Models of Virus-Immune Dynamics and Drug Resistant Virus Infections

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dc.contributor.advisor Kevin Gross, Committee Member en_US
dc.contributor.advisor Charlie Smith, Committee Member en_US
dc.contributor.advisor Alun Lloyd, Committee Chair en_US Soberano, Lisa Albert en_US 2010-04-02T18:12:37Z 2010-04-02T18:12:37Z 2006-09-26 en_US
dc.identifier.other etd-05012006-010714 en_US
dc.description.abstract Models for the activity of a virus within a host describe the interaction between virus, the cells they infect and the attempts of the body's immune response to remove the infection. We aim to improve these models by incorporating more detailed, and more realistic, descriptions of the immune response. One particular application that is of interest involves the administration of drug treatment during acute infections, with the aim of understanding the dynamics of co-circulating wild-type and drug resistant viruses. Two models are presented that suggest improvements for the portrayal of the immune response. The first is based on existing basic infection models for acute viruses. The second is based upon recent experimental results show that a brief exposure to a pathogen can cause the CD8+ cytotoxic T lymphocytes (CTLs), of the immune system to undergo a programmed set of divisions, including sustained proliferation, giving rise to effector cells, which can kill infected cells, followed by the production and maintenance of memory cells. In the co-infection model of wild-type and drug resistant viruses, a target cell limited model is also used. Previous results suggested that the level of immune response maintained during therapy is the key to suppressing the peak load of resistant virus. Our results, however, suggest that suppression of a resistant strain is not solely dependent on the immune response, but also on the availability of target cells. A spatial virus-immune model is presented in an appendix, which allows multiple target regions within the host to be infected by one or more viruses. Another model is introduced which allows multiple viruses to infect the same target region, with immune specific responses to each virus. en_US
dc.rights I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to NC State University or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. en_US
dc.subject drug resistant en_US
dc.subject virus infections en_US
dc.subject CTLs en_US
dc.subject cytotoxic T lymphocytes en_US
dc.subject T cells en_US
dc.subject killer T cells en_US
dc.subject immune response en_US
dc.subject virus en_US
dc.subject resistant en_US
dc.subject virus dynamics en_US
dc.subject drug resistant virus en_US
dc.subject virus-immune en_US
dc.subject ODEs en_US
dc.subject virus-immune dynamics en_US
dc.subject infections en_US
dc.title Models of Virus-Immune Dynamics and Drug Resistant Virus Infections en_US MS en_US thesis en_US Biomathematics en_US

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