AS03- and MF59-Adjuvanted Influenza Vaccines in Children
Identifieur interne : 000F25 ( Pmc/Curation ); précédent : 000F24; suivant : 000F26AS03- and MF59-Adjuvanted Influenza Vaccines in Children
Auteurs : Amanda L. Wilkins [Australie] ; Dmitri Kazmin [États-Unis] ; Giorgio Napolitani [Royaume-Uni] ; Elizabeth A. Clutterbuck [Royaume-Uni] ; Bali Pulendran [États-Unis] ; Claire-Anne Siegrist [Suisse] ; Andrew J. Pollard [Royaume-Uni]Source :
- Frontiers in Immunology [ 1664-3224 ] ; 2017.
Abstract
Influenza is a major cause of respiratory disease leading to hospitalization in young children. However, seasonal trivalent influenza vaccines (TIVs) have been shown to be ineffective and poorly immunogenic in this population. The development of live-attenuated influenza vaccines and adjuvanted vaccines are important advances in the prevention of influenza in young children. The oil-in-water emulsions MF59 and adjuvant systems 03 (AS03) have been used as adjuvants in both seasonal adjuvanted trivalent influenza vaccines (ATIVs) and pandemic monovalent influenza vaccines. Compared with non-adjuvanted vaccine responses, these vaccines induce a more robust and persistent antibody response for both homologous and heterologous influenza strains in infants and young children. Evidence of a significant improvement in vaccine efficacy with these adjuvanted vaccines resulted in the use of the monovalent (A/H1N1) AS03-adjuvanted vaccine in children in the 2009 influenza pandemic and the licensure of the seasonal MF59 ATIV for children aged 6 months to 2 years in Canada. The mechanism of action of MF59 and AS03 remains unclear. Adjuvants such as MF59 induce proinflammatory cytokines and chemokines, including CXCL10, but independently of type-1 interferon. This proinflammatory response is associated with improved recruitment, activation and maturation of antigen presenting cells at the injection site. In young children MF59 ATIV produced more homogenous and robust transcriptional responses, more similar to adult-like patterns, than did TIV. Early gene signatures characteristic of the innate immune response, which correlated with antibody titers were also identified. Differences were detected when comparing child and adult responses including opposite trends in gene set enrichment at day 3 postvaccination and, unlike adult data, a lack of correlation between magnitude of plasmablast response at day 7 and antibody titers at day 28 in children. These insights show the utility of novel approaches in understanding new adjuvants and their importance for developing improved influenza vaccines for children.
Url:
DOI: 10.3389/fimmu.2017.01760
PubMed: 29326687
PubMed Central: 5733358
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<front><div type="abstract" xml:lang="en"><p>Influenza is a major cause of respiratory disease leading to hospitalization in young children. However, seasonal trivalent influenza vaccines (TIVs) have been shown to be ineffective and poorly immunogenic in this population. The development of live-attenuated influenza vaccines and adjuvanted vaccines are important advances in the prevention of influenza in young children. The oil-in-water emulsions MF59 and adjuvant systems 03 (AS03) have been used as adjuvants in both seasonal adjuvanted trivalent influenza vaccines (ATIVs) and pandemic monovalent influenza vaccines. Compared with non-adjuvanted vaccine responses, these vaccines induce a more robust and persistent antibody response for both homologous and heterologous influenza strains in infants and young children. Evidence of a significant improvement in vaccine efficacy with these adjuvanted vaccines resulted in the use of the monovalent (A/H1N1) AS03-adjuvanted vaccine in children in the 2009 influenza pandemic and the licensure of the seasonal MF59 ATIV for children aged 6 months to 2 years in Canada. The mechanism of action of MF59 and AS03 remains unclear. Adjuvants such as MF59 induce proinflammatory cytokines and chemokines, including CXCL10, but independently of type-1 interferon. This proinflammatory response is associated with improved recruitment, activation and maturation of antigen presenting cells at the injection site. In young children