Document Type

Thesis - University Access Only

Award Date

1995

Degree Name

Master of Science (MS)

Department / School

Biology and Microbiology

First Advisor

Christopher C.L. Chase

Abstract

Bovine herpesvirus 1 (BHV -1) is a respiratory disease pathogen that causes millions of dollars in losses to the cattle industry each year. Primary BHV-1 infections provide an opportunity for secondary bacterial infections resulting in shipping fever pneumonia, a highly contagious disease of feedlot cattle. The cellular pathogenesis caused by BHV-1 infection has been well documented. However, few studies have measured the initial cellular changes that occur when BHV-1 infects target cells. This thesis project examined the ability of BHV-1 to stimulate cellular signal transduction pathways that activate cellular DNA synthesis and compare its ability to replicate in actively dividing and quiescent cells. The results of these studies indicate that BHV -1 does not stimulate changes in cytoplasmic Ca2+ and pH upon attachment to cells nor does it alter host cell DNA synthesis upon attachment to or infection of host cells. BHV -1 infection of quiescent cells did not produce a detectable amount of viral DNA synthesis at 24 hours post infection, indicating that viral replication may be cell cycle dependent. BHV-1 infection of actively dividing cells was shown to proceed more efficiently with greater virus production and protein synthesis compared with quiescent cells. These differences were due to a characteristic of the quiescent cells such as a limited quantity of the cellular factors needed by BHV-1. The data in this thesis project provide evidence that BHV-1 's in vitro preference for dividing cells is based on characteristics associated with those cells being in the DNA synthesis phase of the cell cycle. Consequently, BHV-1 has no need to stimulate a cell signal transduction pathway that activates cellular DNA synthesis. These observations are significant because they explain why stressed cattle are more susceptible to BHV-1 infection. Stress causes an animal's cells to become more active thus creating an intracellular environment favorable to BHV-1 replication. Studying the cell signal transduction cascade stimulated by virus-receptor interactions can lead to identification of BHV-1 's cellular receptor and the design of antiviral therapies that prevent infection.

Library of Congress Subject Headings

Cattle -- Virus diseases
Herpesvirus diseases in animals
Cellular signal transduction
Cell cycle

Format

application/pdf

Publisher

South Dakota State University

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Rights Statement

In Copyright