Sam earned his Ph.D. from Rice University in 2005, studying the biology of adenoviral gene therapy vectors and vector targeting in the laboratory of Michael Barry now at Mayo Clinic in Rochester, MN. He then trained as a postdoc from 2005-2008 with Michelle Ozbun at the University of New Mexico, focusing on human papillomavirus (HPV) infection. Sam came to The University of Arizona in 2008 as an assistant research professor in the BIO5 Institute and joined the Department of Immunobiology as an assistant professor in 2011.
Human papillomaviruses (HPVs) are the most prevalent sexually transmitted infection and cause 5% of cancers worldwide. These viruses infect and replicate in cutaneous and mucosal epithelium. Proliferating basal keratinocytes are the target cells of initial infection, but the complete viral replication cycle is dependent on the differentiation of infected basal cells as they move upward through the stratified epithelium. We focus on understanding the mechanisms and implications of virus entry and subcellular trafficking during HPV infection, and strive to understand how these processes may contribute to viral persistence.
Major projects include 1) identifying the cellular proteins, pathways, and factors required for HPV infection and understanding the mechanistic basis for their role and 2) understanding the viral capsid proteins and their role in infection from a structural/functional perspective. Through these studies we hope to discover new mechanisms of viral membrane penetration, unveil new aspects of cell biology regarding mechanisms of protein trafficking and transport, and identify potential targets for therapeutic and prophylactic intervention.