MF59 ATIV produced more homogenous and robust transcriptional responses, more similar to adult-like patterns, than did TIV. Early gene signatures characteristic of the innate immune response, which correlated with antibody titers were also identified. Differences were detected when comparing child and adult responses including opposite trends in gene set enrichment at day 3 postvaccination and, unlike adult data, a lack of correlation between magnitude of plasmablast response at day 7 and antibody titers at day 28 in children. These insights show the utility of novel approaches in understanding new adjuvants and their importance for developing improved influenza vaccines for children.</p>
</div>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Immunol</journal-id>
<journal-id journal-id-type="iso-abbrev">Front Immunol</journal-id>
<journal-id journal-id-type="publisher-id">Front. Immunol.</journal-id>
<journal-title-group><journal-title>Frontiers in Immunology</journal-title>
</journal-title-group>
<issn pub-type="epub">1664-3224</issn>
<publisher><publisher-name>Frontiers Media S.A.</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">29326687</article-id>
<article-id pub-id-type="pmc">5733358</article-id>
<article-id pub-id-type="doi">10.3389/fimmu.2017.01760</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Immunology</subject>
<subj-group><subject>Review</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>AS03- and MF59-Adjuvanted Influenza Vaccines in Children</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Wilkins</surname>
<given-names>Amanda L.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
<uri xlink:type="simple" xlink:href="http://frontiersin.org/people/u/431793"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>Kazmin</surname>
<given-names>Dmitri</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://frontiersin.org/people/u/504192"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>Napolitani</surname>
<given-names>Giorgio</given-names>
</name>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Clutterbuck</surname>
<given-names>Elizabeth A.</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>4</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://frontiersin.org/people/u/69503"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>Pulendran</surname>
<given-names>Bali</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff5"><sup>5</sup>
</xref>
<xref ref-type="aff" rid="aff6"><sup>6</sup>
</xref>
<xref ref-type="aff" rid="aff7"><sup>7</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Siegrist</surname>
<given-names>Claire-Anne</given-names>
</name>
<xref ref-type="aff" rid="aff8"><sup>8</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Pollard</surname>
<given-names>Andrew J.</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>4</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://frontiersin.org/people/u/197671"></uri>
</contrib>
</contrib-group>
<aff id="aff1"><sup>1</sup>
<institution>The Royal Children’s Hospital Melbourne</institution>
,<addr-line>Melbourne, VIC</addr-line>
,<country>Australia</country>
</aff>
<aff id="aff2"><sup>2</sup>
<institution>Emory Vaccine Center, Emory University</institution>
,<addr-line>Atlanta, GA</addr-line>
,<country>United States</country>
</aff>
<aff id="aff3"><sup>3</sup>
<institution>Medical Research Council (MRC), Human Immunology Unit, University of Oxford</institution>
,<addr-line>Oxford</addr-line>
,<country>United Kingdom</country>
</aff>
<aff id="aff4"><sup>4</sup>
<institution>Oxford Vaccine Group, Department of Paediatrics, University of Oxford, The NIHR Oxford Biomedical Research Centre</institution>
,<addr-line>Oxford</addr-line>
,<country>United Kingdom</country>
</aff>
<aff id="aff5"><sup>5</sup>
<institution>Department of Pathology, Emory University School of Medicine</institution>
,<addr-line>Atlanta, GA</addr-line>
,<country>United States</country>
</aff>
<aff id="aff6"><sup>6</sup>
<institution>Department of Pathology, and Microbiology & Immunology, Stanford University</institution>
,<addr-line>Stanford, CA</addr-line>
,<country>United States</country>
</aff>
<aff id="aff7"><sup>7</sup>
