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The first model we are evaluating is human influenza virus in mice. Influenza virus is a negative sense RNA virus, which the CDC estimates causes between 9.2 million and 35.6 million illnesses each year in the United States.[1] In the current influenza season, H3N2 viruses have been the predominant subclade of influenza A virus in circulation.[2] Development of a mouse model for influenza H3N2 virus infection has been difficult. In these studies, we endeavored to mouse-adapt influenza A/Hong Kong/4801/2014 H3N2 virus by serial passaging in AG129 mice. This virus strain was chosen as it overlaps in serotype with the current influenza H3N2 virus in circulation.[2] Initial passaging was unsuccessful, with no detectable increase in virus titer. However, when we used Mannan, an innate immune suppressant, as an aid in adapting the virus to mice, we observed an increase in virus titers in the lung between passage 1 to passage 3.

The second model we are evaluating is mouse Norovirus as a model for Human Norovirus infections. Human Norovirus is a positive sense RNA virus responsible for approximately 685 million cases every year across the world.[3] Therefore identification of antiviral agents for treatment of human norovirus is a priority. We screened potential antiviral compounds in vitro utilizing a mouse macrophage cell line. rupintrivir, favipiravir, carbodine, and anicomycin were all observed to have antiviral effects in vitro. In vivo screening of carbodine will be completed in the mouse model as there is no human norovirus model in vivo.

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Faculty Mentor

E. Bart Tarbet

Departmental Honors Advisor

Lee F. Rickords

Capstone Committee Member

Dennis Welker