Okamoto Lab/Division of Infectious Disease  Institute for Advanced Co-Creation Studies

Our research focusses on the pathogenesis of hepatitis viruses, such as Hepatitis C virus and Hepatitis B virus, and mosquito-borne flaviviruses, such as Japanese encephalitis virus (JEV), Dengue virus (DENV) and Zika virus (ZIKV). It remains unclear how these viruses induce a variety of diseases in hosts. We aim to understand the molecular mechanisms involved in the pathogenicity of these viral infections through molecular biology and animal models.

Pathogenicity of hepatitis viruses

HCV induces chronic infection and leads to development of steatosis, cirrhosis, and hepatocellular carcinoma. Among its 10 viral proteins, the HCV core protein forms a viral particle and induces steatosis and hepatocellular carcinoma in a transgenic mice model. This suggests that the HCV core protein is strongly associated with liver disease during chronic hepatitis C infection. Our research focusses on the maturation of the HCV core protein by a signal peptide peptidase (SPP) and how maturation is essential for viral particle formation and the development of liver diseases. We would like to clarify why maturation of the HCV core protein is needed for its function, especially in the context of liver diseases.

Pathology of mosquito-borne flavivirus and development of new antiviral drugs

Diseases caused by infection with mosquito-borne flaviviruses, one of which is microcephaly caused by infection with Zika virus, have become a serious problem worldwide. Mosquito-borne flaviviruses spread via virus-infected mosquitos. While the host range of viruses are generally limited, mosquito-borne flavivirus can propagate in both mosquitos and mammals. We study how mosquito-borne flavivirus are able to infect mosquitos and mammals and how transmission between mosquitos and mammals contributes to the development of diseases.





  • Prof.: Toru Okamoto
  • Assit. Prof.: Tatsuya Suzuki
  • Postdoc.: Yumi Ito



  • (1) Novel anti-flavivirus drugs targeting the nucleolar distribution of core protein. Tokunaga M., et al. Virology 2019 541:41-51
    (2) Infection with flaviviruses requires BCLXL for cell survival. Suzuki T. & Okamoto T., et al., PLoS Pathog. 2018 Sep 27; 14 (9):e1007299.
    (3)Characterization of SPP inhibitors suppressing propagation of HCV and protozoa. Hirano J. & Okamoto T., et al., Proc Natl Acad Sci U S A. 2017 Dec 12;114 (50):E10782-E10791.
    (4) TRC8-dependent degradation of hepatitis C virus immature core protein regulates viral propagation and pathogenesis. Aizawa S. & Okamoto T., et al., Nat. Commun. 2016 May 6; 12(5): e1005610