HIV-1 infection typically involves a long clinical latency stage during which CD4 counts decline slowly. For the later part of the clinical latency stage it was found recently that this is a highly dynamic phase characterized by rapid turnover rates. Clinical latency can therefore be considered as a quasi-equilibrium state in which CD4 and HIV-1 turnover are in almost perfect balance. Here we consider this quasi-equilibrium to be the stable steady state of a simple host-parasite model in which the parasite (HIV-1) level is determined by the availability of infectable hosts (activated CD4+ T cells). Such models adequately account for the clinical data on the evolution of drug resistant mutants appearing after the administration of anti-HIV drugs. The model suggests a novel therapeutic approach for AIDS: reducing the CD4 count slightly will strongly reduce the HIV load. Combining this anti-CD4 treatment with conventional anti-HIV therapy would prevent the outgrowth of drug resistant mutants.