The CTL response plays a central part in deciding the outcome of viral infections. Evidence from host and viral genetics, gene expression microarrays and assays of T‐cell phenotype and function indicate that individual differences in the efficiency of the virus‐specific CTL response strongly determine the outcome of infection with the human retroviruses HTLV‐1 and HIV‐1. It is now believed that differences in anti‐viral CTL efficiency or “quality” at the single‐cell level are critical in determining the efficacy of the host response to viruses. However, it is difficult to identify and quantify the reasons for this apparent individual variation in CTL efficiency, because of the chronic course of infection and the dynamical complexity of the equilibrium that is established between the virus and the host immune response. Specifically, it is unclear whether the observed variations among infected hosts, i.e. in the frequency, phenotype and function or quality of T cells, are the causes or effects – or both – of the variation in the efficiency of virus control.