<institution>Institute for Immunology, Transplantation and Infection, Stanford University</institution>
,<addr-line>Stanford, CA</addr-line>
,<country>United States</country>
</aff>
<aff id="aff8"><sup>8</sup>
<institution>University of Geneva</institution>
,<addr-line>Geneva</addr-line>
,<country>Switzerland</country>
</aff>
<author-notes><fn fn-type="edited-by"><p>Edited by: Rino Rappuoli, GlaxoSmithKline, Italy</p>
</fn>
<fn fn-type="edited-by"><p>Reviewed by: Raffael Nachbagauer, Icahn School of Medicine at Mount Sinai, United States; Aldo Tagliabue, ALTA, Italy</p>
</fn>
<corresp content-type="corresp" id="cor1">*Correspondence: Amanda L. Wilkins, <email>tolson.amanda@gmail.com</email>
</corresp>
<fn fn-type="other" id="fn001"><p>Specialty section: This article was submitted to Vaccines and Molecular Therapeutics, a section of the journal Frontiers in Immunology</p>
</fn>
</author-notes>
<pub-date pub-type="epub"><day>13</day>
<month>12</month>
<year>2017</year>
</pub-date>
<pub-date pub-type="collection"><year>2017</year>
</pub-date>
<volume>8</volume>
<elocation-id>1760</elocation-id>
<history><date date-type="received"><day>15</day>
<month>9</month>
<year>2017</year>
</date>
<date date-type="accepted"><day>27</day>
<month>11</month>
<year>2017</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2017 Wilkins, Kazmin, Napolitani, Clutterbuck, Pulendran, Siegrist and Pollard.</copyright-statement>
<copyright-year>2017</copyright-year>
<copyright-holder>Wilkins, Kazmin, Napolitani, Clutterbuck, Pulendran, Siegrist and Pollard</copyright-holder>
<license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p>
</license>
</permissions>
<abstract><p>Influenza is a major cause of respiratory disease leading to hospitalization in young children. However, seasonal trivalent influenza vaccines (TIVs) have been shown to be ineffective and poorly immunogenic in this population. The development of live-attenuated influenza vaccines and adjuvanted vaccines are important advances in the prevention of influenza in young children. The oil-in-water emulsions MF59 and adjuvant systems 03 (AS03) have been used as adjuvants in both seasonal adjuvanted trivalent influenza vaccines (ATIVs) and pandemic monovalent influenza vaccines. Compared with non-adjuvanted vaccine responses, these vaccines induce a more robust and persistent antibody response for both homologous and heterologous influenza strains in infants and young children. Evidence of a significant improvement in vaccine efficacy with these adjuvanted vaccines resulted in the use of the monovalent (A/H1N1) AS03-adjuvanted vaccine in children in the 2009 influenza pandemic and the licensure of the seasonal MF59 ATIV for children aged 6 months to 2 years in Canada. The mechanism of action of MF59 and AS03 remains unclear. Adjuvants such as MF59 induce proinflammatory cytokines and chemokines, including CXCL10, but independently of type-1 interferon. This proinflammatory response is associated with improved recruitment, activation and maturation of antigen presenting cells at the injection site. In young children MF59 ATIV produced more homogenous and robust transcriptional responses, more similar to adult-like patterns, than did TIV. Early gene signatures characteristic of the innate immune response, which correlated with antibody titers were also identified. Differences were detected when comparing child and adult responses including opposite trends in gene set enrichment at day 3 postvaccination and, unlike adult data, a lack of correlation between magnitude of plasmablast response at day 7 and antibody titers at day 28 in children. These insights show the utility of novel approaches in understanding new adjuvants and their importance for developing improved influenza vaccines for children.</p>
</abstract>
<kwd-group><kwd>adjuvant</kwd>
<kwd>influenza vaccine</kwd>
<kwd>MF59</kwd>
<kwd>AS03</kwd>
<kwd>children</kwd>
</kwd-group>
<counts><fig-count count="1"></fig-count>
<table-count count="1"></table-count>
<equation-count count="0"></equation-count>
<ref-count count="189"></ref-count>
<page-count count="17"></page-count>
<word-count count="13700"></word-count>
</counts>
</article-meta>
</front>
</pmc>
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