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Peer reviewedOpen accessTuberculosisHIV infectionAIDS

Population-level genome sequencing reveals distinct Mycobacterium tuberculosis intrahost mutational trajectories in simian immunodeficiency virus-coinfected and antiretroviral treated non-human primates

mSystems·

Michael C. Chao, Michael R. Chase, Shoko Wakabayashi, Andrew J. Vickers, Byron Roman, Forrest Hopkins, Peter H. Culviner, Maximillian G. Marin, Pauline Maiello, Collin R. Diedrich, Zandrea Ambrose, Philana Ling Lin, Qingyun Liu, Sarah M. Fortune

DOI
10.1128/msystems.00329-26
PMID
42505123
PMCID
OpenAlex
W7171470455
Study type
Journal article
Publisher
American Society for Microbiology
Article type
journal-article
Integrity
current

Why this research matters now

The abstract frames the work in relation to tuberculosis and HIV coinfection, noting that TB remains a major cause of mortality, particularly among people living with HIV. The study may be relevant to understanding pathogen evolution under immune and treatment-related pressures, but the supplied evidence is from a non-human primate model rather than a clinical intervention study.

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Structured evidence summary

Research question

The article asks how Mycobacterium tuberculosis changes genetically within hosts during infection, particularly under simian immunodeficiency virus coinfection and antiretroviral treatment in a non-human primate model.

Study design

The study used whole-genome sequencing of M. tuberculosis populations from infected tissue samples. The abstract describes 477 tissues from 20 non-human primates, with comparison across SIV coinfection and antiretroviral treatment conditions.

Population and setting

The setting was an experimental non-human primate model of tuberculosis infection. The sampled population included animals with M. tuberculosis infection, including groups with SIV coinfection and groups receiving antiretroviral therapy with virological suppression.

Main findings

The authors report 116 mutations arising during infection, including tissue-enriched mutations and mutations appearing across multiple tissues during dissemination. They describe differing mutational patterns by treatment group, including greater mutation frequency and bacterial expansion in SIV-infected hosts and more oxidative damage-associated mutations in coinfected animals receiving ART. They also report recurrent involvement of lipid metabolism and polyketide synthase genes, with some primate-derived mutations also observed independently in human clinical isolates.

Public-health relevance

The abstract frames the work in relation to tuberculosis and HIV coinfection, noting that TB remains a major cause of mortality, particularly among people living with HIV. The study may be relevant to understanding pathogen evolution under immune and treatment-related pressures, but the supplied evidence is from a non-human primate model rather than a clinical intervention study.

Important limitations

The summary is limited to the supplied single-article abstract and metadata and requires the original paper for decision-grade interpretation. Directly evident constraints include use of a non-human primate model and a sample of 20 animals, so applicability to human disease cannot be established from the supplied abstract alone.

GIDS interpretation

For discoverability, this article is indexed around tuberculosis, HIV/AIDS, and treatment-related context, with emphasis on pathogen genomics and coinfection. It should be treated as single-article literature evidence only, not as confirmation of any surveillance signal.

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Related GIDS surveillance

Literature context does not validate, explain, or change a surveillance signal. Exact and contextual relationships are shown separately.

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Evidence relationships

This article has 6 auditable classifier relationships to diseases, places, topics, and study design.

about diseaseaddresses topicevaluates interventionhas pathogen typestudied population settinguses study design