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Natural variation in host feeding behaviors impacts host disease and pathogen transmission potential
Animals ranging from mosquitoes to humans often vary their feeding behavior when infected or merely exposed to pathogens. These so‐called “sickness behaviors” are part of the innate immune response with many consequences, including avoiding orally transmitted pathogens. Fully understanding the role...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9992943/ https://www.ncbi.nlm.nih.gov/pubmed/36911315 http://dx.doi.org/10.1002/ece3.9865 |
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author | Pfenning‐Butterworth, Alaina C. Vetter, Rachel E. Hite, Jessica L. |
author_facet | Pfenning‐Butterworth, Alaina C. Vetter, Rachel E. Hite, Jessica L. |
author_sort | Pfenning‐Butterworth, Alaina C. |
collection | PubMed |
description | Animals ranging from mosquitoes to humans often vary their feeding behavior when infected or merely exposed to pathogens. These so‐called “sickness behaviors” are part of the innate immune response with many consequences, including avoiding orally transmitted pathogens. Fully understanding the role of this ubiquitous behavior in host defense and pathogen evolution requires a quantitative account of its impact on host and pathogen fitness across environmentally relevant contexts. Here, we use a zooplankton host and fungal pathogen as a case study to ask if infection‐mediated feeding behaviors vary across pathogen exposure levels and natural genetic variation in susceptibility to infection. Then, we connect these changes in behavior to pathogen transmission potential (spore yield) and fitness and growth costs to the host. Our results validate a protective effect of altered feeding behavior during pathogen exposure while also revealing significant variation in the magnitude of this response across host susceptibility and pathogen exposure levels. Across all four host genotypes, feeding rates were negatively correlated with susceptibility to infection and transmission potential. The most susceptible genotypes exhibited either strong anorexia, reducing food intake by 26%–42%, (“Standard”) or pronounced hyperphagia, increasing food intake by 20%–54% (“A45”). Together, these results suggest that infection‐mediated changes in host feeding behavior—which are traditionally interpreted as immunopathology— may in fact serve as crucial components of host defense strategies and warrant further investigation. |
format | Online Article Text |
id | pubmed-9992943 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-99929432023-03-09 Natural variation in host feeding behaviors impacts host disease and pathogen transmission potential Pfenning‐Butterworth, Alaina C. Vetter, Rachel E. Hite, Jessica L. Ecol Evol Research Articles Animals ranging from mosquitoes to humans often vary their feeding behavior when infected or merely exposed to pathogens. These so‐called “sickness behaviors” are part of the innate immune response with many consequences, including avoiding orally transmitted pathogens. Fully understanding the role of this ubiquitous behavior in host defense and pathogen evolution requires a quantitative account of its impact on host and pathogen fitness across environmentally relevant contexts. Here, we use a zooplankton host and fungal pathogen as a case study to ask if infection‐mediated feeding behaviors vary across pathogen exposure levels and natural genetic variation in susceptibility to infection. Then, we connect these changes in behavior to pathogen transmission potential (spore yield) and fitness and growth costs to the host. Our results validate a protective effect of altered feeding behavior during pathogen exposure while also revealing significant variation in the magnitude of this response across host susceptibility and pathogen exposure levels. Across all four host genotypes, feeding rates were negatively correlated with susceptibility to infection and transmission potential. The most susceptible genotypes exhibited either strong anorexia, reducing food intake by 26%–42%, (“Standard”) or pronounced hyperphagia, increasing food intake by 20%–54% (“A45”). Together, these results suggest that infection‐mediated changes in host feeding behavior—which are traditionally interpreted as immunopathology— may in fact serve as crucial components of host defense strategies and warrant further investigation. John Wiley and Sons Inc. 2023-03-07 /pmc/articles/PMC9992943/ /pubmed/36911315 http://dx.doi.org/10.1002/ece3.9865 Text en © 2023 The Authors. Ecology and Evolution published by John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Pfenning‐Butterworth, Alaina C. Vetter, Rachel E. Hite, Jessica L. Natural variation in host feeding behaviors impacts host disease and pathogen transmission potential |
title | Natural variation in host feeding behaviors impacts host disease and pathogen transmission potential |
title_full | Natural variation in host feeding behaviors impacts host disease and pathogen transmission potential |
title_fullStr | Natural variation in host feeding behaviors impacts host disease and pathogen transmission potential |
title_full_unstemmed | Natural variation in host feeding behaviors impacts host disease and pathogen transmission potential |
title_short | Natural variation in host feeding behaviors impacts host disease and pathogen transmission potential |
title_sort | natural variation in host feeding behaviors impacts host disease and pathogen transmission potential |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9992943/ https://www.ncbi.nlm.nih.gov/pubmed/36911315 http://dx.doi.org/10.1002/ece3.9865 |
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