Back to the Future: Lessons Learned From the 1918 Influenza Pandemic
Identifieur interne : 000F24 ( Pmc/Curation ); précédent : 000F23; suivant : 000F25Back to the Future: Lessons Learned From the 1918 Influenza Pandemic
Auteurs : Kirsty R. Short [Australie] ; Katherine Kedzierska [Australie] ; Carolien E. Van De Sandt [Australie, Pays-Bas]Source :
- Frontiers in Cellular and Infection Microbiology [ 2235-2988 ] ; 2018.
Abstract
2018 marks the 100-year anniversary of the 1918 influenza pandemic, which killed ~50 million people worldwide. The severity of this pandemic resulted from a complex interplay between viral, host, and societal factors. Here, we review the viral, genetic and immune factors that contributed to the severity of the 1918 pandemic and discuss the implications for modern pandemic preparedness. We address unresolved questions of why the 1918 influenza H1N1 virus was more virulent than other influenza pandemics and why some people survived the 1918 pandemic and others succumbed to the infection. While current studies suggest that viral factors such as haemagglutinin and polymerase gene segments most likely contributed to a potent, dysregulated pro-inflammatory cytokine storm in victims of the pandemic, a shift in case-fatality for the 1918 pandemic toward young adults was most likely associated with the host's immune status. Lack of pre-existing virus-specific and/or cross-reactive antibodies and cellular immunity in children and young adults likely contributed to the high attack rate and rapid spread of the 1918 H1N1 virus. In contrast, lower mortality rate in in the older (>30 years) adult population points toward the beneficial effects of pre-existing cross-reactive immunity. In addition to the role of humoral and cellular immunity, there is a growing body of evidence to suggest that individual genetic differences, especially involving single-nucleotide polymorphisms (SNPs), contribute to differences in the severity of influenza virus infections. Co-infections with bacterial pathogens, and possibly measles and malaria, co-morbidities, malnutrition or obesity are also known to affect the severity of influenza disease, and likely influenced 1918 H1N1 disease severity and outcomes. Additionally, we also discuss the new challenges, such as changing population demographics, antibiotic resistance and climate change, which we will face in the context of any future influenza virus pandemic. In the last decade there has been a dramatic increase in the number of severe influenza virus strains entering the human population from animal reservoirs (including highly pathogenic H7N9 and H5N1 viruses). An understanding of past influenza virus pandemics and the lessons that we have learnt from them has therefore never been more pertinent.
Url:
DOI: 10.3389/fcimb.2018.00343
PubMed: 30349811
PubMed Central: 6187080
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<front><div type="abstract" xml:lang="en"><p>2018 marks the 100-year anniversary of the 1918 influenza pandemic, which killed ~50 million people worldwide. The severity of this pandemic resulted from a complex interplay between viral, host, and societal factors. Here, we review the viral, genetic and immune factors that contributed to the severity of the 1918 pandemic and discuss the implications for modern pandemic preparedness. We address unresolved questions of why the 1918 influenza H1N1 virus was more virulent than other influenza pandemics and why some people survived the 1918 pandemic and others succumbed to the infection. While current studies suggest that viral factors such as haemagglutinin and polymerase gene segments most likely contributed to a potent, dysregulated pro-inflammatory cytokine storm in victims of the pandemic, a shift in case-fatality for the 1918 pandemic toward young adults was most likely associated with the host's immune status. Lack of pre-existing virus-specific and/or cross-reactive antibodies and cellular immunity in children and young adults likely contributed to the high attack rate and rapid spread of the 1918 H1N1 virus. In contrast, lower mortality rate in in the older (>30 years) adult population points toward the beneficial effects of pre-existing cross-reactive immunity. In addition to the role of humoral and cellular immunity, there is a growing body of evidence to suggest that individual genetic differences, especially involving single-nucleotide polymorphisms (SNPs), contribute to differences in the severity of influenza virus infections. Co-infections with bacterial pathogens, and possibly measles and malaria, co-morbidities, malnutrition or obesity are also known to affect the severity of influenza disease, and likely influenced 1918 H1N1 disease severity and outcomes. Additionally, we also discuss the new challenges, such as changing population demographics, antibiotic resistance and climate change, which we will face in the context of any future influenza virus pandemic. In the last decade there has been a dramatic increase in the number of severe influenza virus strains entering the human population from animal reservoirs (including highly pathogenic H7N9 and H5N1 viruses). An understanding of past influenza virus pandemics and the lessons that we have learnt from them has therefore never been more pertinent.</p>
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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 Cell Infect Microbiol</journal-id>
<journal-id journal-id-type="iso-abbrev">Front Cell Infect Microbiol</journal-id>
<journal-id journal-id-type="publisher-id">Front. Cell. Infect. Microbiol.</journal-id>
<journal-title-group><journal-title>Frontiers in Cellular and Infection Microbiology</journal-title>
</journal-title-group>
<issn pub-type="epub">2235-2988</issn>
<publisher><publisher-name>Frontiers Media S.A.</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">30349811</article-id>
<article-id pub-id-type="pmc">6187080</article-id>
<article-id pub-id-type="doi">10.3389/fcimb.2018.00343</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Cellular and Infection Microbiology</subject>
<subj-group><subject>Review</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>Back to the Future: Lessons Learned From the 1918 Influenza Pandemic</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Short</surname>
