Group | Tuberculosis Ecology and Evolution

The Tuberculosis Ecology and Evolution Group studies the causes and consequences of genetic diversity in the Mycobacterium tuberculosis complex (MTBC), the bacteria that cause tuberculosis (TB). We combine various disciplines to study 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.

Our research comprises three complementary arms:

  • The global population structure of the MTBC
  • Ecology and evolution of drug-resistant MTBC
  • Genomic epidemiology of TB

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

The 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

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

Cox H et al. Whole genome sequencing has the potential to improve treatment for rifampicin-resistant tuberculosis in high burden settings: a retrospective cohort study. J Clin Microbiol. 2022;60(3):e0236221. DOI: 10.1128/jcm.02362-21

Hiza H et al. CD38 expression by antigen-specific CD4 t cells is significantly restored 5 months after treatment initiation independently of sputum bacterial load at the time of tuberculosis diagnosis. Front Med. 2022;9:821776. DOI: 10.3389/fmed.2022.821776

Maghradze N et al. Developing customized stepwise MIRU-VNTR typing for tuberculosis surveillance in Georgia. PLoS One. 2022;17(3):e0264472. DOI: 10.1371/journal.pone.0264472

Merker M et al. Transcontinental spread and evolution of Mycobacterium tuberculosis W148 European/Russian clade toward extensively drug resistant tuberculosis. Nat Commun. 2022;13:5105. DOI: 10.1038/s41467-022-32455-1

Van Rie A et al. Balancing access to BPaLM regimens and risk of resistance. Lancet Infect Dis. 2022;S1473-3099(22):00543-6. DOI: 10.1016/S1473-3099(22)00543-6