Mycobacterium tuberculosis complex

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The Mycobacterium tuberculosis complex (MTC or MTBC) is a genetically related group of Mycobacterium species that can cause tuberculosis in humans or other animals.

It includes:

In addition, two branches exist which have phylogenetic similarities but are not completely described: the dassie and oryx bacilli. Oryx bacilli has been recently reclassified into a separate subspecies, orygis.[1]

Members of the MTC can be distinguished from all other bacteria by the presence of 63 conserved signature indels (CSIs) present in diverse proteins that are exclusively shared by these pathogens.[4] Due to their exclusivity for the MTC complex and presence in highly conserved regions of proteins, these CSIs provide novel means for functional and diagnostic studies (including potential targets for development of novel therapeutics).[4]


PCR for detection of M. tuberculosis complex from clinical samples,lanes 1, 3, 5, 7 and 10 are positive samples

As MTBC diverged into different lineages, so did the expression of key and metabolic pathogenic genes, as a result of mutations introducing new TANNNT Pribnow boxes and mutations that impair the function of repressors Transcripcionales. This provides clear evidence that MTBC lineages probably reflect adaptation to different human populations. In fact, modifying gene expression could be a rapid mechanism for physiological adaptation to a new environment without the need to substantially change the genome.[5]

This can be seen reflected in the way that the different MTBC clades have their own transcriptomic signature. Even single-point mutations can completely change the transcriptional profile of a strain. An example is the N1177 strain, which carries a single mutation in the rpoB gene that confers resistance to rifampicin that modified transcription levels of multiple genes.[5]

The role of methylation is more elusive, the mutation inactivation pattern seems to confirm that methylases are not preserved throughout mtBC. Transcriptional adaptation can allow M. tuberculosis isolates to optimize their infectivity and transmission in subtly different environments provided by different human host populations.[5]

See also


  1. 1.0 1.1 van Ingen J, Rahim Z, Mulder A, Boeree MJ, Simeone R, Brosch R, van Soolingen D (April 2012). "Characterization of Mycobacterium orygis as M. tuberculosis complex subspecies". Emerging Infectious Diseases. 18 (4): 653–5. doi:10.3201/eid1804.110888. PMC 3309669. PMID 22469053.
  2. Patterson, S, Drewe, JA, Pfeiffer, DU, Clutton-Brock, TH (2017). "Social and environmental factors affect tuberculosis related mortality in wild meerkats". Journal of Animal Ecology. 86 (3): 442–450. doi:10.1111/1365-2656.12649. PMC 5413830. PMID 28186336.
  3. Vasconcellos SE, Huard RC, Niemann S, Kremer K, Santos AR, Suffys PN, Ho JL (March 2010). "Distinct genotypic profiles of the two major clades of Mycobacterium africanum". BMC Infectious Diseases. 10: 80. doi:10.1186/1471-2334-10-80. PMC 2859774. PMID 20350321.
  4. 4.0 4.1 Gupta, Radhey S. (2018-10-02). "Impact of Genomics on Clarifying the Evolutionary Relationships amongst Mycobacteria: Identification of Molecular Signatures Specific for the Tuberculosis-Complex of Bacteria with Potential Applications for Novel Diagnostics and Therapeutics". High-Throughput. 7 (4): 31. doi:10.3390/ht7040031. ISSN 2571-5135. PMC 6306742. PMID 30279355.
  5. 5.0 5.1 5.2 Chiner-Oms Á, Berney M, Boinett C, González-Candelas F, Young DB, Gagneux S, et al. (September 2019). "Genome-wide mutational biases fuel transcriptional diversity in the Mycobacterium tuberculosis complex". Nature Communications. 10 (1): 3994. Bibcode:2019NatCo..10.3994C. doi:10.1038/s41467-019-11948-6. PMC 6728331. PMID 31488832. Material was copied from this source, which is available under a Creative Commons Attribution 4.0 International License Archived 2017-10-16 at the Wayback Machine.