<given-names>Kirsty R.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/110714/overview"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>Kedzierska</surname>
<given-names>Katherine</given-names>
</name>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
<xref ref-type="corresp" rid="c001"><sup>*</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/50928/overview"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>van de Sandt</surname>
<given-names>Carolien E.</given-names>
</name>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
<xref ref-type="aff" rid="aff4"><sup>4</sup>
</xref>
<xref ref-type="corresp" rid="c002"><sup>*</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/599540/overview"></uri>
</contrib>
</contrib-group>
<aff id="aff1"><sup>1</sup>
<institution>School of Chemistry and Molecular Biosciences, The University of Queensland</institution>
,<addr-line>Brisbane, QLD</addr-line>
,<country>Australia</country>
</aff>
<aff id="aff2"><sup>2</sup>
<institution>Australian Infectious Diseases Research Centre, The University of Queensland</institution>
,<addr-line>Brisbane, QLD</addr-line>
,<country>Australia</country>
</aff>
<aff id="aff3"><sup>3</sup>
<institution>Department of Microbiology and Immunology, The Peter Doherty Institute for Infection and Immunity, University of Melbourne</institution>
,<addr-line>Parkville, VIC</addr-line>
,<country>Australia</country>
</aff>
<aff id="aff4"><sup>4</sup>
<institution>Department of Hematopoiesis, Sanquin Research and Landsteiner Laboratory</institution>
,<addr-line>Amsterdam</addr-line>
,<country>Netherlands</country>
</aff>
<author-notes><fn fn-type="edited-by"><p>Edited by: Yanmin Wan, Fudan University, China</p>
</fn>
<fn fn-type="edited-by"><p>Reviewed by: Ali Ellebedy, Washington University in St. Louis, United States; Daniel Angel Ortiz, Laboratory Corporation of America Holdings (LabCorp), United States</p>
</fn>
<corresp id="c001">*Correspondence: Katherine Kedzierska <email>kkedz@unimelb.edu.au</email>
</corresp>
<corresp id="c002">Carolien E. van de Sandt <email>cvandesandt@unimelb.edu.au</email>
</corresp>
</author-notes>
<pub-date pub-type="epub"><day>08</day>
<month>10</month>
<year>2018</year>
</pub-date>
<pub-date pub-type="collection"><year>2018</year>
</pub-date>
<volume>8</volume>
<elocation-id>343</elocation-id>
<history><date date-type="received"><day>10</day>
<month>8</month>
<year>2018</year>
</date>
<date date-type="accepted"><day>10</day>
<month>9</month>
<year>2018</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2018 Short, Kedzierska and van de Sandt.</copyright-statement>
<copyright-year>2018</copyright-year>
<copyright-holder>Short, Kedzierska and van de Sandt</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) and the copyright owner(s) 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>2018 marks the 100-year anniversary of the 1918 influenza pandemic, which killed ~50 million people worldwide. The severity of this pandemic resulted from a complex interplay between viral, host, and societal factors. Here, we review the viral, genetic and immune factors that contributed to the severity of the 1918 pandemic and discuss the implications for modern pandemic preparedness. We address unresolved questions of why the 1918 influenza H1N1 virus was more virulent than other influenza pandemics and why some people survived the 1918 pandemic and others succumbed to the infection. While current studies suggest that viral factors such as haemagglutinin and polymerase gene segments most likely contributed to a potent, dysregulated pro-inflammatory cytokine storm in victims of the pandemic, a shift in case-fatality for the 1918 pandemic toward young adults was most likely associated with the host's immune status. Lack of pre-existing virus-specific and/or cross-reactive antibodies and cellular immunity in children and young adults likely contributed to the high attack rate and rapid spread of the 1918 H1N1 virus. In contrast, lower mortality rate in in the older (>30 years) adult population points toward the beneficial effects of pre-existing cross-reactive immunity. In addition to the role of humoral and cellular immunity, there is a growing body of evidence to suggest that individual genetic differences, especially involving single-nucleotide polymorphisms (SNPs), contribute to differences in the severity of influenza virus infections. Co-infections with bacterial pathogens, and possibly measles and malaria, co-morbidities, malnutrition or obesity are also known to affect the severity of influenza disease, and likely influenced 1918 H1N1 disease severity and outcomes. Additionally, we also discuss the new challenges, such as changing population demographics, antibiotic resistance and climate change, which we will face in the context of any future influenza virus pandemic. In the last decade there has been a dramatic increase in the number of severe influenza virus strains entering the human population from animal reservoirs (including highly pathogenic H7N9 and H5N1 viruses). An understanding of past influenza virus pandemics and the lessons that we have learnt from them has therefore never been more pertinent.</p>
</abstract>
<kwd-group><kwd>influenza</kwd>
<kwd>pandemic</kwd>
<kwd>1918</kwd>
<kwd>host factors</kwd>
<kwd>viral factors</kwd>
<kwd>external factors</kwd>
<kwd>societal factors</kwd>
<kwd>prevention</kwd>
</kwd-group>
<counts><fig-count count="2"></fig-count>
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Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/PandemieGrippaleV1/Data/Pmc/Curation
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000F24 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Curation/biblio.hfd -nk 000F24 | SxmlIndent | more
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{{Explor lien |wiki= Sante |area= PandemieGrippaleV1 |flux= Pmc |étape= Curation |type= RBID |clé= PMC:6187080 |texte= Back to the Future: Lessons Learned From the 1918 Influenza Pandemic }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Pmc/Curation/RBID.i -Sk "pubmed:30349811" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Pmc/Curation/biblio.hfd \ | NlmPubMed2Wicri -a PandemieGrippaleV1
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