IgG subclass response to human parvovirus B19 infection
Identifieur interne : 001614 ( Istex/Corpus ); précédent : 001613; suivant : 001615IgG subclass response to human parvovirus B19 infection
Auteurs : Rauli Franssila ; Maria Söderlund ; Caroline S. Brown ; Willy J. M Spaan ; Ilkka Sepp L ; Klaus HedmanSource :
- Clinical and Diagnostic Virology [ 0928-0197 ] ; 1996.
English descriptors
- Teeft :
- Acute infection, Acute phase, Background levels, Capsid, Capsid antigen, Capsid proteins, Cell clones, Chronic infection, Convalescence, Diagnostic test, Diagnostic virology, Diphteria toxin, Early convalescence, Epitope, Erythema infectiosum, Flvp1, Flvp1 antigen, Franssila, Haartman institute, Haemophilus influenzae type, High levels, Human parvovirus, Human parvovirus infection, Hydrops fetalis, Igg1, Igg3, Igg4, Igg4 responses, Immunol, Infection, Kurtzman, Late convalescence, Linear epitopes, Monoclonal antibodies, Optimum volume, Other hand, Parvovirus, Past immunity, Primary structure, Recent infection, S6derlund, Serum pool, Serum pools, Subclass, Subclass response, Subclasses igg1, Subclasses igg3, Time point, Time points, Total igg4, Unique portion, Virology, Years days.
Abstract
Abstract: Background: IgG antibodies are essential to immunity against human parvovirus B19 and can neutralize infection both in bone marrow cell cultures infected in vitro and in chronically infected immunosuppressed individuals. Objectives: To assess the levels and response kinetics of IgG subclasses towards individual structural proteins of human parvovirus B19. Study design: Subclasses of IgG for capsid proteins VP1 or VP2 were quantified by EIA using monoclonal antibodies in 30 acutely infected and 30 convalescent patients, as well as in 32 remotely infected and 20 non-infected controls. Results: In all groups of seropositive individuals the predominant subclass for either structural protein was IgG1. Subclass IgG3 was associated with acute infection. By contrast, IgG4 appeared months after infection, and occurred specifically towards VP1. The ratio of VP1-specific subclasses IgG3 and IgG4 provided a diagnostic test for recent infection with a specificity of 98% and a sensitivity of 97%. Conclusions: Comparative measurement of VP1-specific IgG3 and IgG4 is useful in diagnosis. The IgG4 results point to long-term expression of immunologically active VP1 and to T-cell help of Th2 type for B-cells recognizing VP1.
Url:
DOI: 10.1016/0928-0197(96)00156-0
Links to Exploration step
ISTEX:A2A05B052207B90FB3BC3847436BAB6B9C1BEB0FLe document en format XML
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Brown</name><affiliation><mods:affiliation>Department of Virology, University Hospital of Leiden, Leiden, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Spaan, Willy J M" sort="Spaan, Willy J M" uniqKey="Spaan W" first="Willy J. M" last="Spaan">Willy J. M Spaan</name><affiliation><mods:affiliation>Department of Virology, University Hospital of Leiden, Leiden, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Sepp L, Ilkka" sort="Sepp L, Ilkka" uniqKey="Sepp L I" first="Ilkka" last="Sepp L">Ilkka Sepp L</name><affiliation><mods:affiliation>Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author><author><name sortKey="Hedman, Klaus" sort="Hedman, Klaus" uniqKey="Hedman K" first="Klaus" last="Hedman">Klaus Hedman</name><affiliation><mods:affiliation>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A2A05B052207B90FB3BC3847436BAB6B9C1BEB0F</idno><date when="1996" year="1996">1996</date><idno type="doi">10.1016/0928-0197(96)00156-0</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-B9VMBL4H-W/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001614</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001614</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">IgG subclass response to human parvovirus B19 infection</title><author><name sortKey="Franssila, Rauli" sort="Franssila, Rauli" uniqKey="Franssila R" first="Rauli" last="Franssila">Rauli Franssila</name><affiliation><mods:affiliation>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author><author><name sortKey="Soderlund, Maria" sort="Soderlund, Maria" uniqKey="Soderlund M" first="Maria" last="Söderlund">Maria Söderlund</name><affiliation><mods:affiliation>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author><author><name sortKey="Brown, Caroline S" sort="Brown, Caroline S" uniqKey="Brown C" first="Caroline S" last="Brown">Caroline S. Brown</name><affiliation><mods:affiliation>Department of Virology, University Hospital of Leiden, Leiden, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Spaan, Willy J M" sort="Spaan, Willy J M" uniqKey="Spaan W" first="Willy J. M" last="Spaan">Willy J. M