Kyushu University Academic Staff Educational and Research Activities Database
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Iwami Shingo Last modified date:2020.06.17



Graduate School


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Homepage
https://kyushu-u.pure.elsevier.com/en/persons/shingo-iwami
 Reseacher Profiling Tool Kyushu University Pure
http://bio-math10.biology.kyushu-u.ac.jp/english/
Academic Degree
PhD
Country of degree conferring institution (Overseas)
No
Field of Specialization
Theoretical virology & immunology
Total Priod of education and research career in the foreign country
00years00months
Research
Research Interests
  • Computational Virology and Immunology
    keyword : Mathematical model, Virus, Immune system, Experimental data, Quantification
    2011.11~2016.03.
Current and Past Project
  • HIV infection is a chronic infection characterized by an extremely long disease progression. Therefore, in order to prevent the disease spread, we should develop an AIDS vaccine which is effective for a long time. Even now, although it has passed 26 years from the discovery of HIV, we have not developed an effective AIDS vaccine. In this research, by using both mathematical models and animal experiments, I try to understand and inspect immune responses against the infection in rhesus macaques experimentally and theoretically. And, from a view point of theoretical immunology, I search and propose a new idea to develop the vaccine.
Academic Activities
Papers
1. Iwamoto M, Saso W, Sugiyama R, Ishii K, Ohki M, Nagamori S, Suzuki R, Aizaki H, Ryo A, Yun JH, Park SY, Ohtani N, Muramatsu M, Iwami S, Tanaka Y, Sureau C, Wakita T, Watashi K., Epidermal growth factor receptor is a host-entry cofactor triggering hepatitis B virus internalization., Proc Natl Acad Sci U S A, 116(17):8487-8492, 2019.04, Sodium taurocholate cotransporting polypeptide (NTCP) is a host receptor required for hepatitis B virus (HBV) entry. However, HBV susceptibility of NTCP-expressing cells was diverse depending on the culture condition: Stimulation with epidermal growth factor (EGF) potentiated cell susceptibility to HBV infection. Here, we show that EGF receptor (EGFR) critically triggers HBV internalization. In EGFR-knockdown cells, HBV or its preS1-specific fluorescence probe attached to cell surface, but their internalization was attenuated. PreS1 internalization and HBV infection could be rescued by complementation with functional EGFR. Interestingly, the HBV preS1-NTCP complex was internalized concomitant with the endocytotic relocalization of EGFR. Molecular interaction between NTCP and EGFR was documented by immunoprecipitation assay. Upon dissociation from functional EGFR, NTCP no longer functioned to support infection, as demonstrated by three distinct methods, by introduction of either 1) the NTCP point mutation that disrupted the interaction with EGFR, 2) the decoy peptide interrupting with NTCP-EGFR interaction, or 3) the pharmacological inactivation of EGFR. These data cumulatively suggest that EGFR mediates HBV-NTCP internalization to support cell susceptibility to HBV infection. Thus, EGFR provides a yet unidentified missing link from the cell surface HBV-NTCP attachment to the viral evasion beyond the host cell membrane..