A Mathematical Model for the Treatment of Aids-Related Kaposi'S Sarcoma

We formulate a mathematical model to study the dynamics of HIV-1 related Kaposi's Sarcoma (KS) pathogenesis. KS progression is modeled as a dual process involving the primary infection of B cells, which sustains HHV-8 replication and the secondary infection of progenitor cells by HHV-8, which sustains the KS cell replication. We incorporate the pharmacodynamics of highly active antiretroviral therapy (HAART), or combination therapy (HAART plus KS therapy) and consider how each treatment strategy alters the disease progression. Our results indicate that administration of HAART to individuals co-infected with the HIV-1 and HHV-8 viruses can greatly amplify the therapeutic response of low-dose KS therapies. We have found that adherence levels above 85% can significantly reduce the risk of KS and HIV for a treatment periods under 1 year. For longer treatment periods, however, at least 90% adherence level is recommended.