Going to Bat(s) for Studies of Disease Tolerance

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...

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Main Authors: Judith N. Mandl, Caitlin Schneider, David S. Schneider, Michelle L. Baker
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-09-01
Series:Frontiers in Immunology
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fimmu.2018.02112/full
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spelling doaj-5581d7d7b1dc409abc548cb371526b9c2020-11-24T21:47:54ZengFrontiers Media S.A.Frontiers in Immunology1664-32242018-09-01910.3389/fimmu.2018.02112408880Going to Bat(s) for Studies of Disease ToleranceJudith N. Mandl0Judith N. Mandl1Judith N. Mandl2Caitlin Schneider3Caitlin Schneider4David S. Schneider5Michelle L. Baker6Department of Physiology, McGill University, Montreal, QC, CanadaDepartment of Microbiology and Immunology, McGill University, Montreal, QC, CanadaMcGill Research Center for Complex Traits, McGill University, Montreal, QC, CanadaDepartment of Microbiology and Immunology, McGill University, Montreal, QC, CanadaMcGill Research Center for Complex Traits, McGill University, Montreal, QC, CanadaDepartment of Microbiology and Immunology, Stanford University, Stanford, CA, United StatesAustralian Animal Health Laboratory, Health and Biosecurity Business Unit, Commonwealth Scientific and Industrial Research Organisation, Geelong, VIC, AustraliaA 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.https://www.frontiersin.org/article/10.3389/fimmu.2018.02112/fullbats (Chiroptera)viral immunologyhost pathogen interactiondisease tolerancecomparative genome analysesinnate immunity
collection DOAJ
language English
format Article
sources DOAJ
author Judith N. Mandl
Judith N. Mandl
Judith N. Mandl
Caitlin Schneider
Caitlin Schneider
David S. Schneider
Michelle L. Baker
spellingShingle Judith N. Mandl
Judith N. Mandl
Judith N. Mandl
Caitlin Schneider
Caitlin Schneider
David S. Schneider
Michelle L. Baker
Going to Bat(s) for Studies of Disease Tolerance
Frontiers in Immunology
bats (Chiroptera)
viral immunology
host pathogen interaction
disease tolerance
comparative genome analyses
innate immunity
author_facet Judith N. Mandl
Judith N. Mandl
Judith N. Mandl
Caitlin Schneider
Caitlin Schneider
David S. Schneider
Michelle L. Baker
author_sort Judith N. Mandl
title Going to Bat(s) for Studies of Disease Tolerance
title_short Going to Bat(s) for Studies of Disease Tolerance
title_full Going to Bat(s) for Studies of Disease Tolerance
title_fullStr Going to Bat(s) for Studies of Disease Tolerance
title_full_unstemmed Going to Bat(s) for Studies of Disease Tolerance
title_sort going to bat(s) for studies of disease tolerance
publisher Frontiers Media S.A.
series Frontiers in Immunology
issn 1664-3224
publishDate 2018-09-01
description 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.
topic bats (Chiroptera)
viral immunology
host pathogen interaction
disease tolerance
comparative genome analyses
innate immunity
url https://www.frontiersin.org/article/10.3389/fimmu.2018.02112/full
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