On T-cell dynamics and the hyperactivation theory of AIDS pathogenesis.
In an earlier article the author proposed a model of T cell dynamics in which rising activation rates produced falling T-cell counts. Here I show that, in a model of this type, apoptosis and proliferation must nearly balance. Hence, small perturbations of these processes could have large consequences, a fact that may be relevant to AIDS pathogenesis. In addition, I show the model can reproduce all decay rates found by McLean and Michie for cells with radiation-induced chromosome damage, provided that stable damage can proliferate. Memory-cell 'amnesia' is not required. T-cell lifetimes come out much shorter than previously estimated.
Wick
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Fred Hutchinson Cancer Research Center, Seattle, WA 98104-2092, USA. wick@hivnet.fhcrc.org
D000163:Acquired Immunodeficiency Syndrome / Q000209:etiology / Q000276:immunology*; D017209:Apoptosis / Q000276:immunology; D002875:Chromosomes / Q000528:radiation effects; D006801:Humans; D007700:Kinetics; D016014:Linear Models; D008213:Lymphocyte Activation / Q000276:immunology; D018655:Lymphocyte Count; D018448:Models, Immunological; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000502:physiology