTL responses to the same three SIV CTL epitopes, which were restricted by two molecules (Mamu-B*03 and B*04) encoded by their common maternal haplotype. The two rapid progressors did not share this haplotype with the slow progressors, and we were unable to detect CTL responses in these two siblings. These observations implicate products of the Mamu-B*03 and B*04 alleles in resistance to disease progression in this family of SIV-infected macaques, and provide additional evidence that certain MHC class I-restricted CTL responses may play a significant role in delaying the onset of AIDS.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>macaque</json:string><json:string>disease progression</json:string><json:string>haplotype</json:string><json:string>epitope</json:string><json:string>rhesus</json:string><json:string>allele</json:string><json:string>progressors</json:string><json:string>rhesus macaques</json:string><json:string>cdna</json:string><json:string>primer</json:string><json:string>neutralizing</json:string><json:string>immunology</json:string><json:string>ctls</json:string><json:string>slow progressors</json:string><json:string>immunology letters</json:string><json:string>polymorphic</json:string><json:string>viremia</json:string><json:string>kaslow</json:string><json:string>primary viremia</json:string><json:string>progression</json:string><json:string>rapid progressors</json:string><json:string>sibling</json:string><json:string>denaturing gradient</json:string><json:string>peptide</json:string><json:string>locus</json:string><json:string>assay</json:string><json:string>heparinized tubes</json:string><json:string>virus replication</json:string><json:string>immune responses</json:string><json:string>cell line</json:string><json:string>polymorphic region</json:string><json:string>viral loads</json:string><json:string>plasma virus titers</json:string><json:string>plasma dilution</json:string><json:string>elsevier science</json:string><json:string>stable transfectants</json:string><json:string>important role</json:string><json:string>room temperature</json:string><json:string>fresh medium</json:string><json:string>heterogeneous virus stock</json:string><json:string>neutralizing antibody responses</json:string><json:string>pmol primers</json:string><json:string>infectious centers assay</json:string><json:string>urea gradient</json:string><json:string>amino acid sequences</json:string><json:string>aids virus</json:string><json:string>sibling macaques</json:string><json:string>second round</json:string><json:string>generic primers</json:string><json:string>urea gradients</json:string><json:string>cdna bands</json:string><json:string>antibody responses</json:string><json:string>high neutralizing antibody titers</json:string><json:string>allelic differences</json:string><json:string>variable rates</json:string></teeft></keywords><author><json:item><name>David T. Evans</name><affiliations><json:string>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</json:string></affiliations></json:item><json:item><name>Leslie A. Knapp</name><affiliations><json:string>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</json:string></affiliations></json:item><json:item><name>Peicheng Jing</name><affiliations><json:string>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</json:string></affiliations></json:item><json:item><name>Jacque L. Mitchen</name><affiliations><json:string>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</json:string></affiliations></json:item><json:item><name>Marta Dykhuizen</name><affiliations><json:string>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</json:string></affiliations></json:item><json:item><name>David C. Montefiori</name><affiliations><json:string>Department of Surgery, Duke University Medical Center, Center for AIDS Research, Durham NC 27710, USA</json:string></affiliations></json:item><json:item><name>C.David Pauza</name><affiliations><json:string>Department of Pathology and Laboratory, Medicine University of Wisconsin, Madison, WI 53715, USA</json:string></affiliations></json:item><json:item><name>David I. Watkins</name><affiliations><json:string>E-mail: watkins@primate.wisc.edu</json:string><json:string>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Non-human primate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CTL</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MHC</value></json:item></subject><arkIstex>ark:/67375/6H6-04ZXQL8Q-V</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Highly polymorphic HLA class I molecules may influence rates of disease progression of HIV-infected individuals. Recent evidence suggests that individuals who mount vigorous CTL responses to multiple HIV-1 epitopes have reduced viral loads, and survive longer than individuals that make a less robust or less diverse CTL response. It has been difficult, however, to define associations between particular HLA class I alleles and rates of disease progression. This may be due, in part, to the uncontrolled variables associated with naturally acquired HIV infections. Studies using MHC-defined, non-human primates infected with well characterized viral stocks should help to clarify this relationship. To explore the possibility that MHC class I polymorphism can influence disease progression, we infected four Mamu-DRB-identical individuals from a family of MHC-defined rhesus macaques