I am a viral immunologist by training. My research has focused on cytoplasmic mechanisms that detect and inactivate viruses shortly after their entry to the cell. From 2009 to 2017 I worked at the MRC Laboratory of Molecular Biology in Cambridge, UK, where I co-discovered and characterised the novel Fc receptor TRIM21 as a potent antiviral sensor in the group of Dr Leo James. In recent years I have asked whether the spread of misfolded proteins involved in neurodegeneration can be prevented using the same mechanisms that operate against viruses.
Post-doctoral research associate
I have been interested in neurodegeneration from my MSc, and following on from myPhD, I knew that I wanted to focus my career on understanding the mechanisms of neurodegeneration. I carried out my PhD at the Babraham Institute, where I worked on the interaction between GIMAP6, a member of a family of small GTPases that play a role in maintaining lymphocyte populations, and GABARAPL2, an Atg8 homologue. This gave me an insight into autophagy and aspects of cell biology and equipped me for work in the Seaman group, which is based in the Cambridge Institute for Medical Research. Here I was given the opportunity to work on analysing the role endosome-to-Golgi trafficking plays in the trafficking and processing of the amyloid precursor protein and I have identified an important role for PLD3 in this process. Following on from this project, I was keen to broaden my knowledge of neurodegeneration further, and to this end, my project in the McEwan lab will focus on investigating the mechanisms via which TRIM21 can degrade antibody-bound aggregates in animal models of disease with the aim of uncovering the implications this has for various neurodegenerative disorders.