Chou-Zen Giam, Ph.D.

B.S. Chemistry, National Taiwan University, Taipei, Taiwan (05/1975)
Ph. D. Molecular Biology and Biochemistry, University of Connecticut Health Center, Farmington, CT, USA (05/1983)
Post-doctoral Fellow, Laboratory of Molecular Virology, NCI, NIH, Bethesda, MD, USA (09/1987)

The work in my lab revolves around human viruses, with a special emphasis on human T-cell leukemia virus type 1 (HTLV-1), and with occasional forays into other viruses such as HIV and KSHV. We seek a mechanistic understanding of how viral regulatory proteins hijack cellular mediators of mRNA transcription, cell cycle control, and signal transduction to effect viral replication and pathogenesis, especially, oncogenesis. My interest in cancer viruses and human retroviruses developed initially in the early 1980s in the Laboratory of Molecular Virology (LMV) at the NIH where I was a post-doctoral fellow under the direction of Dr. George Khoury. Our major focus at that time was to understand how transcriptional enhancer elements drive eukaryotic mRNA synthesis by studying the HTLV-1 trans-activator, Tax, and its interaction with the cellular transcription machinery. After leaving LMV for the academia, I have been continuously funded by grants from the NIH and other funding agencies (AmFAR, VA, and DoD). We (and others) have since elucidated the mechanism by which Tax activates viral transcription and contributed to current understanding of how HTLV-1 infects, replicates and causes diseases. Due to the global nature of HTLV-1 infection, we frequently collaborate with colleagues in continental US, Asia (Japan, Taiwan, Hong Kong), Europe (France, UK, Germany, Italy, etc.), Africa (Uganda), and South America (Brazil). Together with our domestic and international partners, we seek fundamental understanding of HTLV-1 replication, persistence, and pathogenesis, and strive to translate basic science findings into preventive measures and therapeutic approaches for HTLV-1-associated diseases, especially adult T cell leukemia (ATL). Our current efforts concentrate on (1) elucidating the mechanisms that underlie the genomic instability of ATL cells; (2) understanding how NF-kB hyperactivation drives the induction of cellular senescence; (3) identifying the genetic alterations in ATL cells that facilitate the clonal expansion of HTLV-1-infected T cells based on whole genome sequence information; and (4) uncovering the mechanisms that regulate HTLV-1 latency and reactivation.