Spaan</name><affiliation><mods:affiliation>Department of Virology, University Hospital of Leiden, Leiden, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Sepp L, Ilkka" sort="Sepp L, Ilkka" uniqKey="Sepp L I" first="Ilkka" last="Sepp L">Ilkka Sepp L</name><affiliation><mods:affiliation>Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author><author><name sortKey="Hedman, Klaus" sort="Hedman, Klaus" uniqKey="Hedman K" first="Klaus" last="Hedman">Klaus Hedman</name><affiliation><mods:affiliation>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Clinical and Diagnostic Virology</title><title level="j" type="abbrev">DIAVIR</title><idno type="ISSN">0928-0197</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996">1996</date><biblScope unit="volume">6</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="41">41</biblScope><biblScope unit="page" to="49">49</biblScope></imprint><idno type="ISSN">0928-0197</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0928-0197</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acute infection</term><term>Acute phase</term><term>Background levels</term><term>Capsid</term><term>Capsid antigen</term><term>Capsid proteins</term><term>Cell clones</term><term>Chronic infection</term><term>Convalescence</term><term>Diagnostic test</term><term>Diagnostic virology</term><term>Diphteria toxin</term><term>Early convalescence</term><term>Epitope</term><term>Erythema infectiosum</term><term>Flvp1</term><term>Flvp1 antigen</term><term>Franssila</term><term>Haartman institute</term><term>Haemophilus influenzae type</term><term>High levels</term><term>Human parvovirus</term><term>Human parvovirus infection</term><term>Hydrops fetalis</term><term>Igg1</term><term>Igg3</term><term>Igg4</term><term>Igg4 responses</term><term>Immunol</term><term>Infection</term><term>Kurtzman</term><term>Late convalescence</term><term>Linear epitopes</term><term>Monoclonal antibodies</term><term>Optimum volume</term><term>Other hand</term><term>Parvovirus</term><term>Past immunity</term><term>Primary structure</term><term>Recent infection</term><term>S6derlund</term><term>Serum pool</term><term>Serum pools</term><term>Subclass</term><term>Subclass response</term><term>Subclasses igg1</term><term>Subclasses igg3</term><term>Time point</term><term>Time points</term><term>Total igg4</term><term>Unique portion</term><term>Virology</term><term>Years days</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Background: IgG antibodies are essential to immunity against human parvovirus B19 and can neutralize infection both in bone marrow cell cultures infected in vitro and in chronically infected immunosuppressed individuals. Objectives: To assess the levels and response kinetics of IgG subclasses towards individual structural proteins of human parvovirus B19. Study design: Subclasses of IgG for capsid proteins VP1 or VP2 were quantified by EIA using monoclonal antibodies in 30 acutely infected and 30 convalescent patients, as well as in 32 remotely infected and 20 non-infected controls. Results: In all groups of seropositive individuals the predominant subclass for either structural protein was IgG1. Subclass IgG3 was associated with acute infection. By contrast, IgG4 appeared months after infection, and occurred specifically towards VP1. The ratio of VP1-specific subclasses IgG3 and IgG4 provided a diagnostic test for recent infection with a specificity of 98% and a sensitivity of 97%. Conclusions: Comparative measurement of VP1-specific IgG3 and IgG4 is useful in diagnosis. The IgG4 results point to long-term expression of immunologically active VP1 and to T-cell help of Th2 type for B-cells recognizing VP1.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>igg4</json:string><json:string>subclass</json:string><json:string>parvovirus</json:string><json:string>igg3</json:string><json:string>igg1</json:string><json:string>capsid</json:string><json:string>flvp1</json:string><json:string>virology</json:string><json:string>s6derlund</json:string><json:string>epitope</json:string><json:string>immunol</json:string><json:string>diagnostic virology</json:string><json:string>human parvovirus</json:string><json:string>kurtzman</json:string><json:string>franssila</json:string><json:string>flvp1 antigen</json:string><json:string>serum pools</json:string><json:string>late convalescence</json:string><json:string>background levels</json:string><json:string>convalescence</json:string><json:string>acute infection</json:string><json:string>cell clones</json:string><json:string>serum pool</json:string><json:string>monoclonal antibodies</json:string><json:string>linear epitopes</json:string><json:string>subclass response</json:string><json:string>other hand</json:string><json:string>infection</json:string><json:string>high