Evidence map›Paper›PMID 42509362›Full record

ArticleCurrent microbiology2026

Transcriptional Profiling of Hypo- and Hypervirulent Mycobacterium tuberculosis Isolates Characterised by Differential Expression of the Moa3 Operon.

Jon Mitchell Ambler, Matthys Gerhardus Potgieter, Marisa Klopper, Melanie Grobbelaar, Margaretha De Vos, Samantha Sampson, Robin Mark Warren, Jonathan Blackburn, Nicola Mulder

Abstract read
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Article in Current microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Jon Mitchell AmblerDepartment of Integrative Biomedical Sciences, Institute of Infectious Disease & Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Western Cape, 7925, Cape Town, South Africa. jambler24@gmail.com.
Matthys Gerhardus PotgieterDepartment of Integrative Biomedical Sciences, Institute of Infectious Disease & Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Western Cape, 7925, Cape Town, South Africa.
Marisa KlopperSouth African Medical Research Council Centre for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, Western Cape, 7602, South Africa.
Melanie GrobbelaarSouth African Medical Research Council Centre for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, Western Cape, 7602, South Africa.
Margaretha De VosSouth African Medical Research Council Centre for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, Western Cape, 7602, South Africa.
Samantha SampsonSouth African Medical Research Council Centre for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, Western Cape, 7602, South Africa.
Robin Mark WarrenSouth African Medical Research Council Centre for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, Western Cape, 7602, South Africa.
Jonathan BlackburnDepartment of Integrative Biomedical Sciences, Institute of Infectious Disease & Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Western Cape, 7925, Cape Town, South Africa.
Nicola MulderDepartment of Integrative Biomedical Sciences, Institute of Infectious Disease & Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Western Cape, 7925, Cape Town, South Africa. nicola.mulder@uct.ac.za.ORCID http://orcid.org/0000-0003-4905-0941

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite advances in tuberculosis treatment and prevention, tuberculosis remains a global health threat, responsible for an estimated 1.23 million deaths in 2024 [46], with continued concern over drug-resistant strains. In the Western Cape, South Africa, co-infection of tuberculosis and HIV is a significant public health concern contributing to a higher burden of disease. We compared the transcriptomes of two genetically similar Beijing family strains of Mycobacterium tuberculosis under four different growth conditions, including oxidative stress, using three biological replicates for each isolate. We identified an operon containing genes involved in the biosynthesis of molybdenum cofactor that showed consistently lower levels of expression in the hypervirulent isolate. This pathway is known to play a critical role in numerous metabolic and redox processes, and its dysregulation could contribute to the observed differences in disease severity between the two isolates. The moa genes, which are involved in the biosynthesis of the molybdenum cofactor, have been previously linked to M. tuberculosis virulence through their essential role in redox metabolism and oxidative stress response. Our results support this hypothesis by identifying differential expression of the moa operon as a potential mechanism underlying the differences in disease severity between the two isolates. Furthermore, the minimal genetic differences between these isolates make them an ideal system for further study of this pathway and its contributions to tuberculosis pathogenesis.

Indexed as

Bacterial ProteinsGene Expression ProfilingGene Expression Regulation, BacterialMetalloproteinsMycobacterium tuberculosisOperonTuberculosisCoenzymesHumansMolybdenum CofactorsOxidative StressPteridinesSouth AfricaVirulenceBacterial ProteinsCoenzymesMetalloproteinsMolybdenum CofactorsmolybdopterinPteridines

Identifiers

PMID42509362
PMCPMC13407613

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