My research focuses on two main topics.
The first is HIV-1-mediated aggravation of liver disease in HCV virus co-infectees. Due to the shared routes of infection, HIV-1/HCV co-infection is common, with 15~30% of all HIV-1-infected persons estimated to be co-infected with HCV. In the co-infected patients, HIV-1 is known to accelerate every stage of HCV-mediated liver disease progression. However, the molecular details regarding how co-infection of HIV-1 and HCV brings about a more severe deterioration of the liver than a single infection of HCV are unknown at present.
Second, HIV-1 viral proteins are generated in a stage-specific manner; that is, regulatory proteins, such as Tat, Rev, and Nef, are expressed at the early stage, while structural proteins, such as Gag, Pol, and Env, are produced at the late stage of virus infection. Molecular regulation of viral gene expression in protein production has been studied comprehensively, whereas the elimination processes using the ubiquitin proteasome system for the synthesized proteins after completion of their duties in the infected cells are generally unknown, representing a current gap in understanding the smooth stage-specific transitioning through the HIV-1 life cycle that is crucial to viral pathogenicity.