Rachel E. Simmonds

This paper develops a mathematical model to study the dynamics of Buruli ulcer formation, showing that mycolactone concentration and bacterial diffusion rates influence wound expansion speed.

The paper shows that mycolactone disrupts lysosome function by inhibiting Vacuolar-ATPase biosynthesis through Sec61 inhibition, leading to proteostatic stress and impaired phagocytic response to M. ulcerans.

This study investigates how blocking the Sec61 translocon with mycolactone affects the production of enveloped viruses, finding that some viruses resist this inhibition early in infection.