levels</json:string><json:string>unique portion</json:string><json:string>past immunity</json:string><json:string>hydrops fetalis</json:string><json:string>erythema infectiosum</json:string><json:string>years days</json:string><json:string>recent infection</json:string><json:string>diagnostic test</json:string><json:string>total igg4</json:string><json:string>optimum volume</json:string><json:string>subclasses igg3</json:string><json:string>time points</json:string><json:string>chronic infection</json:string><json:string>capsid antigen</json:string><json:string>capsid proteins</json:string><json:string>time point</json:string><json:string>subclasses igg1</json:string><json:string>acute phase</json:string><json:string>early convalescence</json:string><json:string>igg4 responses</json:string><json:string>human parvovirus infection</json:string><json:string>haartman institute</json:string><json:string>primary structure</json:string><json:string>haemophilus influenzae type</json:string><json:string>diphteria toxin</json:string></teeft></keywords><author><json:item><name>Rauli Franssila</name><affiliations><json:string>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</json:string></affiliations></json:item><json:item><name>Maria Söderlund</name><affiliations><json:string>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</json:string></affiliations></json:item><json:item><name>Caroline S Brown</name><affiliations><json:string>Department of Virology, University Hospital of Leiden, Leiden, The Netherlands</json:string></affiliations></json:item><json:item><name>Willy J.M Spaan</name><affiliations><json:string>Department of Virology, University Hospital of Leiden, Leiden, The Netherlands</json:string></affiliations></json:item><json:item><name>Ilkka Seppälä</name><affiliations><json:string>Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland</json:string></affiliations></json:item><json:item><name>Klaus Hedman</name><affiliations><json:string>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Antigen persistence</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>B-cell immunity</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Diagnosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Epitope</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>IgG subclass</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parvovirus B19</value></json:item></subject><arkIstex>ark:/67375/6H6-B9VMBL4H-W</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>Abstract: Background: IgG antibodies are essential to immunity against human parvovirus B19 and can neutralize infection both in bone marrow cell cultures infected in vitro and in chronically infected immunosuppressed individuals. Objectives: To assess the levels and response kinetics of IgG subclasses towards individual structural proteins of human parvovirus B19. Study design: Subclasses of IgG for capsid proteins VP1 or VP2 were quantified by EIA using monoclonal antibodies in 30 acutely infected and 30 convalescent patients, as well as in 32 remotely infected and 20 non-infected controls. Results: In all groups of seropositive individuals the predominant subclass for either structural protein was IgG1. Subclass IgG3 was associated with acute infection. By contrast, IgG4 appeared months after infection, and occurred specifically towards VP1. The ratio of VP1-specific subclasses IgG3 and IgG4 provided a diagnostic test for recent infection with a specificity of 98% and a sensitivity of 97%. Conclusions: Comparative measurement of VP1-specific IgG3 and IgG4 is useful in diagnosis. The IgG4 results point to long-term expression of immunologically active VP1 and to T-cell help of Th2 type for B-cells recognizing VP1.</abstract><qualityIndicators><score>7.679</score><pdfWordCount>3507</pdfWordCount><pdfCharCount>21624</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>9</pdfPageCount><pdfPageSize>540 x 749 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>181</abstractWordCount><abstractCharCount>1235</abstractCharCount><keywordCount>6</keywordCount></qualityIndicators><title>IgG subclass response to human parvovirus B19 infection</title><pmid><json:string>15566889</json:string></pmid><pii><json:string>0928-0197(96)00156-0</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Mayo Clin. Proc.