As an infection immunologist, my research focuses on understanding how pathogens and our immune system interact and affect each other.
During my PhD at Imperial College London, I integrated my expertise in M.tuberculosis (Mtb)-infection with the remit of the Tuberculosis Research Centre to develop a research programme combining human ex vivo sampling with in vitro cell culture models to decipher determinants of susceptibility to Mtb-infection. I established primary epithelial culture models and identified a key role for airway epithelium in the innate immune response to Mtb mediated by cross-talk with infected human macrophages.

In Prof Clare Jolly’s lab at UCL, I dissect host pathogen interactions between pandemic viruses and their target cells with a focus on HIV-1 and SARS-CoV-2:

HIV-1 infection drives resting T cell plasticity:

HIV-1 remains a major global health burden. Determining how HIV-1 shapes the immunological niche in which it resides to create a permissive environment is central to informing efforts to limit pathogenesis, disturb viral reservoirs and ultimately achieve cure. I have overcome a key roadblock in understanding HIV-T cell interactions by showing that resting memory T cells, which are refractory to cell-free infection, are highly permissive to infection mediated by cell-to-cell spread. Furthermore, I was able to show that during resting memory T cell infection, HIV-1 employs Vpr to reprogram the infected target cell might contribute to viral persistence. We now exploit this system to interrogate whether further native interactions between HIV-1 and resting CF4+ T cells, as they remain poorly understood.

Evolution of SARS-CoV-2 innate antagonism:
Since the start of the SARS-CoV-2 pandemic in 2020, a series of locally and globally dominant lineages, or variants of concern (VOCs), have emerged. Mutations and host adaptation in SARS-CoV-2 VOCs reflect selective pressures on the virus to adapt to its new host. By evolving the ability to potently evade innate and adaptive immune responses, barriers to infection and viral replication, variants increase their potential to transmit from host to host.
I have redirected my expertise and skills in molecular virology and airway epithelial biology to uncover how SARS-CoV-2 engages with the host innate immune response during airway epithelial infection. As part of an ambitious team, I defined the mechanism of SARS-CoV-2 innate sensing by infected epithelial cells and determined the consequences for surrounding professional immune cells through cytokine-mediated signalling networks. We further discovered that Alpha, the first VOC, evolved enhanced innate antagonism by upregulating innate antagonists Orf6, N and Orf9b. Subsequent VOCs have independently evolved similar strategies to antagonise antiviral responses, showing that VOCs share common pathway of adaptation to combat human innate immunity. This work shows that spike and non-spike mutations act in concert to mediate efficient infection and evasion of host immune responses, determining viral success