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During my PhD, I have been investigating the heritability of virulence in HIV. Though the influences of many host and environmental factors on viral load are well understood, the role of the viral genome itself in determining viral load is less clear.

I have adapted a well-established method from population genetics to more accurately estimate the heritability of viral load using a phylogeny of viral sequences. This method enables analysis on incredibly large datasets, and I have investigated the viral genetic contribution to viral load in subtypes B and C in the UK HIV epidemic, using 8,483 and 1,821 sequences, respectively.

I have also recently started my post-doctoral position as part of the PANGEA_HIV initiative, funded by the Bill and Melinda Gates Foundation. I have created a stochastic, agent-based model (DSPS-HIV) that simulates HIV epidemics, which I've used to generate data sets that can be used to assess phylogenetic methods. Disease stage and transmission risk are dependant on viral load, and contact networks are highly customizable.


Prior to starting my PhD, I participated in research on:

  • The link between vitamin D level and colo-rectal cancer stage in a genome-wide analysis study (GWAS) to look for an association between vitamin D level and SNPs on chromosome 16.
  • Evidence of adaptive selection in coding and non-coding genes in Drosophila. Adaptive substitution rates in coding regions and UTRs were analysed by tissue-specific, time-specific, and immune-related gene function.
  • Prey attraction and genetic variation between and within in four geographically separate populations of the carnivorous pitcher plant Sarracenia alata. (Poster presented at the Evolution 2010 Conference in Portland, Oregon.)

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