intravenously with 40 TCID50SIVmac239. Two of these macaques developed severe wasting and were euthanized within 80 days of infection, while the other two survived for more than 400 days without showing any symptoms of disease. Since all four of these macaques were Mamu-DRB-identical, we were able to exclude the MHC class II DRB loci as determinant of disease progression. Interestingly, both of the slow progressors made CTL responses to the same three SIV CTL epitopes, which were restricted by two molecules (Mamu-B*03 and B*04) encoded by their common maternal haplotype. The two rapid progressors did not share this haplotype with the slow progressors, and we were unable to detect CTL responses in these two siblings. These observations implicate products of the Mamu-B*03 and B*04 alleles in resistance to disease progression in this family of SIV-infected macaques, and provide additional evidence that certain MHC class I-restricted CTL responses may play a significant role in delaying the onset of AIDS.</abstract><qualityIndicators><score>9.584</score><pdfWordCount>4584</pdfWordCount><pdfCharCount>27296</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>7</pdfPageCount><pdfPageSize>552 x 770 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>284</abstractWordCount><abstractCharCount>1911</abstractCharCount><keywordCount>3</keywordCount></qualityIndicators><title>Rapid and slow progressors differ by a single MHC class I haplotype in a family of MHC-defined rhesus macaques infected with SIV</title><pmid><json:string>10203034</json:string></pmid><pii><json:string>S0165-2478(98)00151-5</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>Immunology Letters</title><language><json:string>unknown</json:string></language><publicationDate>1999</publicationDate><issn><json:string>0165-2478</json:string></issn><pii><json:string>S0165-2478(00)X0045-4</json:string></pii><volume>66</volume><issue>1–3</issue><pages><first>53</first><last>59</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1999</json:string></date><geogName></geogName><orgName><json:string>Department of Surgery, Duke Uni</json:string><json:string>Medical Center, Center</json:string><json:string>Therion Biologics Corporation, Cambridge</json:string><json:string>Department of Biological Anthropology, Uni</json:string><json:string>Department of Pathology and Laboratory</json:string><json:string>AIDS Research, Durham NC</json:string><json:string>National Institutes of Health CAI</json:string></orgName><orgName_funder><json:string>National Institutes of Health CAI</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>C. David</json:string><json:string>To</json:string></persName><placeName><json:string>Foster City</json:string><json:string>Madison</json:string><json:string>CA</json:string><json:string>WI</json:string><json:string>Cambridge</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>[7,8]</json:string><json:string>[23]</json:string><json:string>[21,25]</json:string><json:string>[6]</json:string><json:string>[22]</json:string><json:string>[17]</json:string><json:string>[14,15]</json:string><json:string>[1]</json:string><json:string>[21]</json:string><json:string>[27]</json:string><json:string>[9,10]</json:string><json:string>[20]</json:string><json:string>[18,19]</json:string><json:string>[26]</json:string><json:string>[34,35]</json:string><json:string>[1,2,33]</json:string><json:string>[28,29]</json:string><json:string>[11,12]</json:string><json:string>[24]</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-04ZXQL8Q-V</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - immunology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - immunology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Immunology</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Immunology and Allergy</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>1999</publicationDate><copyrightDate>1999</copyrightDate><doi><json:string>10.1016/S0165-2478(98)00151-5</json:string></doi><id>DDFDA6C515F749DAEB99FD2069311FAA1C11EDDB</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-04ZXQL8Q-V/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-04ZXQL8Q-V/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-04ZXQL8Q-V/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Rapid and slow progressors differ by a single MHC class I haplotype in a family of MHC-defined rhesus macaques infected with SIV</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>©1999 Elsevier Science B.V.</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</p></availability><date>1999</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 type="content">Fig. 1: The inheritance of alleles at the MHC class I and class II DRB loci in a family of six rhesus macaques. A, The relationships of each of the family members are illustrated in the pedigree. The MHC class I (B) and II DRB (C) loci were analyzed by denaturing gradient gel electrophoresis (DGGE; manuscript in preparation). The identified haplotypes are represented symbolically, a–d, below each family member in the pedigree. The ‘c’ haplotype shown in bold consists of the MHC class I alleles Mamu-A*03, B*03 and B404. B, MHC class I cDNAs were amplified by RT-PCR from PBLs using Mamu-A and B locus-specific primers [24]. A second round of PCR using generic GC-clamped primers was used to amplify a polymorphic region spanning exons 2–3. These products were then separated using 50–65% formamide and urea gradients on 8% polyacrylamide gels. C, The polymorphic second exon of alleles at the Mamu-DRB locus was amplified from genomic DNA using GC-clamped primers. These PCR products were then separated on a 40–65% formamide and urea gradient gel [21]. B and C, DGGE-separated cDNA bands were identified by directly sequencing PCR products reamplified from gel plugs.