Cross-Reactivity, Epitope Spreading, and De Novo Immune Stimulation Are Possible Mechanisms of Cross-Protection of Nonvaccine Human Papillomavirus (HPV) Types in Recipients of HPV Therapeutic Vaccines
Identifieur interne : 000014 ( Pmc/Corpus ); précédent : 000013; suivant : 000015Cross-Reactivity, Epitope Spreading, and De Novo Immune Stimulation Are Possible Mechanisms of Cross-Protection of Nonvaccine Human Papillomavirus (HPV) Types in Recipients of HPV Therapeutic Vaccines
Auteurs : Mayumi Nakagawa ; William Greenfield ; Andrea Moerman-Herzog ; Hannah N. ColemanSource :
- Clinical and Vaccine Immunology : CVI [ 1556-6811 ] ; 2015.
Abstract
Numerous versions of human papillomavirus (HPV) therapeutic vaccines designed to treat individuals with established HPV infection, including those with cervical intraepithelial neoplasia (CIN), are in development because approved prophylactic vaccines are not effective once HPV infection is established. As human papillomavirus 16 (HPV-16) is the most commonly detected type worldwide, all versions of HPV therapeutic vaccines contain HPV-16, and some also contain HPV-18. While these two HPV types are responsible for approximately 70% of cervical cancer cases, there are other high-risk HPV types known to cause malignancy. Therefore, it would be of interest to assess whether these HPV therapeutic vaccines may confer cross-protection against other high-risk HPV types. Data available from a few clinical trials that enrolled subjects with CINs regardless of the HPV type(s) present demonstrated clinical responses, as measured by CIN regression, in subjects with both vaccine-matched and nonvaccine HPV types. The currently available evidence demonstrating cross-reactivity, epitope spreading, and
Url:
DOI: 10.1128/CVI.00149-15
PubMed: 25947147
PubMed Central: 4478515
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PMC:4478515Le document en format XML
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Immune Stimulation Are Possible Mechanisms of Cross-Protection of Nonvaccine Human Papillomavirus (HPV) Types in Recipients of HPV Therapeutic Vaccines</title>
<author><name sortKey="Nakagawa, Mayumi" sort="Nakagawa, Mayumi" uniqKey="Nakagawa M" first="Mayumi" last="Nakagawa">Mayumi Nakagawa</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA</nlm:aff>
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</author>
<author><name sortKey="Greenfield, William" sort="Greenfield, William" uniqKey="Greenfield W" first="William" last="Greenfield">William Greenfield</name>
<affiliation><nlm:aff id="aff2">Department of Obstetrics & Gynecology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA</nlm:aff>
</affiliation>
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<author><name sortKey="Moerman Herzog, Andrea" sort="Moerman Herzog, Andrea" uniqKey="Moerman Herzog A" first="Andrea" last="Moerman-Herzog">Andrea Moerman-Herzog</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA</nlm:aff>
</affiliation>
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<author><name sortKey="Coleman, Hannah N" sort="Coleman, Hannah N" uniqKey="Coleman H" first="Hannah N." last="Coleman">Hannah N. Coleman</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Cross-Reactivity, Epitope Spreading, and <italic>De Novo</italic>
Immune Stimulation Are Possible Mechanisms of Cross-Protection of Nonvaccine Human Papillomavirus (HPV) Types in Recipients of HPV Therapeutic Vaccines</title>
<author><name sortKey="Nakagawa, Mayumi" sort="Nakagawa, Mayumi" uniqKey="Nakagawa M" first="Mayumi" last="Nakagawa">Mayumi Nakagawa</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA</nlm:aff>
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<author><name sortKey="Greenfield, William" sort="Greenfield, William" uniqKey="Greenfield W" first="William" last="Greenfield">William Greenfield</name>
<affiliation><nlm:aff id="aff2">Department of Obstetrics & Gynecology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA</nlm:aff>
</affiliation>
</author>
<author><name sortKey="Moerman Herzog, Andrea" sort="Moerman Herzog, Andrea" uniqKey="Moerman Herzog A" first="Andrea" last="Moerman-Herzog">Andrea Moerman-Herzog</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA</nlm:aff>
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<author><name sortKey="Coleman, Hannah N" sort="Coleman, Hannah N" uniqKey="Coleman H" first="Hannah N." last="Coleman">Hannah N. Coleman</name>
<affiliation><nlm:aff id="aff1">Department of Pathology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA</nlm:aff>
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<series><title level="j">Clinical and Vaccine Immunology : CVI</title>
<idno type="ISSN">1556-6811</idno>
<idno type="eISSN">1556-679X</idno>
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<front><div type="abstract" xml:lang="en"><p>Numerous versions of human papillomavirus (HPV) therapeutic vaccines designed to treat individuals with established HPV infection, including those with cervical intraepithelial neoplasia (CIN), are in development because approved prophylactic vaccines are not effective once HPV infection is established. As human papillomavirus 16 (HPV-16) is the most commonly detected type worldwide, all versions of HPV therapeutic vaccines contain HPV-16, and some also contain HPV-18. While these two HPV types are responsible for approximately 70% of cervical cancer cases, there are other high-risk HPV types known to cause malignancy. Therefore, it would be of interest to assess whether these HPV therapeutic vaccines may confer cross-protection against other high-risk HPV types. Data available from a few clinical trials that enrolled subjects with CINs regardless of the HPV type(s) present demonstrated clinical responses, as measured by CIN regression, in subjects with both vaccine-matched and nonvaccine HPV types. The currently available evidence demonstrating cross-reactivity, epitope spreading, and <italic>de novo</italic>
