Going to Bat(s) for Studies of Disease Tolerance
Identifieur interne : 000572 ( Pmc/Checkpoint ); précédent : 000571; suivant : 000573Going to Bat(s) for Studies of Disease Tolerance
Auteurs : Judith N. Mandl [Canada] ; Caitlin Schneider [Canada] ; David S. Schneider [États-Unis] ; Michelle L. Baker [Australie]Source :
- Frontiers in Immunology [ 1664-3224 ] ; 2018.
Abstract
A majority of viruses that have caused recent epidemics with high lethality rates in people, are zoonoses originating from wildlife. Among them are filoviruses (e.g., Marburg, Ebola), coronaviruses (e.g., SARS, MERS), henipaviruses (e.g., Hendra, Nipah) which share the common features that they are all RNA viruses, and that a dysregulated immune response is an important contributor to the tissue damage and hence pathogenicity that results from infection in humans. Intriguingly, these viruses also all originate from bat reservoirs. Bats have been shown to have a greater mean viral richness than predicted by their phylogenetic distance from humans, their geographic range, or their presence in urban areas, suggesting other traits must explain why bats harbor a greater number of zoonotic viruses than other mammals. Bats are highly unusual among mammals in other ways as well. Not only are they the only mammals capable of powered flight, they have extraordinarily long life spans, with little detectable increases in mortality or senescence until high ages. Their physiology likely impacted their history of pathogen exposure and necessitated adaptations that may have also affected immune signaling pathways. Do our life history traits make us susceptible to generating damaging immune responses to RNA viruses or does the physiology of bats make them particularly tolerant or resistant? Understanding what immune mechanisms enable bats to coexist with RNA viruses may provide critical fundamental insights into how to achieve greater resilience in humans.
Url:
DOI: 10.3389/fimmu.2018.02112
PubMed: 30294323
PubMed Central: 6158362
Affiliations:
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PMC:6158362Le document en format XML
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<front><div type="abstract" xml:lang="en"><p>A majority of viruses that have caused recent epidemics with high lethality rates in people, are zoonoses originating from wildlife. Among them are filoviruses (e.g., Marburg, Ebola), coronaviruses (e.g., SARS, MERS), henipaviruses (e.g., Hendra, Nipah) which share the common features that they are all RNA viruses, and that a dysregulated immune response is an important contributor to the tissue damage and hence pathogenicity that results from infection in humans. Intriguingly, these viruses also all originate from bat reservoirs. Bats have been shown to have a greater mean viral richness than predicted by their phylogenetic distance from humans, their geographic range, or their presence in urban areas, suggesting other traits must explain why bats harbor a greater number of zoonotic viruses than other mammals. Bats are highly unusual among mammals in other ways as well. Not only are they the only mammals capable of powered flight, they have extraordinarily long life spans, with little detectable increases in mortality or senescence until high ages. Their physiology likely impacted their history of pathogen exposure and necessitated adaptations that may have also affected immune signaling pathways. Do our life history traits make us susceptible to generating damaging immune responses to RNA viruses or does the physiology of bats make them particularly tolerant or resistant? Understanding what immune mechanisms enable bats to coexist with RNA viruses may provide critical fundamental insights into how to achieve greater resilience in humans.</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 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">30294323</article-id>
<article-id pub-id-type="pmc">6158362</article-id>
<article-id pub-id-type="doi">10.3389/fimmu.2018.02112</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>Going to Bat(s) for Studies of Disease Tolerance</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Mandl</surname>
<given-names>Judith N.</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<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/459230/overview"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>Schneider</surname>
<given-names>Caitlin</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Schneider</surname>
<given-names>David S.</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>4</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Baker</surname>
<given-names>Michelle L.</given-names>
</name>