</note><note type="content">Table 1: Summary of immune responses and disease progression in four MHC-defined, SIV-infected sibling macaques</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Rapid and slow progressors differ by a single MHC class I haplotype in a family of MHC-defined rhesus macaques infected with SIV</title><author xml:id="author-0000"><persName><forename type="first">David T.</forename><surname>Evans</surname></persName><affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Leslie A.</forename><surname>Knapp</surname></persName><affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Peicheng</forename><surname>Jing</surname></persName><affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Jacque L.</forename><surname>Mitchen</surname></persName><affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Marta</forename><surname>Dykhuizen</surname></persName><affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</affiliation></author><author xml:id="author-0005"><persName><forename type="first">David C.</forename><surname>Montefiori</surname></persName><affiliation>Department of Surgery, Duke University Medical Center, Center for AIDS Research, Durham NC 27710, USA</affiliation></author><author xml:id="author-0006"><persName><forename type="first">C.David</forename><surname>Pauza</surname></persName><affiliation>Department of Pathology and Laboratory, Medicine University of Wisconsin, Madison, WI 53715, USA</affiliation></author><author xml:id="author-0007"><persName><forename type="first">David I.</forename><surname>Watkins</surname></persName><email>watkins@primate.wisc.edu</email><note type="correspondence"><p>Corresponding author. Tel.: +1-608-265-3380; fax: +1-608-263-4031</p></note><affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</affiliation></author><idno type="istex">DDFDA6C515F749DAEB99FD2069311FAA1C11EDDB</idno><idno type="ark">ark:/67375/6H6-04ZXQL8Q-V</idno><idno type="DOI">10.1016/S0165-2478(98)00151-5</idno><idno type="PII">S0165-2478(98)00151-5</idno></analytic><monogr><title level="j">Immunology Letters</title><title level="j" type="abbrev">IMLET</title><idno type="pISSN">0165-2478</idno><idno type="PII">S0165-2478(00)X0045-4</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1999"></date><biblScope unit="volume">66</biblScope><biblScope unit="issue">1–3</biblScope><biblScope unit="page" from="53">53</biblScope><biblScope unit="page" to="59">59</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1999</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Highly polymorphic HLA class I molecules may influence rates of disease progression of HIV-infected individuals. Recent evidence suggests that individuals who mount vigorous CTL responses to multiple HIV-1 epitopes have reduced viral loads, and survive longer than individuals that make a less robust or less diverse CTL response. It has been difficult, however, to define associations between particular HLA class I alleles and rates of disease progression. This may be due, in part, to the uncontrolled variables associated with naturally acquired HIV infections. Studies using MHC-defined, non-human primates infected with well characterized viral stocks should help to clarify this relationship. To explore the possibility that MHC class I polymorphism can influence disease progression, we infected four Mamu-DRB-identical individuals from a family of MHC-defined rhesus macaques intravenously with 40 TCID50SIVmac239. Two of these macaques developed severe wasting and were euthanized within 80 days of infection, while the other two survived for more than 400 days without showing any symptoms of disease. Since all four of these macaques were Mamu-DRB-identical, we were able to exclude the MHC class II DRB loci as determinant of disease progression. Interestingly, both of the slow progressors made CTL responses to the same three SIV CTL epitopes, which were restricted by two molecules (Mamu-B*03 and B*04) encoded by their common maternal haplotype. The two rapid progressors did not share this haplotype with the slow progressors, and we were unable to detect CTL responses in these two siblings. These observations implicate products of the Mamu-B*03 and B*04 alleles in resistance to disease progression in this family of SIV-infected macaques, and provide additional evidence that certain MHC class I-restricted CTL responses may play a significant role in delaying the onset of AIDS.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Non-human primate</term></item><item><term>CTL</term></item><item><term>MHC</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1999">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-04ZXQL8Q-V/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>IMLET</jid><aid>3003</aid><ce:pii>S0165-2478(98)00151-5</ce:pii><ce:doi>10.1016/S0165-2478(98)00151-5</ce:doi><ce:copyright type="full-transfer" year="1999">Elsevier Science B.V.