I am an Assistant professor at Infection disease biology at LSHTM and hold an honorary position at Welcome Sagner Institute.
My current main focus is understanding the fundamental biology of Treponema pallidum subps. pallidum, the infectious agent of syphilis. Supported by an ERC Starting Grant, my group aims to advance our understaing of T. palldium pathogenisis while bridging basic and clinical research with the goal to inform future syphilis vaccine development.

Treponema pallidum (TP), the causative agent of syphilis, along with other pathogenic spirochetes, forms a distinct evolutionary clade with unique features, including periplasmic endoflagella, minimal genomes, and outer membranes lacking lipopolysaccharides. These features enable TP to navigate viscous environments, breach biological barriers, and evade host immune responses, leading to syphilis, which affects over 7 million people globally each year, including 1 million pregnant women, and causes 200,000 stillbirths annually, making it the second leading cause of stillbirths after malaria.

Research on TP is hindered by its dependence on host cells for growth, complicating in vitro cultivation and leaving critical questions unanswered. We are addressing these gaps by unraveling TP's distinctive biology and host interactions, using multi-omics approaches and cutting-edge techniques like spatial transcriptomics. Specifically, we are focusing on TP's host dependencies to optimize axenic (cell-free) culture conditions. We are also interested in TP adhesins and are characterizing their roles in attachment and the cell cycle, positioning them as prime vaccine candidates to block infection at its earliest stage. Finally, we are optimizing and establishing infection models for syphilis, such as foreskin explants to understand the initiation of infection and placental explants to understand how TP crosses the placental membrane. These models will allow us to investigate host–pathogen interactions in settings that closely mimic human disease.