We are developing precision molecular tools to study how pathogenic bacteria survive and infect, enabling the design of new antimicrobial therapies.
As soon as new antimicrobial drugs are discovered and used in the clinic, pathogenic bacteria inevitably evolve resistance, driving an unsustainable cycle threatening the twentieth century's improvements to public health.
Antibiotics revolutionised modern medicine, but once again millions of lives are threatened by pathogenic bacteria like M. tuberculosis, which causes tuberculosis, the deadliest infectious disease and one of the top 10 causes of death worldwide.
Working at the interface of genetics, chemistry, and machine learning, we use chemical 'probes' to systematically and precisely disrupt the cellular machinery of M. tuberculosis and study the consequences of this disruption on its ability to survive, infect, and resiliently evolve resistance.
With this approach, we seek to bridge the gap between understanding pathogen biology and designing new therapeutic strategies.