- Evaluating viral infection/amplification as a virus-cell interaction
- Elucidating molecular mechanisms of latent and persistent viral infections
- Therapeutics that disrupt the virus-host interaction
- Pathology of viruses that infect the central nervous system
- Interactions between retrotransposons and viruses
Control and regulate viral life cycles by disclosing the elaborate tactics
There is still debate on whether viruses are living organisms or a complex of organic materials and genomic information. Once a virus invades a cell, it transforms the cellular environment so that it can replicate and thrive. This process, from entry into the cell to replication, involves a number of intricate mechanisms. The lab is investigating these mechanisms by using hepatitis B virus (Hepatitis B virus) (HBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV) as its models. Ultimately, the goal is to find ways to prevent and control the pathogenic effects of infection. (See figures 1 and 2).
Viruses that infect the central nervous system (CNS), i.e. brain and spinal cord, bring some extra challenges. Subacute sclerosing panencephalitis (SSPE) caused by the measles virus and deafness due to the mumps virus are examples of virus infection-mediated disorders. Guillain-Barre syndrome, an intractable disease, is associated with viral infection. Some studies propose the hypothesis that viral infection could be the cause of many mental illnesses. We are studying the pathological mechanisms of viral infection in the CNS with emphasis on bornavirus and influenza virus, whose infection could induce behavioral abnormalities, resembling to psychiatric disorders, in animal models (Figure 3).
About 40% of the host genome consists of retrotransposons. Like retroviruses, they can reverse transcribe and insert their transcripts into other loci of the genome. Recently, it has become evident that retrotransposons can reverse transcribe RNA virus sequences. We are exploring the mechanism and physiological significance of interactions between retrotransposons and viruses. We are particularly interested in why the genome devotes such a large volume to retrotransposons (Figure 4).