immune stimulation as possible mechanisms of cross-protection conferred by investigational HPV therapeutic vaccines is discussed.</p>
</div>
</front>
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<pmc article-type="review-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Clin Vaccine Immunol</journal-id>
<journal-id journal-id-type="iso-abbrev">Clin. Vaccine Immunol</journal-id>
<journal-id journal-id-type="hwp">cdli</journal-id>
<journal-id journal-id-type="pmc">cvi</journal-id>
<journal-id journal-id-type="publisher-id">CVI</journal-id>
<journal-title-group><journal-title>Clinical and Vaccine Immunology : CVI</journal-title>
</journal-title-group>
<issn pub-type="ppub">1556-6811</issn>
<issn pub-type="epub">1556-679X</issn>
<publisher><publisher-name>American Society for Microbiology</publisher-name>
<publisher-loc>1752 N St., N.W., Washington, DC</publisher-loc>
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<article-meta><article-id pub-id-type="pmid">25947147</article-id>
<article-id pub-id-type="pmc">4478515</article-id>
<article-id pub-id-type="publisher-id">00149-15</article-id>
<article-id pub-id-type="doi">10.1128/CVI.00149-15</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Minireview</subject>
</subj-group>
</article-categories>
<title-group><article-title>Cross-Reactivity, Epitope Spreading, and <italic>De Novo</italic>
Immune Stimulation Are Possible Mechanisms of Cross-Protection of Nonvaccine Human Papillomavirus (HPV) Types in Recipients of HPV Therapeutic Vaccines</article-title>
<alt-title alt-title-type="running-head">Minireview</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author" corresp="yes"><name><surname>Nakagawa</surname>
<given-names>Mayumi</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Greenfield</surname>
<given-names>William</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>b</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Moerman-Herzog</surname>
<given-names>Andrea</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Coleman</surname>
<given-names>Hannah N.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>a</sup>
</xref>
</contrib>
<aff id="aff1"><label>a</label>
Department of Pathology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA</aff>
<aff id="aff2"><label>b</label>
Department of Obstetrics & Gynecology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA</aff>
</contrib-group>
<contrib-group><contrib contrib-type="editor"><name><surname>Papasian</surname>
<given-names>C. J.</given-names>
</name>
<role>Editor</role>
</contrib>
</contrib-group>
<author-notes><corresp id="cor1">Address correspondence to Mayumi Nakagawa, <email>mnakagawa@uams.edu</email>
.</corresp>
<fn fn-type="other"><p><bold>Citation</bold>
Nakagawa M, Greenfield W, Moerman-Herzog A, Coleman HN. 2015. Cross-reactivity, epitope spreading, and <italic>de novo</italic>
immune stimulation are possible mechanisms of cross-protection of nonvaccine human papillomavirus (HPV) types in recipients of HPV therapeutic vaccines. Clin Vaccine Immunol 22:679–687. doi:<ext-link ext-link-type="uri" xlink:href="http://dx.doi.org/10.1128/CVI.00149-15">10.1128/CVI.00149-15</ext-link>
.</p>
</fn>
</author-notes>
<pub-date pub-type="epub"><day>6</day>
<month>5</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="ppub"><month>7</month>
<year>2015</year>
</pub-date>
<volume>22</volume>
<issue>7</issue>
<fpage>679</fpage>
<lpage>687</lpage>
<permissions><copyright-statement>Copyright © 2015, American Society for Microbiology. All Rights Reserved.</copyright-statement>
<copyright-year>2015</copyright-year>
<copyright-holder>American Society for Microbiology</copyright-holder>
</permissions>
<self-uri content-type="pdf" xlink:href="zcd00715000679.pdf"></self-uri>
<abstract><p>Numerous versions of human papillomavirus (HPV) therapeutic vaccines designed to treat individuals with established HPV infection, including those with cervical intraepithelial neoplasia (CIN), are in development because approved prophylactic vaccines are not effective once HPV infection is established. As human papillomavirus 16 (HPV-16) is the most commonly detected type worldwide, all versions of HPV therapeutic vaccines contain HPV-16, and some also contain HPV-18. While these two HPV types are responsible for approximately 70% of cervical cancer cases, there are other high-risk HPV types known to cause malignancy. Therefore, it would be of interest to assess whether these HPV therapeutic vaccines may confer cross-protection against other high-risk HPV types. Data available from a few clinical trials that enrolled subjects with CINs regardless of the HPV type(s) present demonstrated clinical responses, as measured by CIN regression, in subjects with both vaccine-matched and nonvaccine HPV types. The currently available evidence demonstrating cross-reactivity, epitope spreading, and <italic>de novo</italic>
immune stimulation as possible mechanisms of cross-protection conferred by investigational HPV therapeutic vaccines is discussed.</p>
</abstract>
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