Files in this item



application/pdf9503181.pdf (5MB)Restricted to U of Illinois
(no description provided)PDF


Title:The effect of envelope glycoprotein gI on the replication of pseudorabies virus in porcine alveolar macrophages
Author(s):Dworak, Linda Jane
Doctoral Committee Chair(s):Hahn, Edwin C.
Department / Program:Biology, Microbiology
Biology, Veterinary Science
Discipline:Biology, Microbiology
Biology, Veterinary Science
Degree Granting Institution:University of Illinois at Urbana-Champaign
Subject(s):Biology, Microbiology
Biology, Veterinary Science
Abstract:Pseudorabies (PrV) is an alphaherpesvirus disease of swine. The lungs are a main site of viral replication and alveolar macrophages (PAM) are productively infected. Programs for the eradication of PrV are currently underway in the United States and Europe. Most of the PrV vaccines used in the programs are genetically engineered for deletion of the envelope glycoprotein gI because of the association of gI with virulence.
The objectives of this study were: (1) To determine the consequences of gI deletion on the infectivity of PrV in porcine macrophage compartments, and (2) To localize the stage in the viral replication cycle when gI exerts an effect on the production of PrV in PAM. Experiments utilized a gI-deletion mutant (gI$\sp-$) and the isogenic parental wild-type strain (Ka) to specifically define the effect of gI in the virus-macrophage interaction.
The PrV infection was evaluated in porcine peripheral blood monocytes, PAM, and bone marrow cells. Virus production and cytopathic effect in the immune cells were compared to infection of PK-15, a permissive, non-immune, porcine kidney cell line that served as an indicator of baseline cell susceptibility. The parameters examined included adsorption, penetration, viral DNA synthesis, maturation, release, and pathogenic effects of the virus on the cell.
Results demonstrated that deletion of the gI-encoding region enhanced viral replication and production of infectious progeny in macrophages. In PAM, modulation of Ka replication occurred at a stage following penetration and preceding viral DNA synthesis. The phenomenon was cell type-specific, occurring with pronounced regularity in macrophages but not in PK-15 cells. Host cell protein synthesis was depressed overall in both Ka and gI$\sp-$-infected cells, but the lower yield of Ka was accompanied by a less pronounced depression. Ka suppressed endogenous levels of interferon-alpha in PAM, whereas gI$\sp-$ induced higher levels of interferon. The evidence suggests that the gI-encoding region is associated with slowing the initial rate of production of infectious virus in PrV-infected PAM. The results serve as a reminder that although a gene deletion may attenuate virulence of a pathogen in the whole animal, it may also endow the virus with a greater ability to infect certain cell types.
Issue Date:1994
Rights Information:Copyright 1994 Dworak, Linda Jane
Date Available in IDEALS:2011-05-07
Identifier in Online Catalog:AAI9503181
OCLC Identifier:(UMI)AAI9503181

This item appears in the following Collection(s)

Item Statistics