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Principal Investigator

Dr. John H. Connor

John Connor

Email: jhconnor@bu.edu
B.A. Swarthmore College
Ph.D in Pharmacology, Duke University

Protein synthesis is a central issue in virus replication. Though viruses absolutely need to make new proteins to replicate, they do not carry their own protein synthesis machinery. Instead, they utilize the protein synthethesis machinery of their host. My research interests are in understanding how a virus accomplishes this hostile takeover of the host machinery. I work with a prototype negative strand RNA virus, vesicular stomatitis virus (VSV) that is currently being developed as a potential antitumor agent. VSV turns off all host protein synthesis following infection, but the host protein synthesis machinery translates large amounts of viral protein. Using genetic, molecular biological, and rational mutagenesis approaches, we are investigating how VSV interacts with and dominates the host translation machinery.

Our studies have shown an important role for multi-protein translation initiation complexes. Changes in the phosphorylation and makeup of these complexes correlates closely with the switch from host to viral protein synthesis. Currently the laboratory is working to determine how VSV infection is altering these complexes to favor viral translation. Our studies on VSV translation have also led us to the finding that VSV is capable of replicating under hypoxic cell stress, a difficult to treat microenvironment of solid tumors. We are currently developing new ways to use VSV as a means to target hypoxic tumor cells for destruction.



Post-Docs

Michelle Toomey Olsen

Michelle Toomey Olsen

Email: mtoomey5@bu.edu
B.S. Biochemistry, Bridgewater State College
Ph.D Molecular and Cell Biology and Biochemistry, Boston University

My project focuses on understanding viral-host interactions, specifically investigating the cellular pathways important for Ebola infection. Using the EBOV minigenome system and small molecule inhibitors, I am exploring the role of polyamines and hypusination in viral gene expression and replication. Understanding the basic way a virus is taking over the cell may provide insight into the pathogenicity of Ebola as well as provide the ability to target host factors involved in viral replication.

John Ruedas

John Ruedas

Email: jruedas@bu.edu
Ph.D. San Diego State University

I joined Dr. Connor’s lab in June of 2015. I am currently involved in developing a multiplexed diagnostic assay with our collaborators to detect hemorrhagic fever viruses in blood. This assay is being developed as a field-applicable rapid-detection system that will test patients for specific viral infections such as Ebola, Marburg, and Lassa. Rapid diagnosis will in turn help determine available treatments options that are specific for the infection. I am also involved in generating new recombinant viruses for the lab to study. Specifically, I am generating Vesicular Stomatitis Viruses (VSV) that are pseudotyped with surface glycoproteins from hemorrhagic fever viruses. VSV viruses that express these surface glycoproteins can be used as research tools for viral entry mechanisms, help screen for new antibodies that bind to the glycoprotein, and serve as novel vaccine vectors.



Graduate Students

Emily Speranza

Emily Speranza

Email: speranza@bu.edu
B.A. Biology and Mathematics, Carroll College
Current: Ph.D. Bioinformatics Program, Boston University

My project is focused on understanding the host response to viral hemmorhagic fever. I use a combination of RNA-Seq, microarray, and nanostring data and understand how the host response is different between different infections (Lassa, Marburg, and Ebola) and to understand the differences in the host response between survivors and non-survivors.




Labatory Technicians

Maohua Lei

Maohua Lee

Email: malei@bu.edu









A.J. Devaux

AJ Devaux

Email: ajdevaux@bu.edu
B.S. Biology, UMass Boston








Ali Soucy

Ali Soucy

Email: alisoucy@bu.edu
B.S. Nutritional Sciences, University of New Hampshire