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Please use this identifier to cite or link to this item: http://arks.princeton.edu/ark:/88435/dsp01xd07gs85z
Title: Modeling Hepatitis C Virus and Human Immunodeficiency Virus Coinfection and the Development of Hepatocellular Carcinoma
Authors: Renschler, Christine Kathryn
Advisors: Tarnita, Corina
Department: Ecology and Evolutionary Biology
Class Year: 2014
Abstract: Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) are the sources of two highly prevalent chronic viral infections. Shared routes of transmission make coinfection with these pathogens common. Since the introduction of highly active antiretroviral treatment (HAART), there has been a decrease in AIDS related deaths. As a result of increased life expectancy, coinfected individuals have more time to develop complications from HCV. In areas where HAART is available, chronic HCV infection has become a major threat to HIV infected individuals (Taylor et al., 2012). Studies have shown that the course of HCV is more aggressive under the conditions of coinfection. The main long-term effects of chronic HCV are ultimately cirrhosis and hepatocellular carcinoma (HCC). Recently, Chakrabarty & Murray (2012) created a model to examine the long-term course of HCV monoinfection to the development of HCC. Understanding the within-host dynamics of coinfection is crucial for designing treatment strategies. As an extension to their model, the model created for this study investigates the impact of coinfection with HIV on the development of HCC. The model consists of a deterministic ODE model that tracks the progress to equilibrium levels of infection, followed by a stochastic model that uses hepatocyte turnover to predict progression to hepatocellular carcinoma. Consistent with the literature, results show that the introduction
Extent: 45 pages
URI: http://arks.princeton.edu/ark:/88435/dsp01xd07gs85z
Type of Material: Princeton University Senior Theses
Language: en_US
Appears in Collections:Ecology and Evolutionary Biology, 1992-2016

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