Reading immune restoration through Mycobacterium tuberculosis intrahost evolution
- 1Key Laboratory of Systems Health Science of Zhejiang Province, School of Life Science, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou, China
- 2Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing, China
Abstract
Antiretroviral therapy (ART) suppresses human immunodeficiency virus replication, but does not fully restore protection against tuberculosis. The relevant mechanisms are still poorly understood. M. C. Chao, M. R. Chase, S. Wakabayashi, A. J. Vickers, et al. (mSystems 11:e00329-26, 2026, https://doi.org/10.1128/msystems.00329-26) use population-level Mycobacterium tuberculosis genome sequencing in macaques to show that similar bacterial burdens can conceal different evolutionary trajectories: simian immunodeficiency virus coinfection primarily increases opportunities for mutation through replication, whereas ART-treated animals show a distinct enrichment of oxidative damage-associated variants. We argue that the principal value of this work is conceptual. Pathogen genomes may provide a time-integrated, but indirect, readout of local immune ecology. To translate these genomic signatures into a framework for evaluating immune restoration, future studies should pair host and pathogen measurements, experimentally validate the mechanisms generating these mutations, and longitudinally link tissue-level selection to persistence, reactivation, and transmission.
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BibTeX
@article{teng2026reading,
title = {{Reading immune restoration through Mycobacterium tuberculosis intrahost evolution}},
author = {Lin Teng and Guangzhi Zhang},
journal = {mSystems},
year = {2026},
month = sep,
doi = {10.1128/msystems.00953-26},
url = {https://doi.org/10.1128/msystems.00953-26},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Reading immune restoration through Mycobacterium tuberculosis intrahost evolution
AU - Lin Teng
AU - Guangzhi Zhang
PY - 2026
DA - 2026/09/22
JO - mSystems
DO - 10.1128/msystems.00953-26
UR - https://doi.org/10.1128/msystems.00953-26
AB - Antiretroviral therapy (ART) suppresses human immunodeficiency virus replication, but does not fully restore protection against tuberculosis. The relevant mechanisms are still poorly understood. M. C. Chao, M. R. Chase, S. Wakabayashi, A. J. Vickers, et al. (mSystems 11:e00329-26, 2026, https://doi.org/10.1128/msystems.00329-26) use population-level Mycobacterium tuberculosis genome sequencing in macaques to show that similar bacterial burdens can conceal different evolutionary trajectories: simian immunodeficiency virus coinfection primarily increases opportunities for mutation through replication, whereas ART-treated animals show a distinct enrichment of oxidative damage-associated variants. We argue that the principal value of this work is conceptual. Pathogen genomes may provide a time-integrated, but indirect, readout of local immune ecology. To translate these genomic signatures into a framework for evaluating immune restoration, future studies should pair host and pathogen measurements, experimentally validate the mechanisms generating these mutations, and longitudinally link tissue-level selection to persistence, reactivation, and transmission.
SN - 2379-5077
ER -