</ce:copyright></item-info><head><ce:title>Rapid and slow progressors differ by a single MHC class I haplotype in a family of MHC-defined rhesus macaques infected with SIV</ce:title><ce:author-group><ce:author><ce:given-name>David T.</ce:given-name><ce:surname>Evans</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Leslie A.</ce:given-name><ce:surname>Knapp</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Peicheng</ce:given-name><ce:surname>Jing</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Jacque L.</ce:given-name><ce:surname>Mitchen</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Marta</ce:given-name><ce:surname>Dykhuizen</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>David C.</ce:given-name><ce:surname>Montefiori</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>c</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>C.David</ce:given-name><ce:surname>Pauza</ce:surname><ce:cross-ref refid="AFF4"><ce:sup>d</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>David I.</ce:given-name><ce:surname>Watkins</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF4"><ce:sup>d</ce:sup></ce:cross-ref><ce:cross-ref refid="CORR1">*</ce:cross-ref><ce:e-address>watkins@primate.wisc.edu</ce:e-address></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Present address: Department of Biological Anthropology, University of Cambridge Downing Street, Cambridge CB2 3DZ, UK</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Department of Surgery, Duke University Medical Center, Center for AIDS Research, Durham NC 27710, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF4"><ce:label>d</ce:label><ce:textfn>Department of Pathology and Laboratory, Medicine University of Wisconsin, Madison, WI 53715, USA</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Tel.: +1-608-265-3380; fax: +1-608-263-4031</ce:text></ce:correspondence></ce:author-group><ce:date-received day="19" month="10" year="1998"></ce:date-received><ce:date-accepted day="18" month="11" year="1998"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Highly polymorphic HLA class I molecules may influence rates of disease progression of HIV-infected individuals. Recent evidence suggests that individuals who mount vigorous CTL responses to multiple HIV-1 epitopes have reduced viral loads, and survive longer than individuals that make a less robust or less diverse CTL response. It has been difficult, however, to define associations between particular <ce:italic>HLA</ce:italic> class I alleles and rates of disease progression. This may be due, in part, to the uncontrolled variables associated with naturally acquired HIV infections. Studies using MHC-defined, non-human primates infected with well characterized viral stocks should help to clarify this relationship. To explore the possibility that MHC class I polymorphism can influence disease progression, we infected four Mamu-DRB-identical individuals from a family of MHC-defined rhesus macaques intravenously with 40 TCID<ce:inf>50</ce:inf>SIV<ce:inf>mac</ce:inf>239. Two of these macaques developed severe wasting and were euthanized within 80 days of infection, while the other two survived for more than 400 days without showing any symptoms of disease. Since all four of these macaques were Mamu-DRB-identical, we were able to exclude the MHC class II DRB loci as determinant of disease progression. Interestingly, both of the slow progressors made CTL responses to the same three SIV CTL epitopes, which were restricted by two molecules (Mamu-B*03 and B*04) encoded by their common maternal haplotype. The two rapid progressors did not share this haplotype with the slow progressors, and we were unable to detect CTL responses in these two siblings. These observations implicate products of the Mamu-B*03 and B*04 alleles in resistance to disease progression in this family of SIV-infected macaques, and provide additional evidence that certain MHC class I-restricted CTL responses may play a significant role in delaying the onset of AIDS.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Non-human primate</ce:text></ce:keyword><ce:keyword><ce:text>CTL</ce:text></ce:keyword><ce:keyword><ce:text>MHC</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Rapid and slow progressors differ by a single MHC class I haplotype in a family of MHC-defined rhesus macaques infected with SIV</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Rapid and slow progressors differ by a single MHC class I haplotype in a family of MHC-defined rhesus macaques infected with SIV</title></titleInfo><name type="personal"><namePart type="given">David T.</namePart><namePart type="family">Evans</namePart><affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Leslie A.</namePart><namePart type="family">Knapp</namePart><affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peicheng</namePart><namePart type="family">Jing</namePart><affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jacque L.</namePart><namePart type="family">Mitchen</namePart><affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marta</namePart><namePart type="family">Dykhuizen</namePart><affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David C.</namePart><namePart type="family">Montefiori</namePart><affiliation>Department of Surgery, Duke University Medical Center, Center for AIDS Research, Durham NC 27710, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.David</namePart><namePart type="family">Pauza</namePart><affiliation>Department of Pathology and Laboratory, Medicine University of Wisconsin, Madison, WI 53715, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David I.