Graduate Studies

 

First Advisor

Daniel C. Ciobanu

Degree Name

Doctor of Philosophy (Ph.D.)

Committee Members

Dustin Loy, Seth Harris, Hiep Vu

Department

Integrative Biomedical Sciences

Date of this Version

5-2025

Document Type

Dissertation

Citation

A dissertation presented to the faculty of the Graduate College at the University of Nebraska in partial fulfillment of requirements for the degree of Doctor of Philosophy

Major: Integrative Biomedical Sciences

Under the supervision of Professor Daniel C. Ciobanu

Lincoln, Nebraska, May 2025

Comments

Copyright 2025, Christian Willis Eaton. Used by permission

Abstract

Viruses and their hosts exist in an evolutionary arms race, with evolutionary promotion of host genetic-based defense mechanisms and evolution of virus genetic-based mechanisms to overcome host defenses. Viruses are capable of much more rapid evolution and adaptation than their hosts, often leading to the use of host cellular mechanisms to promote viral infection and replication. In this study, we describe the generation of a detection assay for atypical porcine pestivirus (APPV), designed to target the viral 5’ UTR, a region of the viral genome which sees less mutations than the protein coding regions. This assay was generated to be capable of detecting multiple global strains of APPV. Additionally, we describe an in vivo challenge of pigs from two distinct synaptogyrin 2 (SYNGR2) genotypes. These pigs were coinfected with porcine circovirus type 2b (PCV2b) and porcine reproductive and respiratory syndrome virus (PRRSV). We validated a previous study that showed a SYNGR2 genotype-dependent outcome of PCV2b infection, and showed that SYNGR2 genotype did not influence PRRSV replication over the course of the challenge period. Subsequently, we utilized an in vitro model of infection of WT and SYNGR2 KO MDBK and Vero cells for SYNGR2-dependent outcome of bovine viral diarrhea virus type 1 (BVDV-1) and Lone Star virus (LSV), respectively. We determined that host cell SYNGR2 KO did not influence the replication of either BVDV-1 or LSV.

Advisor: Daniel C. Ciobanu

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