Thesis (Ph. D.)--Michigan State University. Fisheries and Wildlife, 2008. / Title from PDF t.p. (Proquest, viewed on Aug. 20, 2009) Includes bibliographical references. Also issued in print.

Thesis (M.S.)--Brock University, 2009. / Includes bibliographical references (leaves 121-136).

Objective: To develop an original survey on public attitudes, knowledge and practices on West Nile Virus (WNV), mosquitoes, and pesticides. We sought to gain insight on what personal protective behaviors (PPBs) are used by the public and whether the public is supportive of pesticide use in combating the threat of WNV. An effective WNV control program must take into account the public's attitudes regarding PPBs and what would influence their use of PPBs. The survey findings will be used to develop a new educational plan for the West Nile Virus Surveillance and Control Program of Delaware County. We sought to determine if knowledge and concern about one's personal risk of contracting WNV were driving forces in one's use of PPBs and support of pesticide use. Results: The sample population was highly informed on WNV and used many PPBs. Knowledge of WNV and concern about contracting WNV were not significant predictors of PPB use or pesticide support. However, odds ratios indicate an increased odds of being in the high PPB group with increasing knowledge. Knowing someone who has or has had WNV was a factor in PPB use, although the outcome of WNV infection is rarely reported. Older age predicted greater PPB use while higher education predicted a lack of support for pesticide use. Conclusion: Future surveys of the public knowledge will need to reach a more diverse population than that of the current study. It appears that many people are using PPBs despite not believing in their efficacy at preventing mosquito bites and WNV. Future studies should seek to identify what is motivating people to use these PPBs, besides knowledge of WNV and concern for their health. / Public Health

West Nile Virus (WNV) first appeared in Texas equids during June 2002. It has since spread rapidly across the state and apparently become endemic. Data from outbreaks occurring between 2002 and 2004 were analyzed to determine hotspots of equine WNV disease, identify environmental factors associated with outbreaks, and to create risk maps of locations with horses at a higher risk of the disease. Kriging was used to model the smoothed WNV attack rates, and interpolated rates were mapped to describe the spatial distribution of WNV disease risk in Texas. A retrospective time-space analysis using a Poisson model was conducted on each year’s data to identify clusters with high attack rates. The resulting overlapping yearly clusters were considered areas of hyperendemicity (hotspots). The counties identified as hotspots included Hockley, Lubbock, and Lynn (primary cluster) and Leon and Roberstson (secondary cluster). Environmental and geographic features were added to the disease maps and analyzed to determine possible environmental factors associated with outbreaks. Locations in close proximity to lakes, bird breeding routes, migratory flyway zones, crop farm and agricultural land, and all dense vegetation were found to be important environmental predictors. Finally, risk maps were created that combined surveillance data on WNV positive mosquito collections and wild bird WNV cases with previously identified environmental risk factors to predict areas of high occurrence of WNV. These risk maps could be used to implement various preventative measures to reduce the transmission of WNV in the Texas equine industry.

Between the years 2006-2007, Harris County, located at the heart of the Houston metropolitan area, experienced a nearly 90% decline in the number of female mosquitoes which tested positive for the West Nile virus. Different theories exist as to why such a precipitous drop occurred and this study attempts to determine the extent to which climatic variability between the two years played a role. The Mosquito Control Division of Harris County Public Health and Environmental Services gathered the data on vectors and reservoirs. Then using GIS, spatial analysis, and geostatistical tools the vector and reservoir data was compared to climatic data to investigate any changes in viral distribution. Previous studies of the area until now have used a limited amount of climatic data; this study seeks to improve the resolution of climatic data analyzed. A higher resolution of data was achieved by including as-of-yet unused data from a network of over 150 gauges maintained by various state and local agencies in addition to previously used data from NOAA COOP stations. Using this dense network of station's values for precipitation, temperature and other climatic variables were interpolated for all of Harris County and used in the analysis. Based on results, water availability was the most likely out of all the climatic variables to the precipitous drop of West Nile virus positive female mosquitoes from 2006-2007. Correlations between all climatic variables and mosquito abundance and West Nile virus positives showed mixed results compared to a previous study in the same area.

West Nile Virus (WNV) first appeared in Texas equids during June 2002. It has since spread rapidly across the state and apparently become endemic. Data from outbreaks occurring between 2002 and 2004 were analyzed to determine hotspots of equine WNV disease, identify environmental factors associated with outbreaks, and to create risk maps of locations with horses at a higher risk of the disease. Kriging was used to model the smoothed WNV attack rates, and interpolated rates were mapped to describe the spatial distribution of WNV disease risk in Texas. A retrospective time-space analysis using a Poisson model was conducted on each year's data to identify clusters with high attack rates. The resulting overlapping yearly clusters were considered areas of hyperendemicity (hotspots). The counties identified as hotspots included Hockley, Lubbock, and Lynn (primary cluster) and Leon and Roberstson (secondary cluster). Environmental and geographic features were added to the disease maps and analyzed to determine possible environmental factors associated with outbreaks. Locations in close proximity to lakes, bird breeding routes, migratory flyway zones, crop farm and agricultural land, and all dense vegetation were found to be important environmental predictors. Finally, risk maps were created that combined surveillance data on WNV positive mosquito collections and wild bird WNV cases with previously identified environmental risk factors to predict areas of high occurrence of WNV. These risk maps could be used to implement various preventative measures to reduce the transmission of WNV in the Texas equine industry.

