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Faculty of Graduate Studies

Veerle Appels

  • B.Sc. (University of Victoria, 2024)
Notice of the Final Oral Examination for the Degree of Master of Science

Topic

Characterizing the three-way interplay between the virus, bacteria, and host during influenza A virus-Staphylococcus aureus coinfection

Department of Biochemistry and Microbiology

Date & location

  • Monday, July 20, 2026
  • 9:00 A.M.
  • Clearihue Building, Room B017

Examining Committee

Supervisory Committee

  • Dr. Mariya Goncheva, Department of Biochemistry and Microbiology, University of Victoria (Supervisor)
  • Dr. Lauren Davey, Department of Biochemistry and Microbiology, UVic (Member)
  • Dr. Marie-Eve Tremblay, School of Medical Sciences, UVic (Outside Member)

External Examiner

  • Dr. Caren Helbing, Department of Biochemistry and Microbiology, UVic 

Chair of Oral Examination

  • Dr. Barbara Ehlting, Department of Biology, UVic 

Abstract

Influenza A virus (IAV) is a respiratory pathogen responsible for seasonal flu epidemics and historical pandemics. IAV infection is often complicated by secondary bacterial infections, where Staphylococcus aureus is the most common etiology. Together, IAV-S. aureus coinfection causes significant increases in morbidity and mortality and has been shown to increase the virulence of both pathogens. We established an in vitro model of IAV-S. aureus coinfection in human lung cells, identifying that the presence of S. aureus increases the amount of infectious virus particles produced by approximately 10-fold. We further examined the viral, bacterial, and host contributors to this proviral effect. S. aureus Fibronectin Binding Protein A (FnbA), a cell-wall associated adhesin, was found to mediate this proviral effect. Mass spectrometry and Western blots identified two host proteins: Vacuolar Protein Sorting 26 Retromer Complex Component Associated Protein A (VPS26A) and Vesicle Trafficking 1 (VTA1), which are reduced in the presence of S. aureus expressing FnbA at 12 hours post infection (hpi). We found no changes in the levels of intracellular viral nucleoprotein (NP) during coinfection. We then examined coinfection in a model of primary respiratory epithelial cells differentiated at the air-liquid interface, and further validated the proviral effect in this model. Overall, these experiments give insight into the mechanisms whereby S. aureus is modulating host proteins to promote IAV proliferation, which allows for the identification of therapeutic targets in drug development.

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