Unit | Tuberculosis Ecology and Evolution

TB Research in the BSL3-Laboratory at Swiss TPH

Tuberculosis is an infectious disease caused by the bacterium Mycobacterium tuberculosis (Mtb), one of the deadliest pathogens known to humankind. In the Tuberculosis Ecology and Evolution Unit, we study the causes and consequences of genetic diversity in the Mycobacterium tuberculosis complex (MTBC).

Through the combined strengths of state-of-the-art BSL3 facilities, expert genomics capacity, and international collaborations, we’re equipped to investigate the fundamental biology of Mtb alongside the molecular epidemiology of TB across the world.

We focus on understanding the global diversity of the MTBC, the evolutionary forces that drive this diversity, and the phenotypic consequences of this diversity for the biology and the epidemiology of TB.

Main Research Areas of the Tuberculosis Ecology and Evolution Unit

The Global Population Structure of the MTBC

The human-adapted MTBC comprises seven phylogenetic lineages that are associated with different regions of the world. We use comparative whole genome sequencing to study the differences between these lineages and the evolutionary forces shaping this diversity. We combine various –omics technologies with functional assays and epidemiological data to investigate the phenotypic consequences of this diversity. Read more

Genomic epidemiology of TB

Recent advances in whole-genome sequencing have revolutionized molecular epidemiological investigation of TB. We use such genomic epidemiological approaches to study the transmission dynamics of TB in Switzerland and in TB-endemic countries. We also explore the micro-evolution of MTBC in individual patients during treatment. More information

Ecology and Evolution of Drug-Resistant MTBC

Drug resistance poses a growing threat to global health. When drug-resistant bacteria first emerge, they are often less transmissible than susceptible strains – this is because drug resistance in bacteria is often associated with a reduction in Darwinian fitness. However, evolution is a continuous process, and drug-resistant bacteria readily adapt and regain the ability to transmit. This process is mediated by compensatory mutations. Further information

Latest Publications

All Publications

Arbués A, Schmidiger S, Reinhard M, Borrell S, Gagneux S, Portevin D. Soluble immune mediators orchestrate protective in vitro granulomatous responses across Mycobacterium tuberculosis complex lineages. Elife. 2025;13. DOI: 10.7554/eLife.99062

Goig G.A et al. Transmission as a key driver of resistance to the new tuberculosis drugs. N Engl J Med. 2025;392(1):97-99. DOI: 10.1056/NEJMc2404644

Goig G.A et al. Ecology, global diversity and evolutionary mechanisms in the Mycobacterium tuberculosis complex. Nat Rev Microbiol. 2025(in press). DOI: 10.1038/s41579-025-01159-w

Koele S.E et al. Cardiac safety of bedaquiline, delamanid and moxifloxacin co-administered with or without varying doses of sutezolid or delpazolid for the treatment of drug-susceptible TB. J Antimicrob Chemother. 2025;80(8):2305-2313. DOI: 10.1093/jac/dkaf210

Maghradze N et al. Linking genetic and phenotypic bedaquiline resistance in Mycobacterium tuberculosis strains from Georgia. PLoS One. 2025;20(7):e0326794. DOI: 10.1371/journal.pone.0326794