Bruce W Banfield, Ph.D

Bruce W Banfield

Faculty Bio

Education and Training:
B.Sc., Biochemistry, University of British Columbia, 1984-1988
Ph.D., Microbiology and Immunology, University of British Columbia, 1988-1994
Post-Doctoral Fellow, Microbiology and Immunology, University of British Columbia, 1994-1996
Visiting Research Fellow, Molecular Biology, Princeton University, 1996-1999

Academic Appointments:
Assistant Professor, Department of Microbiology, University of Colorado Health Sciences Center, 1999
Associate Professor, Department of Microbiology, University of Colorado Health Sciences Center, 2006
Associate Professor, Department of Microbiology and Immunology, Queen's University, 2007
Professor, Department of Biomedical and Molecular Sciences, Queen's University, 2013

Active Funding:
Canadian Institutes of Health Research, Operating Grant, "Functions of the herpesvirus tegument"
Natural Science and Engineering Council of Canada, Discovery Grant, "Remodeling of the nuclear membrane during herpesvirus assembly"

Research Interests:
Viruses are selective and efficient nucleic acid delivery devices that serve as excellent tools for studying complex macromolecular assemblies as well as core cellular functions. The order Herpesvirales is a very large group of viruses that infect animals ranging from oysters to elephants. The model herpesvirus studied in the Banfield laboratory is the important human pathogen, herpes simplex virus type 2 (HSV-2), a large virus encoding 74 distinct proteins. HSV-2 virions are complex machines containing almost 100 different proteins. Approximately half of these structural proteins are encoded by the viral genome and the other half are of cellular origin. All herpes virions share a layered structure: a linear double-stranded DNA genome encased by an icosahedral nucleocapsid, which is surrounded by a lipid envelope embedded with glycoproteins. Between the nucleocapsid and the envelope lies a proteinaceous layer called the tegument. During infection, the virion nucleocapsid and tegument components enter the cell cytoplasm. The tegument proteins delivered into the cytoplasm during infection have the opportunity to perform a variety of functions prior to new virus gene expression. A widely held view is that a key role for incoming tegument proteins is to establish an environment within the cell that is conducive to virus replication. In keeping with this view, our research focuses on the analysis of several viral tegument proteins and how they counteract different intrinsic cellular antiviral defense mechanisms aimed at restricting the production of new viruses. Additionally, many tegument proteins play fundamental roles in virus assembly and mediate the release of newly formed virions from the cell. Our laboratory is actively engaged in determining the role of tegument components in the assembly and release of herpesvirus virions from infected cells.

Last Modified: 2018-01-08