• Ph.D., Cornell University, 1972
• B.S., Bowling Green State University, 1967

Research Interests: Work in the Gooding laboratory focuses on the interactions between infectious viruses and host immune defense mechanisms. Gooding and co-workers have described several countermeasures in human group C adenoviruses that protect the virus-infected cell from destruction by host cytokines of the TNF family as well as from lysis by anti-viral cytotoxic T cells. This group is also investigating the mechanisms of adenovirus persistence in human tonsil and adenoid tissues. Adenoviral DNA has been localized to T lymphocytes within mucosal lymphoid tissues, suggesting a possible latency mechanism. Current investigation focuses on identifying which T cell subsets harbor the virus and determining what signals lead to reactivation of viral replication in vitro. In addition, the group has established a model system in a human T lymphocyte cell line that mimics the behavior of the virus in tonsil T cells. This model will facilitate detailed analysis of the atypical virus life cycle that permits long-term association of the virus with T lymphocytes in vivo. One current hypothesis is that viral genes responsible for neutralizing host defense are uniquely regulated and act to protect the persistently infected T cell from destruction.

Overall, it is anticipated that this work will contribute to a variety of different approaches to human disease from the development of viral vaccines, where genes that interfere with vaccine effectiveness will be identified and deleted from the immunizing strain, to the use of adenovirus as a vector for gene transfer, where viral genes that dampen host responsiveness will be expressed at high levels to prevent elimination of the transferred gene. In addition, the finding of adenovirus, with its known capacity for mutagenesis, in T cells that continue to divide provides strong incentive to reevaluate the real-life oncogenic potential of this DNA "tumor" virus.