Research

Our lab primarily focuses on the molecular virology of HIV-1, but we have expanded research into Hepatitis B virus and Human Papillomavirus. Read below for more information on our ongoing projects!

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Human Immunodeficiency Virus (HIV)

Maddi Bandini

My overall goal is to determine how HIV-1 Vif induces metaphase arrest followed by cell death during HIV-1 replication, and whether Vif can be targeted as a cancer therapeutic. Vif is an HIV-1 accessory protein essential for viral replication and is known to degrade the host restriction factor APOBEC3G. Currently, we are working with Dr. Aussie Suzuki to define the molecular features of Vif-associated cell-cycle arrest.

 

Ryan Behrens

 

James Bruce

My research has focused on virus/host interactions. Characterizing how viruses utilize cellular pathways enhances our understanding of both the viral lifecycle and the normal function of these cellular processes. My work has shown that HIV-1 proteins such as Envelope (Env), Tat, and Vpr regulate the cellular sulfonation, transcription, cell cycle, and DNA damage pathways to facilitate efficient viral replication.

Lauren Kelly

Previous work from our lab and Lloyd Smith’s group identified dehydroamino acids (DHAA), a rare post-translational modification, in HIV-1 virions. The regulation and ramifications of this modification in the context of viral infection have yet to be determined. My work focuses on 1) determining the impact this modification has on viral infection and 2) identifying and characterizing key DHAA-regulatory proteins.

Hepatitis B Virus (HBV)

Jorge Guerrero

Host Zinc-finger Antiviral Protein (ZAP) targets CpG dinucleotides, and our preliminary data indicates that HBV may be using its high CpG content to keep viral products low and evade a strong immune response. My project involves studying HBV through genomic and gene expression analysis to discover how it establishes its reservoir early during infection while evading the immune response.

Human Papillomavirus (HPV)

Kerry Smith

I’m working on repurposing HIV-1 protease inhibitors (PIs) for targeting HPV-related diseases by decreasing the levels of HPVs’ critical oncoproteins, E6 and E7. Currently, we are trying to dissect the mechanism of HIV-1 PIs in HPV-associated cancer cells.