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This paper develops a predictive mathematical model of cell infection, host immune response and viral replication that reproduces observed long-term trends in human immunodeficiency virus (HIV) pathogenesis. Cell activation induced by repeated exposure to many different antigens is proposed as the principal mechanism of providing target cells for HIV infection and, hence, of CD4+ T cell depletion, with regulation of the overall T cell pool size causing concomitant CD8 pool increases. The model correctly predicts the cross-patient variability in disease progression, the rate of which is found to depend on the efficacy of anti-HIV cytotoxic T lymphocyte responses, overall viral pathogenicity and random effects. The model also predicts a variety of responses to anti-viral therapy, including episodic residual viral replication and discordant responses and we find that such effects can be suppressed by increasing the potency of treatment.

Original publication




Journal article


Proceedings. Biological sciences

Publication Date





2085 - 2095


Department of Infectious Disease Epidemiology, Imperial College of Science, Technology and Medicine, St Mary's Campus, Norfolk Place, Paddington, London W2 1PG, UK.


T-Lymphocytes, Cytotoxic, Humans, HIV-1, HIV Infections, Antigens, Anti-HIV Agents, Viral Load, Models, Biological, Time Factors