Sir Henry Dale Fellow, Group Leader
Statistical genomics of host pathogen interactions
I am a group leader at the Experimental Medicine Division of Nuffield Department of Medicine. I received my undergraduate degree in Engineering in 2009 and a DPhil in Statistical Genetics from the University of Oxford in 2014. I was awarded a Royal Society and Wellcome Trust Sir Henry Dale Fellowship in 2020 to start my independent research career.
My main research focus is understanding host pathogen interactions using genetic data and developing statistical methods to integrate heterogeneous sources of data in infectious diseases. Traditionally, genetic studies of infectious diseases have sought to explain between-individual variation in disease phenotypes by assessing genetic factors separately in humans or pathogens, under the assumption that these factors are independent. Although reasonable for some variants, there is strong evidence that genetic interactions between host and viruses play a major role in viral disease aetiology. My aim is to integrate host and viral genomic data from the same patients to better understand viral pathogenesis and between-individual heterogeneity in disease outcomes. We are generating and analysing paired host-virus genomic data from large and well-characterised HBV, HCV and HIV infected cohorts and will investigate (a) host polymorphisms linked with viral sequence variation, (b) virus sites under strong host genetic selective pressures, (c) host and virus genetic factors independently contributing to disease phenotypes and (d) host-virus genetic interactions contributing to disease phenotypes.
My research is interdisciplinary, and I am interested in a wide range of subjects. Methodology and application areas include: Statistical Genetics, Bayesian Statistics, Machine Learning, Population Genetics, Bioinformatics, Immunology, Pathogen Evolution, Microbiology and Host-Pathogen Interaction.
For an up-to-date and full list of my publication please visit my Google Scholar page.
T cell assays differentiate clinical and subclinical SARS-CoV-2 infections from cross-reactive antiviral responses
Ogbe A. et al, (2021), Nature Communications, 12
Risk of Reactivation of Hepatitis B Virus (HBV) and Tuberculosis (TB) and Complications of Hepatitis C Virus (HCV) Following Tocilizumab Therapy: A Systematic Review to Inform Risk Assessment in the COVID-19 Era
Campbell C. et al, (2021), Frontiers in Medicine, 8
Using host genetics to infer the global spread and evolutionary history of HCV subtype 3a
Lin S-K. et al, (2021), Virus Evolution
Divergent trajectories of antiviral memory after SARS-Cov-2 infection
Tomic* A. et al, (2021)
High cure rates for HCV genotype 6 in advanced liver fibrosis with 12 weeks sofosbuvir and daclatasvir: The Vietnam SEARCH Study
Flower B. et al, (2021), Open Forum Infectious Diseases