Dr. Van Doorslaer received his BS and MS from the University of Leuven, Belgium. He left the land of beer and chocolate to pursue a Ph.D. in the lab of Dr. Robert Burk, at the Albert Einstein College of Medicine in New York. For his post-doctoral work, he joined the lab of Dr. McBride located within the National Institute of Allergy and Infectious Disease at the NIH.

Dr. Van Doorslaer recently joined the faculty of the School of Animal and Comparative Biomedical Sciences at the University of Arizona. He later joined the Immunobiology faculty. Dr. Van Doorslaer also holds appointments within the BIO5 Institute, and the cancer biology and genetics GIDP. His current research combines thorough evolutionary analysis with state-of-the-art molecular techniques to understand why certain DNA viruses are oncogenic. His lab is particularly interested in a subset of human oncogenic papillomaviruses.

The red queen hypothesis states that the host-parasite arms race results in an uneasy balance. Many persistent viruses have co-evolved along-side their hosts for millions of years. Under normal conditions, most persistent viruses do not cause overt disease in the host. Papillomaviruses have evolved to usurp the cellular machinery to complete their life-cycle. The papillomaviral lifecycle perturbs the normal differentiation cycle of the infected cell, forcing cells to divide far beyond their natural lifespan. It is feasible that the continued insult provided by replicating viruses eventually results in malignant transformation of the infected cell. However, while the persistent infection is key to viral oncogenesis, many long-term persisting viruses do not cause cancer. We use cutting-edge technologies and approaches to elucidate which viral phenotypes are associated with oncogenic progression. The pathways targeted by these viruses may represent powerful targets for therapeutic intervention.