title: Anti-CD4 therapy for AIDS suggested by mathematical models.
abstract: 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.
authors: Theoretical Biology, Utrecht University, The Netherlands.
authors: R J
authors: RJ
authors: De Boer
authors: C A
authors: CA
authors: Boucher
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000276:immunology* / Q000628:therapy*; D015703:Antigens, CD / Q000276:immunology*; D000998:Antiviral Agents / Q000627:therapeutic use; D015704:CD4 Antigens / Q000276:immunology*; D018791:CD4 Lymphocyte Count; D015497:HIV-1; D006790:Host-Parasite Interactions; D006801:Humans; D019259:Lamivudine; D008962:Models, Theoretical; D016047:Zalcitabine / Q000031:analogs & derivatives / Q000627:therapeutic use
chemical_list: D015703:Antigens, CD; D000998:Antiviral Agents; D015704:CD4 Antigens; D019259:Lamivudine; D016047:Zalcitabine