Rapid adaptation to a novel pathogen through disease tolerance in a wild songbird
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F23%3A10466487" target="_blank" >RIV/00216208:11310/23:10466487 - isvavai.cz</a>
Result on the web
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=hW4xS9FHt" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=hW4xS9FHt</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1371/journal.ppat.1011408" target="_blank" >10.1371/journal.ppat.1011408</a>
Alternative languages
Result language
angličtina
Original language name
Rapid adaptation to a novel pathogen through disease tolerance in a wild songbird
Original language description
Author summaryWhen organisms encounter a novel pathogen, they can adapt to it in two ways: by killing the pathogen (known as resistance) or reducing the damage incurred while not directly killing the pathogen (known as disease tolerance). Although much work has focused on resistance, we understand less about how animals achieve disease tolerance or how quickly disease tolerance can evolve. Here we show that a wild bird species (the house finch) has evolved disease tolerance to a novel bacterial pathogen quickly (within similar to 20-25 years, at most similar to 15 generations). In house finches, this pathogen causes severe swelling around the eye and limits their ability to avoid predators. House finch populations that have evolved with this pathogen for longer are more tolerant to it; they show milder eye swelling even though they do not clear the pathogen any more efficiently than their less-tolerant counterparts. Moreover, tolerant finches have fewer immune genes that turn on in response to the infection, suggesting that a more-targeted immune response may facilitate tolerance. As disease tolerance can potentially help humans and animals adapt to new pathogens and also may change the way pathogens spread through animal populations, it is critical we understand how, and how quickly, tolerance evolves. Animal hosts can adapt to emerging infectious disease through both disease resistance, which decreases pathogen numbers, and disease tolerance, which limits damage during infection without limiting pathogen replication. Both resistance and tolerance mechanisms can drive pathogen transmission dynamics. However, it is not well understood how quickly host tolerance evolves in response to novel pathogens or what physiological mechanisms underlie this defense. Using natural populations of house finches (Haemorhous mexicanus) across the temporal invasion gradient of a recently emerged bacterial pathogen (Mycoplasma gallisepticum), we find rapid evolution of tolerance (<25 years). In particular, populations with a longer history of MG endemism have less pathology but similar pathogen loads compared with populations with a shorter history of MG endemism. Further, gene expression data reveal that more-targeted immune responses early in infection are associated with tolerance. These results suggest an important role for tolerance in host adaptation to emerging infectious diseases, a phenomenon with broad implications for pathogen spread and evolution.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
10602 - Biology (theoretical, mathematical, thermal, cryobiology, biological rhythm), Evolutionary biology
Result continuities
Project
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Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2023
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
PLoS Pathogens
ISSN
1553-7366
e-ISSN
1553-7374
Volume of the periodical
19
Issue of the periodical within the volume
6
Country of publishing house
US - UNITED STATES
Number of pages
21
Pages from-to
e1011408
UT code for WoS article
001004437500001
EID of the result in the Scopus database
2-s2.0-85164040743