Researcher's Profile


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Research Outline      2014-10-02 00:03:00

Our laboratory is interested in understanding how Hepatitis B virus (HBV) persists within the host under the antiviral therapy and host immune pressure. Although current antiviral nucleos(t)ide analogues (NAs) effectively suppress HBV replication by inhibiting viral reverse transcriptases, they cannot cure chronic hepatitis B. Covalently closed circular (ccc) DNA, the replicative template of HBV, is not affected by NAs and persists within the infected hepatocytes even after years of treatment. Therefore, it is critical to understand the mechanisms involving the regulation of the activity and stability of HBV cccDNA . Curing chronic hepatitis B may need elimination of all infected hepatocytes and/or silencing of HBV cccDNA activity. Our laboratory thus aims to explore the mechanisms regulating the formation and activity of HBV cccDNA and all the potential strategies that can eradicate persistent HBV for the ultimate goal of curing chronic HBV infection.

We are also interested in understanding the role of T cell immunity in influenza virus infection. Current inactivated flu vaccine induces robust neutralizing antibodies against the surface viral proteins HA and NA, but often requires annual reformulation because of the high mutation rate of these viral proteins resulting from antigenic drift and antigenic shift. On the contrary, T cell immunity against the more conserved internal viral proteins exhibits cross-reactivity against wider ranges of influenza virus strains. It has been shown that T cell immunity can reduce morbidity and mortality caused by influenza viruses, although it cannot prevent infection. Therefore, we aim to investigate the determinants in generation and maintenance of robust and effective T cell immune response against influenza viruses.