This study characterizes the adaptive evolution of the zoonotic pathogen *Bordetella hinzii* within a patient with interleukin-12 receptor β1 deficiency. Genomic sequencing of 24 isolates revealed extensive within-host diversification, driven by an E96 substitution in the DNA polymerase III ε-subunit, causing proofreading deficiency. This led to mutations in DNA repair genes, altered mutational spectra, and metabolic adaptations. An excess of G:C > T:A transversions suggested oxidative stress. The study highlights the role of host immune phenotype in shaping pathogen evolution post-zoonotic infection.
Publisher
Nature Communications
Published On
Jul 23, 2021
Authors
A. Launay, C.-J. Wu, A. Dualanto Chiang, J.-H. Youn, P. P. Khil, J. P. Dekker
Tags
Bordetella hinzii
zoonotic pathogen
genomic sequencing
mutational spectra
oxidative stress
host immune phenotype
adaptive evolution
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