</title><language><json:string>unknown</json:string></language><volume>70</volume><pages><first>261</first><last>265</last></pages></serie><host><title>Clinical and Diagnostic Virology</title><language><json:string>unknown</json:string></language><publicationDate>1996</publicationDate><issn><json:string>0928-0197</json:string></issn><pii><json:string>S0928-0197(00)X0001-3</json:string></pii><volume>6</volume><issue>1</issue><pages><first>41</first><last>49</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>5000</json:string><json:string>1996</json:string></date><geogName></geogName><orgName><json:string>Zymed Laboratories, San Francisco</json:string><json:string>University Hospital of Leiden, Leiden, The Netherlands</json:string><json:string>Haartman Institute, University of Helsinki, Helsinki, Finland Received</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName></persName><placeName><json:string>Uppsala</json:string><json:string>Finland</json:string><json:string>UK</json:string><json:string>Helsinki</json:string><json:string>Denmark</json:string><json:string>Sweden</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Mosmann et al., 1986</json:string><json:string>Bird et al., 1990</json:string><json:string>Ulrich et al., 1995</json:string><json:string>Ozawa et al., 1987</json:string><json:string>Aalberse et al., 1983</json:string><json:string>Mortimer et al., 1983</json:string><json:string>Linde et al., 1988</json:string><json:string>Wagner et al., 1995</json:string><json:string>Aversa et al., 1993</json:string><json:string>Cohen et al., 1983</json:string><json:string>Lundkvist et al., 1993</json:string><json:string>Lundgren et al., 1989</json:string><json:string>Romagnani, 1994</json:string><json:string>Wierenga et al., 1990</json:string><json:string>Gascan et al., 1991</json:string><json:string>Maizels et al., 1995</json:string><json:string>Brown et al., 1990</json:string><json:string>Anand et al., 1987</json:string><json:string>Griffin et al., 1994</json:string><json:string>Kurtzman et al.</json:string><json:string>Frickhofen and Young, 1992</json:string><json:string>Anderson et al., 1984</json:string><json:string>Kurtzman et al., 1989</json:string><json:string>Saikawa et al., 1993</json:string><json:string>Ozawa and Young, 1987</json:string><json:string>Faden et al., 1992</json:string><json:string>Lambin et al., 1993</json:string><json:string>R. Franssila et al.</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-B9VMBL4H-W</json:string></ark><categories><wos></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - biomedical research</json:string><json:string>3 - virology</json:string></scienceMetrix><scopus><json:string>1 - Life Sciences</json:string><json:string>2 - Immunology and Microbiology</json:string><json:string>3 - Virology</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><json:string>4 - immunopathologie</json:string></inist></categories><publicationDate>1996</publicationDate><copyrightDate>1996</copyrightDate><doi><json:string>10.1016/0928-0197(96)00156-0</json:string></doi><id>A2A05B052207B90FB3BC3847436BAB6B9C1BEB0F</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-B9VMBL4H-W/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-B9VMBL4H-W/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6H6-B9VMBL4H-W/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a">IgG subclass response to human parvovirus B19 infection</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">ELSEVIER</publisher><availability><licence><p>elsevier</p></licence></availability><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M"></p><date>1996</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">Section title: Report</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">IgG subclass response to human parvovirus B19 infection</title><author xml:id="author-0000"><persName><forename type="first">Rauli</forename><surname>Franssila</surname></persName><note type="correspondence"><p>Corresponding author. Fax: + 358 0 434 6491.</p></note><affiliation>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Maria</forename><surname>Söderlund</surname></persName><affiliation>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Caroline S</forename><surname>Brown</surname></persName><affiliation>Department of Virology, University Hospital of Leiden, Leiden, The Netherlands</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Willy J.M</forename><surname>Spaan</surname></persName><affiliation>Department of Virology, University Hospital of Leiden, Leiden, The Netherlands</affiliation></author><author xml:id="author-0004"><persName><forename type="first">Ilkka</forename><surname>Seppälä</surname></persName><affiliation>Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Klaus</forename><surname>Hedman</surname></persName><affiliation>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</affiliation></author><idno type="istex">A2A05B052207B90FB3BC3847436BAB6B9C1BEB0F</idno><idno type="ark">ark:/67375/6H6-B9VMBL4H-W</idno><idno type="DOI">10.1016/0928-0197(96)00156-0</idno><idno type="PII">0928-0197(96)00156-0</idno></analytic><monogr><title