%0 Journal Article
%T Mathematical Modeling of the HIV/Kaposi¡¯s Sarcoma Coinfection Dynamics in Areas of High HIV Prevalence
%A E. Lungu
%A T. J. Massaro
%A E. Ndelwa
%A N. Ainea
%A S. Chibaya
%A N. J. Malunguza
%J Computational and Mathematical Methods in Medicine
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/753424
%X We formulate a deterministic system of ordinary differential equations to quantify HAART treatment levels for patients co-infected with HIV and Kaposi's Sarcoma in a high HIV prevalence setting. A qualitative stability analysis of the equilibrium states is carried out and we find that the disease-free equilibrium is globally attracting whenever the reproductive number . A unique endemic equilibrium exists and is locally stable whenever . Therefore, reducing to below unity should be the goal for disease eradication. Provision of HAART is shown to provide dual benefit of reducing HIV spread and the risk of acquiring another fatal disease for HIV/AIDS patients. By providing treatment to 10% of the HIV population, about 87% of the AIDS population acquire protection against coinfection with HIV and Kaposi's Sarcoma (KS). Most sub-Sahara African countries already have programmes in place to screen HIV. Our recommendation is that these programmes should be expanded to include testing for HHV-8 and KS counseling. 1. Introduction Kaposi's Sarcoma is a cancer that occurs mostly in humans with suppressed immune systems [1]. The development of this cancer depends upon prior infection to the human herpesvirus-8 (HHV-8) [2], a virus which is usually transmitted either sexually or via saliva [3]. For HIV-related Kaposi's Sarcoma development, immunosuppression is a necessary causal factor [2]. Because HIV is an immunosuppressive virus, it promotes the development of Kaposi's Sarcoma in individuals dually infected with both viruses (HIV and HHV-8) and this combination has proved to be fatal and has made Kaposi's Sarcoma the fourth largest killer of people living with HIV/AIDS in sub-Sahara Africa [4]. In competent immune systems, acquisition of HHV-8 does not guarantee the development of KS; in fact, most individuals with a strong immune response could remain latently infected with HHV-8 throughout their lifetime [2]. The HIV-1 growth factors stimulate the immune cells including the healthy and infected B-cells to proliferate. The activation of latently infected B-cells to proliferate only leads to production of more HHV-8 that, according to the theory proposed by Foreman et al. [2], may be responsible for infection of progenitor cells of endothelial origin, which once infected with HHV-8 develop into Kaposi's Sarcoma cells [2]. Recent research findings [12] show that highly active antiretroviral therapy (HAART) for HIV significantly decreases (and, in some instances, completely forces the cancer into remission) KS activity in a patient, but such treatment is only
%U http://www.hindawi.com/journals/cmmm/2013/753424/