Dr. Marcel A. Behr, MD, M.Sc., FRCPC
McGill University Health Centre
1001 boul Décarie
Glen Block E, Office #EM3.3212
Montréal, QC H4A 3J1 Canada
Phone: 514 934-1934 (42815)
email: marcel.behr [at] mcgill.ca
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 is the Associate Program Leader of the Infectious Diseases and Immunity in Global Health Program at the Research Institute of the McGill University Health Centre since 2016 and in 2017 he became the co-Director the McGill Interdisciplinary Initiative in Infection and Immunity (McGill-i4). He is the interim director of 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:
- M. tuberculosis evolution. We used genomic approaches to define the micro-evolution of the M. tuberculosis complex (Mostowy et al, Journal of Infectious Diseases, 2002, cited 292 times) and M. bovis BCG vaccines (Mostowy and Behr et al, Vaccine, 2003, cited 134 times). We then used multi-locus sequence analysis to derive a genus-level appreciation of the macro-evolution of M. tuberculosis from related non-tuberculous mycobacteria (Veyrier, BMC Evolutionary Biology, 2009, reviewed in Veyrier et al, 2011, Trends in Microbiology). This work led to the genomic comparison of M. tuberculosis with the environmental species M. kansasii, revealing both genomic conservation across the species and candidates to explain the phenotypic differences (Wang et al, Genome Biology and Evolution, 2015)
- Mycobacterium avium genomics. Using multi-locus sequence analysis, we derived a phylogeny of this diverse group of organisms, 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 genome of M. avium paratuberculosis (Alexander et al, J. Bacteriology, 2009) and study their role in the micro-evolution of this subspecies (Wang et al, J. Bacteriology, 2016). Our appreciation of the species was captured in a comprehensive review (Turenne et al, Clin Micro Reviews, 2007, cited 235 times). This work also enabled me to assemble a team to produce the first text book of paratuberculosis since 1913 (Behr & Collins, Paratuberculosis: Organism, Disease, Control - published by CAB International, 2010).
- NOD2 and mycobacterial infection. We showed that NOD2 mediates host resistance to mycobacterial infection, using ex vivo and in vivo studies of Nod2-/- mice during pulmonary mycobacterial infection (Divangahi et al, J. Immunology, 2008). In this work, we showed that NOD2 not only mediates innate recognition of mycobacteria, but also instructs mycobacteria-specific adaptive immune responses. We showed that this effect is systemic, as a similar phenotype was observed whether the mycobacteria were delivered into the lungs or via intramuscular injection. This paper has been cited 211 times in a variety of journals, including the New England Journal of Medicine and Nature Immunology.
- NOD2 and N-glycolyl muramyl dipeptide (MDP). Using a ‘genetics squared’ approach, we showed that NOD2-dependent immune recognition depends on the presence of the bacterial NamH enzyme which converts N-acetyl MDP into the unusual molecule N-glycolyl MDP. The N-glycolyl MDP was shown to be more potent and more efficacious at inducing classical NOD2-dependent responses (Coulombe et al, J. Exp Med, 2009). This first paper used the model organism M. smegmatis and has been cited 163 times in journals such as Science, Ann Rev Immunol, Immunity, etc. More recently, we confirmed these findings in an independent set of experiments using the pathogen M. tuberculosis (Hansen et al, JID, 2013). Together these papers indicate that NOD2 is exquisitely tuned to recognition of mycobacterial peptidoglycan.
- TB molecular epidemiology. Using genotyping tools, such as RFLP, MIRU and spoligotyping, we described three vastly different epidemiologic situations in Quebec, Canada. In Montreal, the majority of TB is reactivation disease from over 80 countries (Kulaga et al, CMAJ, 2002), providing a snapshot of the global strain diversity of M. tuberculosis (Reed et al, JCM, 2009, cited 178 times). In rural Quebec, there is a founder strain of M. tuberculosis that causes false-positive genotypic matching due to shared ancestry rather than transmission (Nguyen et al, JCM, 2003). This founder strain spread with the Fur Trade, explaining its presence in rural settings of Western Canada (Pepperell et al, PNAS, 2011). In Nunavik, there is an extremely high degree of strain sharing, indicative of ongoing transmission within villages of a single bacterial clone introduced in the early 20th century (Nguyen et al, AmJRCCM, 2003; Lee et al, JID, 2015; Lee et al, PNAS, 2015).