level="j">Clinical and Diagnostic Virology</title><title level="j" type="abbrev">DIAVIR</title><idno type="pISSN">0928-0197</idno><idno type="PII">S0928-0197(00)X0001-3</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996"></date><biblScope unit="volume">6</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="41">41</biblScope><biblScope unit="page" to="49">49</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1996</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Background: IgG antibodies are essential to immunity against human parvovirus B19 and can neutralize infection both in bone marrow cell cultures infected in vitro and in chronically infected immunosuppressed individuals. Objectives: To assess the levels and response kinetics of IgG subclasses towards individual structural proteins of human parvovirus B19. Study design: Subclasses of IgG for capsid proteins VP1 or VP2 were quantified by EIA using monoclonal antibodies in 30 acutely infected and 30 convalescent patients, as well as in 32 remotely infected and 20 non-infected controls. Results: In all groups of seropositive individuals the predominant subclass for either structural protein was IgG1. Subclass IgG3 was associated with acute infection. By contrast, IgG4 appeared months after infection, and occurred specifically towards VP1. The ratio of VP1-specific subclasses IgG3 and IgG4 provided a diagnostic test for recent infection with a specificity of 98% and a sensitivity of 97%. Conclusions: Comparative measurement of VP1-specific IgG3 and IgG4 is useful in diagnosis. The IgG4 results point to long-term expression of immunologically active VP1 and to T-cell help of Th2 type for B-cells recognizing VP1.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Antigen persistence</term></item><item><term>B-cell immunity</term></item><item><term>Diagnosis</term></item><item><term>Epitope</term></item><item><term>IgG subclass</term></item><item><term>Parvovirus B19</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996">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-B9VMBL4H-W/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: 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:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>DIAVIR</jid><aid>96001560</aid><ce:pii>0928-0197(96)00156-0</ce:pii><ce:doi>10.1016/0928-0197(96)00156-0</ce:doi><ce:copyright type="unknown" year="1996"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Report</ce:textfn></ce:dochead><ce:title>IgG subclass response to human parvovirus B19 infection</ce:title><ce:author-group><ce:author><ce:given-name>Rauli</ce:given-name><ce:surname>Franssila</ce:surname><ce:cross-ref refid="COR1"><ce:sup>∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Maria</ce:given-name><ce:surname>Söderlund</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Caroline S</ce:given-name><ce:surname>Brown</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Willy J.M</ce:given-name><ce:surname>Spaan</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Ilkka</ce:given-name><ce:surname>Seppälä</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>c</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Klaus</ce:given-name><ce:surname>Hedman</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Virology, University Hospital of Leiden, Leiden, The Netherlands</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Corresponding author. Fax: + 358 0 434 6491.</ce:text></ce:correspondence></ce:author-group><ce:date-received day="28" month="7" year="1995"></ce:date-received><ce:date-accepted day="25" month="9" year="1995"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para><ce:bold>Background:</ce:bold> IgG antibodies are essential to immunity against human parvovirus B19 and can neutralize infection both in bone marrow cell cultures infected in vitro and in chronically infected immunosuppressed individuals.</ce:simple-para><ce:simple-para><ce:bold>Objectives:</ce:bold> To assess the levels and response kinetics of IgG subclasses towards individual structural proteins of human parvovirus B19.</ce:simple-para><ce:simple-para><ce:bold>Study design:</ce:bold> Subclasses of IgG for capsid proteins VP1 or VP2 were quantified by EIA using monoclonal antibodies in 30 acutely infected and 30 convalescent patients, as well as in 32 remotely infected and 20 non-infected controls.</ce:simple-para><ce:simple-para><ce:bold>Results:</ce:bold> In all groups of seropositive individuals the predominant subclass for either structural protein was IgG1. Subclass IgG3 was associated with acute infection. By contrast, IgG4 appeared months after infection, and occurred specifically towards VP1. The ratio of VP1-specific subclasses IgG3 and IgG4 provided a diagnostic test for recent infection with a specificity of 98% and a sensitivity of 97%.