<xref ref-type="aff" rid="aff5"><sup>5</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/471241/overview"></uri>
</contrib>
</contrib-group>
<aff id="aff1"><sup>1</sup>
<institution>Department of Physiology, McGill University</institution>
,<addr-line>Montreal, QC</addr-line>
,<country>Canada</country>
</aff>
<aff id="aff2"><sup>2</sup>
<institution>Department of Microbiology and Immunology, McGill University</institution>
,<addr-line>Montreal, QC</addr-line>
,<country>Canada</country>
</aff>
<aff id="aff3"><sup>3</sup>
<institution>McGill Research Center for Complex Traits, McGill University</institution>
,<addr-line>Montreal, QC</addr-line>
,<country>Canada</country>
</aff>
<aff id="aff4"><sup>4</sup>
<institution>Department of Microbiology and Immunology, Stanford University</institution>
,<addr-line>Stanford, CA</addr-line>
,<country>United States</country>
</aff>
<aff id="aff5"><sup>5</sup>
<institution>Australian Animal Health Laboratory, Health and Biosecurity Business Unit, Commonwealth Scientific and Industrial Research Organisation</institution>
,<addr-line>Geelong, VIC</addr-line>
,<country>Australia</country>
</aff>
<author-notes><fn fn-type="edited-by"><p>Edited by: Irah L. King, McGill University, Canada</p>
</fn>
<fn fn-type="edited-by"><p>Reviewed by: Christopher J. A. Duncan, Newcastle University, United Kingdom; Anna-Lena Spetz, Stockholm University, Sweden</p>
</fn>
<corresp id="c001">*Correspondence: Judith N. Mandl <email>judith.mandl@mcgill.ca</email>
</corresp>
<fn fn-type="other" id="fn001"><p>This article was submitted to Viral Immunology, a section of the journal Frontiers in Immunology</p>
</fn>
</author-notes>
<pub-date pub-type="epub"><day>20</day>
<month>9</month>
<year>2018</year>
</pub-date>
<pub-date pub-type="collection"><year>2018</year>
</pub-date>
<volume>9</volume>
<elocation-id>2112</elocation-id>
<history><date date-type="received"><day>18</day>
<month>6</month>
<year>2018</year>
</date>
<date date-type="accepted"><day>28</day>
<month>8</month>
<year>2018</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2018 Mandl, Schneider, Schneider and Baker.</copyright-statement>
<copyright-year>2018</copyright-year>
<copyright-holder>Mandl, Schneider, Schneider and Baker</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>A majority of viruses that have caused recent epidemics with high lethality rates in people, are zoonoses originating from wildlife. Among them are filoviruses (e.g., Marburg, Ebola), coronaviruses (e.g., SARS, MERS), henipaviruses (e.g., Hendra, Nipah) which share the common features that they are all RNA viruses, and that a dysregulated immune response is an important contributor to the tissue damage and hence pathogenicity that results from infection in humans. Intriguingly, these viruses also all originate from bat reservoirs. Bats have been shown to have a greater mean viral richness than predicted by their phylogenetic distance from humans, their geographic range, or their presence in urban areas, suggesting other traits must explain why bats harbor a greater number of zoonotic viruses than other mammals. Bats are highly unusual among mammals in other ways as well. Not only are they the only mammals capable of powered flight, they have extraordinarily long life spans, with little detectable increases in mortality or senescence until high ages. Their physiology likely impacted their history of pathogen exposure and necessitated adaptations that may have also affected immune signaling pathways. Do our life history traits make us susceptible to generating damaging immune responses to RNA viruses or does the physiology of bats make them particularly tolerant or resistant? Understanding what immune mechanisms enable bats to coexist with RNA viruses may provide critical fundamental insights into how to achieve greater resilience in humans.</p>
</abstract>
<kwd-group><kwd>bats (Chiroptera)</kwd>
<kwd>viral immunology</kwd>
<kwd>host pathogen interaction</kwd>
<kwd>disease tolerance</kwd>
<kwd>comparative genome analyses</kwd>
<kwd>innate immunity</kwd>
</kwd-group>
<counts><fig-count count="1"></fig-count>
<table-count count="0"></table-count>
<equation-count count="0"></equation-count>
<ref-count count="139"></ref-count>
<page-count count="13"></page-count>
<word-count count="12026"></word-count>
</counts>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>Australie</li>
<li>Canada</li>
<li>États-Unis</li>
</country>
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<tree><country name="Canada"><noRegion><name sortKey="Mandl, Judith N" sort="Mandl, Judith N" uniqKey="Mandl J" first="Judith N." last="Mandl">Judith N. Mandl</name>
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