- Understanding the role of oxidative stress in viral infections
- Interaction of ethanol and hepatitis C virus (HSV)
- Mechanisms of chemical-biological and virus-host interactions to identify novel targets for therapy
- Mechanism and function of alternate frames decoding during HCV infection
Recent findings from Professor Choi's laboratory suggest that:
- HCV induces oxidative stress by specific modulation of host gene expression
- This perburbation of the host redox status has significant effects on HCV genome and its replication
- Increased oxidative stress is likely to promote the development and progression of severe liver diseases, including hepatocellular carcinoma
- Ethanol, an important cofactor in liver diseases, elevates complete replication of HCV at physiologically relevant doses
- F protein (also known as ARFP, Core+1/F, and p17) has important biological functions during HCV infection
Profess Choi has studies in progress to define the underlying mechanisms as well as in vivo relevance of these findings.
- Ph. D., 1999 — University of Southern California
- B.S., 1992 — University of California, Los Angeles
