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

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

Pathogenicity of hepatitis viruses

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


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

Infectious diseases by infection with mosquito-borne flavivirus, one of which is microcephaly by infection with Zika virus, have become a serious problem worldwide . Mosquito-borne flavivirus spreads infection through blood feeding of virus-infected mosquito. While host ranges of virus infection are generally limited, mosquito-borne flavivirus can propagate mosquito and mammals. We study how mosquito-borne flavivirus infects mosquito and mammals and how transmission between mosquito and mammals is associate to development of diseases





  • Prof.: Toru Okamoto
  • Asst. Prof.: Tatsuya Suzuki
  • SA Asst. Prof.: Yumi Ito



  • (1) How Do Flaviviruses Hijack Host Cell Functions by Phase Separation? Saito A. et al., Viruses 2021 Jul 28;13(8):1479.
    (2) Engineered ACE2 receptor therapy overcomes mutational escape of SARS-CoV-2. Higuchi Y. et al., 2021 Jun 21;12(1):3802.
    (3) Hepatitis C virus modulates signal peptide peptidase to alter host protein processing. Hirano et al., Proc Natl Acad Sci U S A. 2021 Jun 1;118(22):e2026184118
    (4) Infection with flaviviruses requires BCLXL for cell survival. Suzuki T. & Okamoto T., et al., PLoS Pathog. 2018 Sep 27; 14 (9):e1007299.
    (5) 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.
    (6) 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