The principal aim of this work is to try to understand why the range of experience with respect to HIV infection is so diverse. Hence, why does one individual experience a long latency period (or relatively low success of antipathetic mutation) compared to another.
The answer, it is felt, lies in the priming and level of fitness of the immune response of the individual and the various factors which influence this. If such "priming patterns" can be recognised, even anticipated, then in the long term we may have a way of typing and intervening for the individual. Unfortunately, understanding how the immune system is "imprinted" by experience of antigenic invasion and diversity is not straightforward. What assumptions can we make about the nature of this that can be modelled, tested, argued and what is the best way to grow a picture of the cell interactions and see how the endpoints might arise. What exactly is involved in antigenic diversity? How variable is the mutation rate and the viral load? What is the importance of cell mobility and how realistic is this in terms of cross-infection and sub-system involvement? How important then is the cross-reactivity?
To investigate these questions an agent-based approach is used. A large-scale, parallel, implementation is necessary, to explicitly account for lymph nodes and the connection between these. Simulations with hundreds of lymph nodes and more than one billion immune cells permit investigation of localised effects such as early HIV infection in the GI tract.
This work was mainly carried out during my Ph.D., supervised by
Prof. Heather J. Ruskin and
Dr. Martin Crane.
For the latest details on this work, please refer to the publication list. Alternatively, you may also contact me directly.
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