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

Barbara Szomolay; Edward M. Lungu

doi:10.1142/S0218339014500247

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

Barbara Szomolay, Edward M. Lungu

Mathematics & Statistical Sciences

Research output: Contribution to journal › Article › peer-review

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Abstract

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.

Original language	English
Pages (from-to)	495-522
Number of pages	28
Journal	Journal of Biological Systems
Volume	22
Issue number	3
DOIs	https://doi.org/10.1142/S0218339014500247
Publication status	Published - Sept 1 2014

All Science Journal Classification (ASJC) codes

Ecology
Agricultural and Biological Sciences (miscellaneous)
Applied Mathematics

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abstract = "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.",

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AB - 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.

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

Abstract

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