Dr. Marcel A. Behr, MD, M.Sc., FRCPC
McGill University Health Centre
1001 boul Décarie
Glen Block E, Office #E05.1808
Montréal, QC H4A 3J1 Canada
Phone: 514 934-1934 (42815)
email: marcel.behr [at] mcgill.ca
Lab website: www.mcgill.ca/molepi
Infectious Diseases: https://www.mcgill.ca/infect-diseases/
MI4: https://www.mcgill.ca/mi4/
McGill TB Centre website: https://www.mcgill.ca/tb
IDIGH Program: https://idigh.ca/en/
Twitter: @mbehr_mcgill
Dr. Behr is a clinician-scientist with appointments of Full Professor in the Department of Medicine and Associate member in the departments of Epidemiology and Biostatistics as well as Microbiology and Immunology. He is the founding Director of the McGill International TB Centre and led it from 2012 to 2018. He was the Associate Program Leader of the Infectious Diseases and Immunity in Global Health Program at the Research Institute of the McGill University Health Centre from 2016 to 2023. In 2017 he became the co-Director the McGill Interdisciplinary Initiative in Infection and Immunity (MI4) and became its Director in late 2021. He is the Director of the McGill Infectious Diseases Division.
Dr. Behr trained at the University of Toronto, Queen’s, McGill and Stanford. His work has been recognized in Quebec (Chercheur National Award of the FRSQ), Canada (Joe Doupe Award of the Clinical Society for Clinical Investigation, Fellow of the Canadian Academy of Health Sciences and of the Royal Society of Canada) and beyond (Election to the American Society for Clinical Investigation and Fellow of the American Academy of Microbiology). Dr. Behr’s lab uses bacterial genetics to study the epidemiology and pathogenesis of mycobacterial diseases.
Most significant contributions:
Research in the Behr lab that employs bacterial genetic methods to study the epidemiology and pathogenesis of mycobacterial diseases. Our work has been cited ~ 25,000 times with an h-index of 80. Highlights include the following:
- Mycobacterium tuberculosis evolution. We used microarrays to define the micro-evolution of the M. tuberculosis complex (MTC) (Mostowy et al, JID, 2002) and M. bovis BCG vaccines (Mostowy et al, Vaccine, 2003). We then described the macro-evolution of M. tuberculosis from non-tuberculous mycobacteria (Veyrier, BMC Evolutionary Biology, 2009), such as M. kansasii (Wang, Genome Biology and Evolution, 2015). To reorient TB research, we imputed the ancestor of the M. tuberculosis complex (called MTBC 0 ) and shared this sequence through Tuberculist as the new ‘North Star’ for TB research (Harrison, Microbial Genomics, 2024).
- Mycobacterium avium. Using multi-locus sequence analysis, we derived a phylogeny of M. avium, revealing a mix of environmental organisms and pathogenic clones (Turenne et al, J. Bacteriology, 2008). This enabled us to identify horizontal gene transfer events that define the pathogen M. avium paratuberculosis (Alexander et al, J. Bacteriology, 2009). Our appreciation of the species was captured in a comprehensive review (Turenne et al, Clin Micro Reviews, 2007) and served as the basis for editing two reference textbooks on Paratuberculosis (2010, 2020).
- NOD2 and mycobacterial infection. We showed that NOD2 mediates innate and adaptive immune responses to mycobacterial infection (Divangahi et al, J. Immunology,
2008). Then, using a ‘genetics squared’ approach, we showed that NOD2-dependent immune recognition is tuned to the modified mycobacterial peptidoglycan, where the C2 position of muramic acid has an unusual N-glycolyl group instead of the typical N-acetyl moiety (Coulombe et al, J. Exp Med, 2009). N-glycolyl MDP is now commercially available through InvivoGen as an immunologic reagent. -
Tuberculosis molecular epidemiology. Using bacterial genotyping, our group has evaluated TB transmission over space and time. We tracked TB within a village that suffered a TB surge (Lee et al, JID, 2015) and characterized the evolution of that founder strain (Lee et al, PNAS, 2015). We demonstrated the importance of reinfection after treatment in South Africa (Verver, Am J Resp Crit Care Med, 2005). Our work showed that M. orygis (not M. bovis) is the cause of zoonotic TB in India (Duffy et al, Lancet Microbe, 2020), resulting in an updated WHO definition (https://doi.org/10.1016/S1473-3099(24)00180-4). These genomic epidemiology studies, complemented by historic literature, reinforced the importance of fast disease after infection (Behr et al, BMJ, 2018; BMJ, 2019) and led to the WHO changing its guidance on the global burden of M. tuberculosis infection (https://bit.ly/3UROiZF).
(updated June 2024)