Susan Marriott is a Professor of Virology and Microbiology at Baylor College of Medicine in Houston, Texas.  She earned her PhD from Kansas State University for  studying viral replication under the mentorship of Richard A Consigli. She subsequently carried out postdoctoral training at the National Institutes of Health in Bethesda MD in the lab of John N Brady where she began to study the mechanism of cellular transformation mediated by retroviruses.  She joined the faculty at Baylor College of Medicine in 1991 and has developed an active research program focusing on the role of genomic instability in human retroviral transformation  Over the years. she has participated as a member of numerous grant review panels for the National Institutes of Health and the American Cancer Society and  was invited as speaker at national and international conferences and has published extensively on viral carcinogenesis. Susan Marriott is a Professor of Virology and Microbiology at Baylor College of Medicine in Houston, Texas.  She earned her PhD from Kansas State University for  studying viral replication under the mentorship of Richard A Consigli. She subsequently carried out postdoctoral training at the National Institutes of Health in Bethesda MD in the lab of John N Brady where she began to study the mechanism of cellular transformation mediated by retroviruses.  She joined the faculty at Baylor College of Medicine in 1991 and has developed an active research program focusing on the role of genomic instability in human retroviral transformation  Over the years. she has participated as a member of numerous grant review panels for the National Institutes of Health and the American Cancer Society and  was invited as speaker at national and international conferences and has published extensively on viral carcinogenesis.

Human T-cell leukemia virus type I (HTLV-I) was the first retrovirus shown to cause cancer in humans. The major viral oncoprotein, Tax, is a transcriptional regulator of viral and cellular gene expression, and interacts with many important cellular proteins that regulate cell cycle progression, and cellular responses to DNA damage. The ongoing studies in my lab encompass a broad-based effort to understand the molecular mechanisms of Tax function, and how these functions promote genomic instability and cellular transformation.