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in fitness between these viral phenotypes may allow other factors to tip the balance
in favor of X4 virus and help explain why in about 50% of patients the viral phe-
notype switches from R5 to X4 late in infection (Mosier 2000).
Acknowledgements
I thank the Discipline of Genetics and the School of Molecular and Biomedical Sci-
ence, University of Adelaide, for support, and the South Australian Partnership for
Advanced Computing (SAPAC) for access to high-performance computing resources.
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