Humans are engaged in a non-stop evolutionary struggle with infectious diseases. I seek to understand how natural selection from pathogens has shaped human genetics. My research falls into two areas:
1. Malaria and the red blood cell
The genetic mutations responsible for a variety of human blood conditions - most famously sickle cell anaemia, but also the thalassaemias - make those who carry them less likely to die from malaria. We still do not understand exactly how this malaria protection works. Sickle cell and the thalassaemias are also public health concerns in their own right.
Various populations around the world have experienced malaria for many generations, and ended up with different profiles of malaria protective blood disorder genes. I use models to simulate the possible evolutionary histories behind such profiles. These models help me to understand how genetic blood conditions interact with one another and with the malaria parasite, and make predictions about mechanisms of malaria protection.
Our immune systems protect us from pathogens. A female immune system must also be capable of tolerating a foetus during pregnancy. Immune system genes known as HLAs and KIRs are critical to fighting infection, but there is evidence that they affect pregnancy too. I use mathematical models and computational simulations to understand interactions between HLAs, KIRs and pathogens. I intend to identify the genetic signatures of pathogen and reproductive selection on HLAs and KIRs, and to use models to help predict which genetic combinations lead to different health outcomes.
I am a member of the
Warwick Infectious Disease Epidemiology Research centre