Abstract
We introduce and analyze a within-host dynamical model of the coevolution between rapidly mutating pathogens and the adaptive immune response. Pathogen mutation and a homeostatic constraint on lymphocytes both play a role in allowing the development of chronic infection, rather than quick pathogen clearance. The dynamics of these chronic infections display emergent structure, including branching patterns corresponding to asexual pathogen speciation, which is fundamentally driven by the coevolutionary interaction. Over time, continued branching creates an increasingly fragile immune system, and leads to the eventual catastrophic loss of immune control.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Adaptive Immunity / immunology
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Algorithms
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Biological Evolution*
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Host-Pathogen Interactions / immunology
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Humans
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Immune System / immunology*
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Immune System / microbiology
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Immune System / parasitology
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Infections / immunology*
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Infections / microbiology
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Infections / parasitology
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Models, Immunological
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T-Lymphocytes / immunology*
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T-Lymphocytes / microbiology
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T-Lymphocytes / parasitology
Grants and funding
This material is based upon work supported by the David and Lucile Packard Foundation (
http://www.packard.org), the Office of Naval Research (
http://www.onr.navy.mil) MURI grants N000140810747 and 0001408WR20242, the Institute for Collaborative Biotechnologies (
http://icb.ucsb.edu) through grant W911NF-09-0001 from the U.S. Army Research Office, and the National Science Foundation (
http://www.nsf.gov) Graduate Research Fellowship Program under Grant No. DGE-1144085. The content of the information does not necessarily reflect the position or the policy of the Government, and no official endorsement should be inferred. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.