</ce:simple-para><ce:simple-para><ce:bold>Conclusions:</ce:bold> Comparative measurement of VP1-specific IgG3 and IgG4 is useful in diagnosis. The IgG4 results point to long-term expression of immunologically active VP1 and to T-cell help of T<ce:inf>h</ce:inf>2 type for B-cells recognizing VP1.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Antigen persistence</ce:text></ce:keyword><ce:keyword><ce:text>B-cell immunity</ce:text></ce:keyword><ce:keyword><ce:text>Diagnosis</ce:text></ce:keyword><ce:keyword><ce:text>Epitope</ce:text></ce:keyword><ce:keyword><ce:text>IgG subclass</ce:text></ce:keyword><ce:keyword><ce:text>Parvovirus B19</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>IgG subclass response to human parvovirus B19 infection</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>IgG subclass response to human parvovirus B19 infection</title></titleInfo><name type="personal"><namePart type="given">Rauli</namePart><namePart type="family">Franssila</namePart><affiliation>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</affiliation><description>Corresponding author. Fax: + 358 0 434 6491.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Maria</namePart><namePart type="family">Söderlund</namePart><affiliation>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Caroline S</namePart><namePart type="family">Brown</namePart><affiliation>Department of Virology, University Hospital of Leiden, Leiden, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Willy J.M</namePart><namePart type="family">Spaan</namePart><affiliation>Department of Virology, University Hospital of Leiden, Leiden, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ilkka</namePart><namePart type="family">Seppälä</namePart><affiliation>Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Klaus</namePart><namePart type="family">Hedman</namePart><affiliation>Department of Virology, Haartman Institute, P.O. Box 21, FIN-00014, University of Helsinki, Helsinki, Finland</affiliation><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">1996</dateIssued><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Background: IgG antibodies are essential to immunity against human parvovirus B19 and can neutralize infection both in bone marrow cell cultures infected in vitro and in chronically infected immunosuppressed individuals. Objectives: To assess the levels and response kinetics of IgG subclasses towards individual structural proteins of human parvovirus B19. Study design: Subclasses of IgG for capsid proteins VP1 or VP2 were quantified by EIA using monoclonal antibodies in 30 acutely infected and 30 convalescent patients, as well as in 32 remotely infected and 20 non-infected controls. Results: In all groups of seropositive individuals the predominant subclass for either structural protein was IgG1. Subclass IgG3 was associated with acute infection. By contrast, IgG4 appeared months after infection, and occurred specifically towards VP1. The ratio of VP1-specific subclasses IgG3 and IgG4 provided a diagnostic test for recent infection with a specificity of 98% and a sensitivity of 97%. Conclusions: Comparative measurement of VP1-specific IgG3 and IgG4 is useful in diagnosis. The IgG4 results point to long-term expression of immunologically active VP1 and to T-cell help of Th2 type for B-cells recognizing VP1.</abstract><note type="content">Section title: Report</note><subject><genre>Keywords</genre><topic>Antigen persistence</topic><topic>B-cell immunity</topic><topic>Diagnosis</topic><topic>Epitope</topic><topic>IgG subclass</topic><topic>Parvovirus B19</topic></subject><relatedItem type="host"><titleInfo><title>Clinical and Diagnostic Virology</title></titleInfo><titleInfo type="abbreviated"><title>DIAVIR</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">1996</dateIssued></originInfo><identifier type="ISSN">0928-0197</identifier><identifier type="PII">S0928-0197(00)X0001-3</identifier><part><date>1996</date><detail type="volume"><number>6</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="issue-pages"><start>1</start><end>78</end></extent><extent unit="pages"><start>41</start><end>49</end></extent></part></relatedItem><identifier type="istex">A2A05B052207B90FB3BC3847436BAB6B9C1BEB0F</identifier><identifier type="ark">ark:/67375/6H6-B9VMBL4H-W</identifier><identifier type="DOI">10.1016/0928-0197(96)00156-0</identifier><identifier type="PII">0928-0197(96)00156-0</identifier><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></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-B9VMBL4H-W/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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