Date of Award:

8-2023

Document Type:

Thesis

Degree Name:

Master of Public Health (MPH)

Department:

Animal, Dairy, and Veterinary Sciences

Committee Chair(s)

E. Bart Tarbet

Committee

E. Bart Tarbet

Committee

Jane Kelly

Committee

Brett L. Hurst

Abstract

The Coronavirus Disease-2019 (COVID-19) pandemic, caused by the virus known as Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), has entered into its fourth year, and has lead to hundreds of millions of people infected, millions of deaths, and millions more facing an uncertain future of long-term health consequences as a result of infection. This devastating pandemic has led to economic instability and massive strains on the public health, healthcare, and mental healthcare systems as we have struggled to keep up with the rapid evolution of the virus. Among the most frustrating elements of this evolution is the emergence of new variants of the virus that can increase transmission, increase disease severity, and/or decrease the efficacy of vaccinations and therapeutics. It is important to remain vigilant in our surveillance of new variants to ensure the treatments and preventions we have in place are still effective. Additionally, these changes may require researchers to change animal models of SARS-CoV-2 to match the current variants. The Institute for Antiviral Research at Utah State University developed mouse models for each of the major variants in a mouse genetically modified to express the human angiotensin converting enzyme 2 (hACE2) receptor that SARS-CoV-2 uses to enter human cells. Expression of the hACE2 receptor makes the mice susceptible to infection with SARS-CoV-2 and allows the comparison of variants within this mouse model. We evaluated the mice for survival, weight loss, clinical and neurological sources, actively replicating virus in different organs, and microscopic analysis of different tissues to observe the damage caused by the variants in the mice. We observed a prolonged time to clinical signs, and a prolonged time to death in the variants after the original pandemic virus, and ultimately saw no deaths in the mice infected with the Omicron subvariant BA.2, along with minimal clinical signs.

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