</namePart><namePart type="family">Watkins</namePart><affiliation>E-mail: watkins@primate.wisc.edu</affiliation><affiliation>Wisconsin Regional Primate Research Center, University of Wisconsin, 1220 Capitol Ct., Madison, WI 53715, USA</affiliation><description>Corresponding author. Tel.: +1-608-265-3380; fax: +1-608-263-4031</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length 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>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1999</dateIssued><copyrightDate encoding="w3cdtf">1999</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Highly polymorphic HLA class I molecules may influence rates of disease progression of HIV-infected individuals. Recent evidence suggests that individuals who mount vigorous CTL responses to multiple HIV-1 epitopes have reduced viral loads, and survive longer than individuals that make a less robust or less diverse CTL response. It has been difficult, however, to define associations between particular HLA class I alleles and rates of disease progression. This may be due, in part, to the uncontrolled variables associated with naturally acquired HIV infections. Studies using MHC-defined, non-human primates infected with well characterized viral stocks should help to clarify this relationship. To explore the possibility that MHC class I polymorphism can influence disease progression, we infected four Mamu-DRB-identical individuals from a family of MHC-defined rhesus macaques intravenously with 40 TCID50SIVmac239. Two of these macaques developed severe wasting and were euthanized within 80 days of infection, while the other two survived for more than 400 days without showing any symptoms of disease. Since all four of these macaques were Mamu-DRB-identical, we were able to exclude the MHC class II DRB loci as determinant of disease progression. Interestingly, both of the slow progressors made CTL responses to the same three SIV CTL epitopes, which were restricted by two molecules (Mamu-B*03 and B*04) encoded by their common maternal haplotype. The two rapid progressors did not share this haplotype with the slow progressors, and we were unable to detect CTL responses in these two siblings. These observations implicate products of the Mamu-B*03 and B*04 alleles in resistance to disease progression in this family of SIV-infected macaques, and provide additional evidence that certain MHC class I-restricted CTL responses may play a significant role in delaying the onset of AIDS.</abstract><note type="content">Fig. 1: The inheritance of alleles at the MHC class I and class II DRB loci in a family of six rhesus macaques. A, The relationships of each of the family members are illustrated in the pedigree. The MHC class I (B) and II DRB (C) loci were analyzed by denaturing gradient gel electrophoresis (DGGE; manuscript in preparation). The identified haplotypes are represented symbolically, a–d, below each family member in the pedigree. The ‘c’ haplotype shown in bold consists of the MHC class I alleles Mamu-A*03, B*03 and B404. B, MHC class I cDNAs were amplified by RT-PCR from PBLs using Mamu-A and B locus-specific primers [24]. A second round of PCR using generic GC-clamped primers was used to amplify a polymorphic region spanning exons 2–3. These products were then separated using 50–65% formamide and urea gradients on 8% polyacrylamide gels. C, The polymorphic second exon of alleles at the Mamu-DRB locus was amplified from genomic DNA using GC-clamped primers. These PCR products were then separated on a 40–65% formamide and urea gradient gel [21]. B and C, DGGE-separated cDNA bands were identified by directly sequencing PCR products reamplified from gel plugs.</note><note type="content">Table 1: Summary of immune responses and disease progression in four MHC-defined, SIV-infected sibling macaques</note><subject lang="en"><genre>Keywords</genre><topic>Non-human primate</topic><topic>CTL</topic><topic>MHC</topic></subject><relatedItem type="host"><titleInfo><title>Immunology Letters</title></titleInfo><titleInfo type="abbreviated"><title>IMLET</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><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1999</dateIssued></originInfo><identifier type="ISSN">0165-2478</identifier><identifier type="PII">S0165-2478(00)X0045-4</identifier><part><date>1999</date><detail type="volume"><number>66</number><caption>vol.</caption></detail><detail type="issue"><number>1–3</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>236</end></extent><extent unit="pages"><start>53</start><end>59</end></extent></part></relatedItem><identifier type="istex">DDFDA6C515F749DAEB99FD2069311FAA1C11EDDB</identifier><identifier type="ark">ark:/67375/6H6-04ZXQL8Q-V</identifier><identifier type="DOI">10.1016/S0165-2478(98)00151-5</identifier><identifier type="PII">S0165-2478(98)00151-5</identifier><accessCondition type="use and reproduction" contentType="copyright">©1999 Elsevier Science B.V.</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource><recordOrigin>Elsevier Science B.V., ©1999</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-04ZXQL8Q-V/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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