Models of Virus-Immune Dynamics and Drug Resistant Virus Infections

drug resistant;virus infections;CTLs;cytotoxic T lymphocytes;T cells;killer T cells;immune response;virus;resistant;virus dynamics;drug resistant virus;virus-immune;ODEs;virus-immune dynamics;infections

Soberano, Lisa Albert ; Kevin Gross, Committee Member,Charlie Smith, Committee Member,Alun Lloyd, Committee Chair,Soberano, Lisa Albert ; Kevin Gross ; Committee Member ; Charlie Smith ; Committee Member ; Alun Lloyd ; Committee Chair

University:North Carolina State University

关键词: drug resistant;    virus infections;    CTLs;    cytotoxic T lymphocytes;    T cells;    killer T cells;    immune response;    virus;    resistant;    virus dynamics;    drug resistant virus;    virus-immune;    ODEs;    virus-immune dynamics;    infections;   

Others  :  https://repository.lib.ncsu.edu/bitstream/handle/1840.16/2356/etd.pdf?sequence=1&isAllowed=y

美国|英语

来源: null

【 摘 要 】

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.