Extrinsic and environmental factors are known to affect the transmission of arthropod-borne viruses (arboviruses), including variations in the arthropod vector populations. Differences among these factors have been associated with differential transmission and are sometimes used to control the spread of an arbovirus through a vertebrate population in an effort to prevent or disrupt an outbreak. However, diversity in intrinsic viral populations, such as genetic and phenotypic variability, is not often accounted for when considering alterations in transmission. Presented in this dissertation are four experimental studies that explore the contribution of viral intrinsic factors, especially phenotypic variability, to the transmission potential of arboviruses as judged by modeling parameters such as vectorial capacity (VC) and the basic reproductive number (R0). The overall hypothesis of this research is that phenotypic differences of arboviruses alter the transmission potential of these arboviruses by conferring fitness advantages in either the vector or the vertebrate. Further, these phenotypic differences need not be large in magnitude to affect the relative transmission potential. To investigate this hypothesis, this research determined 1) whether intrinsic viral characteristics can lead to differential transmission in a given locale, 2) whether variability of viral fitness in the mosquito vector can lead to significant differential transmission potential, 3) how our newly formulated methods from our preceding aim could aid in the explanation of a currently puzzling phenomenon in the field of arbovirology, 4) whether phenotypic differences in the vertebrate host alters the potential for transmission, and 5) how identified phenotypic differences in both the vector and vertebrate hosts could act synergistically or antagonistically to alter transmission potential of arboviruses. The research in this dissertation offers a more accurate tool for assessing transmission potential in the vector, provides a new model assessing transmission potential in the vertebrate, and provides several of the necessary steps towards a more appropriate calculation of R0. Our use of R0 based on dynamic phenotypic differences provides a framework for a more dynamic formulation of transmission models, and provides an accessible framework for output validation and reporting to public health stakeholders.
| Identifer | oai:union.ndltd.org:LSU/oai:etd.lsu.edu:etd-07052011-160554 |
| Date | 07 July 2011 |
| Creators | Christofferson, Rebecca C. |
| Contributors | Mores, Christopher N., Macaluso, Kevin R., Elzer, Philip H., Foppa, Ivo M., Kim, Joomyeong |
| Publisher | LSU |
| Source Sets | Louisiana State University |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.lsu.edu/docs/available/etd-07052011-160554/ |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached herein 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 LSU or its agents the non-exclusive license to archive and make accessible, under the conditions specified below and in appropriate University policies, 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. |
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