Michael M.C. LaiDistinguished Professor Molecular Microbiology & Immunology, Neurology School of Medicine |  |
Telephone: 323-442-1748 E-mail: michlai@usc.edu Office: HMR 503 Mail Code: 9094 HSC Education: MD 1968 Medicine - National Taiwan University PhD 1973 University of California, Berkeley Research Topics: Virology, DNA & RNA, Gene Regulation/Transcription PubMed Search Research Keywords Research Description Molecular Biology and Diseases of RNA Viruses The main interest of our laboratory is the study of the molecular biology and pathogenesis of hepatitis C virus, hepatitis delta virus, and murine coronavirus, particularly focusing on the structure and replication of viruses and virus-host interactions with relevance to the mechanism of virus-induced diseases. Hepatitis C Virus. This virus causes the most prevalent form of chronic hepatitis in the U.S. We study the regulation of viral RNA replication and translation. We also investigate the mechanism of viral escape from interferon, and the mechanism of viral persistence. Using a cell culture system established in this laboratory, we are studying the biology of viral infections and the mechanism of viral pathogenesis and oncogenesis. The eventual goals of these projects are to develop new therapy for HCV infection. Hepatitis delta Virus. The virus converts cellular polymerases into RNA-dependent RNA polymerases, which is a unique feature among mammalian viruses. We are utilizing a novel strategy of RNA transfection developed in our laboratory to study the mechanism of RNA-dependent RNA transcription and replication. We are also studying the structure and functions of ribozymes associated with this viral RNA. Selected Publications Vo NV, Oh JW, Lai MM. Identification of RNA ligands that bind hepatitis C virus polymerase selectively and inhibit its RNA synthesis from the natural viral RNA templates. Virology. [ 2003 ] Mar 15;307(2):301-16. PubMed Shi ST, Lee KJ, Aizaki H, Hwang SB, Lai MM. Hepatitis C virus RNA replication occurs on a detergent-resistant membrane that cofractionates with caveolin-2. J Virol. [ 2003 ] Apr;77(7):4160-8. PubMed Gao L, Tu H, Shi ST, Lee KJ, Asanaka M, Hwang SB, Lai MM. Interaction with a ubiquitin-like protein enhances the ubiquitination and degradation of hepatitis C virus RNA-dependent RNA polymerase. J Virol. [ 2003 ] Apr;77(7):4149-59. PubMed Sung VM, Shimodaira S, Doughty AL, Picchio GR, Can H, Yen TS, Lindsay KL, Levine AM, Lai MM. Establishment of B-cell lymphoma cell lines persistently infected with hepatitis C virus in vivo and in vitro: the apoptotic effects of virus infection. J Virol. [ 2003 ] Feb;77(3):2134-46. PubMed Choi KS, Huang P, Lai MM. Polypyrimidine-tract-binding protein affects transcription but not translation of mouse hepatitis virus RNA. Virology. [ 2002 ] Nov 10;303(1):58-68. PubMed Macnaughton TB, Lai MM. Large hepatitis delta antigen is not a suppressor of hepatitis delta virus RNA synthesis once RNA replication is established. J Virol. [ 2002 ] Oct;76(19):9910-9. PubMed Koev G, Duncan RF, Lai MM. Hepatitis C virus IRES-dependent translation is insensitive to an eIF2alpha-independent mechanism of inhibition by interferon in hepatocyte cell lines. Virology. [ 2002 ] Jun 5;297(2):195-202. PubMed Lai MM, Haller JA. Resolution of epithelial ingrowth in a patient treated with 5-fluorouracil. Am J Ophthalmol. [ 2002 ] Apr;133(4):562-4. PubMed Macnaughton TB, Lai MM. Genomic but not antigenomic hepatitis delta virus RNA is preferentially exported from the nucleus immediately after synthesis and processing. J Virol. [ 2002 ] Apr;76(8):3928-35. PubMed Macnaughton TB, Shi ST, Modahl LE, Lai MM. Rolling circle replication of hepatitis delta virus RNA is carried out by two different cellular RNA polymerases. J Virol. [ 2002 ] Apr;76(8):3920-7. PubMed |