We develop a description of HIV mutations based upon a continuum representation of the fitness of the virus, including the interaction of the virus with both specific Th1 lymphocytes as well as cross-reactive cells. This deterministic model allows a straightforward measure of the diversity of viral population and reproduces the observed increase in diversity as the disease progresses in an untreated patient. We use the diversity threshold theory, extending the modelling to track mutations on a continuum. When the diversity threshold is exceeded, the host immune system collapses.