Thesis (M.Sc.)--York University, 2008. Graduate Programme in Biology. / Typescript. Includes bibliographical references (leaves 56-75). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR38744

Thesis (M.S. in entomology)--Washington State University, August 2009. / Title from PDF title page (viewed on Aug. 12, 2009). "Department of Entomology." Includes bibliographical references (p. 65-68).

West Nile virus (WNV) has a worldwide distribution, with this virus having been isolated on all continents except Antarctica. The recent emergence of highly pathogenic strains of WNV associated with increased rates of neurological disease is of great concern given this broad distribution of the virus. Although two vaccines have been licensed for veterinary use, no prophylactic measures have been approved for humans. Similarly, no antivirals are currently available for post-exposure treatment of WNV. Indeed, few therapeutic agents have shown promise when administered after WNV infection in animal models. KUNV is a highly attenuated, Australasian lineage 1 strain of WNV. This attenuation is mediated in part by the limited neuroinvasiveness of this virus. Phylogenetically, KUNV clusters with pathogenic lineage 1 WNV strains, including the isolates which have been associated with 997 deaths in North America since 1999. Recently, it was shown that mice exposed to KUNV were effectively protected from challenge with pathogenic WNV. The KUNV strain used in that study possessed a single amino acid substitution in NS1 protein that affected oligomerization of this protein, resulting in reduced virus replication in vitro and increased attenuation in mice. In the present study, further characterization of this attenuation marker in NS1 protein was undertaken to determine whether it is suitable for inclusion in a live-attenuated KUNV vaccine. Similarly, mapping of the residues that contribute to the dimerization domain surrounding NS1 protein was performed to identify other potential attenuation markers for stabilization of KUNV attenuation. The mutant viruses created in this study also were manipulated to characterize the role of NS1 protein dimerization in flavivirus replication. The results of this work indicate that NS1 protein dimerization is not absolutely required for virus replication or production of secreted oligomers of NS1 protein, which are important for eliciting protective humoral responses. Although replication of KUNV was found to be highly dependent on retention of the conserved amino acid sequence within the dimerization domain, two mutant viruses were generated by introducing substitutions at residue 250 of NS1 protein. The resultant viruses demonstrated reduced replication in vitro and attenuation in mice. Similarly, a non-conservative substitution in NS2A, which was previously shown to reduce the resistance of KUNV to the host interferon response, was able to attenuate KUNV in mice. Inoculation of adult mice with viruses containing mutations at either site afforded complete protection from lethal WNV challenge. However, the substitutions described in the dimerization domain of NS1 protein were unstable, with restoration of virulence being observed in mutant viruses after limited passaging in vitro. Concerns over the stability of attenuating mutations in KUNV and the time taken to characterize new attenuation markers prompted the evaluation of a novel approach to the development of rationally-designed flavivirus vaccines. The introduction of large complements of synonymous codon substitutions reduced KUNV replication in vertebrate cells. Escape mutations were not observed in a KUNV vaccine candidate containing 37 rare codons after repeated passaging in vertebrate cells at a low MOI. Replication of KUNV in C6/36 cells was unaffected by the introduction of large numbers of rare codons, indicating that this cell line exerts limited selective pressure on the codon composition of this virus. This observation indicates that C6/36 cells may be a useful cell line for the propagation of viruses containing this type of mutation. Finally, three monoclonal antibodies (MAbs) which bind to WNV envelope (E) protein were observed to potently neutralize the pathogenic NY99 strain of WNV. Passive administration of one of these antibodies was shown to afford mice protection even when administered seven days after challenge with WNV NY99 strain. Remarkably, this is the same time that mortality is first observed in control groups. These antibodies mapped to the putative receptor binding domain (domain 3) of E protein. However, these antibodies were found to block virus replication at a stage after receptor-binding. Homology modeling was used to propose a mechanism for the blockade of virus infection mediated by MAb binding. This study describes the development and characterization of a promising new vaccine as well as candidate immunotherapeutics for the prophylaxis and post-exposure treatment of WNV disease. This work described herein also has implications for the development of vaccines and antivirals for other flaviviral diseases.

Thesis (M.S.)--Georgia Southern University, 2007. / "A thesis submitted to the Graduate Faculty of Georgia Southern University in partial fulfillment of the requirements for the degree Master of Science." Under the direction of William S. Irby. ETD. Electronic version approved: May 2007. Includes bibliographical references (p. 36-39)