EDUCATION AND POSITIONS HELD:
Bachelor of Medicine, School of Medicine, Kaohsiung Medical Univ. 1984
Ph.D., Department of Microbiology and Immunology., Oregon Health Sciences Univ. USA 1993
Associate Prof., Institute of Clinical Medicine, National Yang-Ming Univ. 1993
Adjunct Associate Investigator, Department of Medical Research and Education. Taipei Veterans General Hospital 1995
Prof., Institute of Clinical Medicine, National Yang-Ming Univ. 2001
RESEARCH INTERESTS:
HIV-1 protease mediates virus maturation by processing viral structural protein Gag precursors during or after virus budding. The PR-mediated virus maturation is necessary for acquisition of viral infectivity. Timing of PR activation appears to be critical for virus assembly as premature PR activation can reduce virion release due to premature cleavage of Gag. Our primary goal is to elucidate the mechanism of PR activation. We also analyze the SARS-CoV structural domains involved in virus particle assembly. BST-2/tetherin has been reported to restrict enveloped virus release by tethering the progeny virions to the cell surface. We investigate the impact of BST-2/tetherin on coronavirus replication and explore whether coronaviruses or SARS-CoV has not yet identified strategy to oppose the BST-2/tetehrin anti-viral function.
愛滋病毒釋出胞外時，病毒的蛋白酵素(PR)將結構蛋白切割之後，病毒才能成熟並具感染力，而蛋白酵素何時活化對病毒顆粒的形成極重要，因為蛋白酵素如提早活化將使結構蛋白提早被分解，導致病毒顆粒無法組裝，我們主要探討愛滋病毒蛋白酵素活化的機制。此外我們也分析SARS冠狀病毒結構蛋白那些區域與病毒顆粒的形成有關。已知寄主細胞BST-2/ tetherin可將組合完成的病毒顆粒沾黏在細胞表面上使病毒無法釋出胞外，我們研究BST-2/tetherin 對冠狀病毒組裝或複製的影響，並探討SARS或其他冠狀病毒是否表現特定因子來抑制BST-2/tetherin的抗病毒作用。