2025/03/31 更新

写真a

タケダ　ミドリ
武田　緑
TAKEDA Midori
所属
医歯学域ヒトレトロウイルス学系 ヒトレトロウイルス学共同研究センター 特任助教
職名
特任助教

学位

  • 博士（医学） （ 2016年3月   岡山大学 ）

経歴

  • 鹿児島大学   総合科学域総合研究学系 ヒトレトロウイルス学共同研究センター   特任助教

    2019年4月 - 現在

  • 鹿児島大学   医歯学域医学系 附属難治ウイルス病態制御研究センター   特任助教

    2018年4月 - 2019年3月

所属学協会

  • 日本分子生物学会

  • 日本ウイルス学会

  • 日本肝臓学会

 

論文

  • Toyodome A., Mawatari S., Eguchi H., Takeda M., Kumagai K., Taniyama O., Ijuin S., Sakae H., Tabu K., Oda K., Ikeda M., Ido A. .  Analysis of the susceptibility of refractory hepatitis C virus resistant to nonstructural 5A inhibitors .  Scientific Reports14 ( 1 ) 16363   2024年7月査読

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    記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Scientific Reports  

    Resistance-associated substitutions (RASs) of hepatitis C virus (HCV) affect the efficacy of direct-acting antivirals (DAAs). In this study, we aimed to clarify the susceptibility of the coexistence of nonstructural (NS) 5A Q24K/L28M/R30Q (or R30E)/A92K RASs, which were observed in patients with DAAs re-treatment failure and to consider new therapeutic agents. We used a subgenomic replicon system in which HCV genotype 1B strain 1B-4 was electroporated into OR6c cells derived from HuH-7 cells (Wild-type [WT]). We converted WT genes to NS5A Q24K/L28M/R30Q/A92K or Q24/L28K/R30E/A92K. Compared with the WT, the Q24K/L28M/R30Q/A92K RASs was 36,000-fold resistant to daclatasvir, 440,000-fold resistant to ledipasvir, 6300-fold resistant to velpatasvir, 3100-fold resistant to elbasvir, and 1.8-fold resistant to pibrentasvir. Compared with the WT, the Q24K/L28M/R30E/A92K RASs was 640,000-fold resistant to daclatasvir and ledipasvir, 150,000-fold resistant to velpatasvir, 44,000-fold resistant to elbasvir, and 1500-fold resistant to pibrentasvir. The Q24K/L28M/R30E/A92K RASs was 816.3 times more resistant to pibrentasvir than the Q24K/L28M/R30Q/A92K RASs. Furthermore, a combination of pibrentasvir and sofosbuvir showed therapeutic efficacy against these RASs. Combination regimens may eradicate HCV with NS5A Q24K/L28M/R30E/A92K RASs.

    DOI： 10.1038/s41598-024-67169-5

    Scopus

    PubMed

    その他リンク： https://www.nature.com/articles/s41598-024-67169-5

  • Li J., Takeda M., Imahatakenaka M., Ikeda M. .  Identification of dihydroorotate dehydrogenase inhibitor, vidofludimus, as a potent and novel inhibitor for influenza virus .  Journal of Medical Virology96 ( 1 ) e29372   2024年1月査読 国際誌

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    記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Journal of Medical Virology  

    Influenza A virus (IAV) infection causes respiratory disease. Recently, infection of IAV H5N1 among mammals are reported in farmed mink. Therefore, to discover antivirals against IAV, we screened a compound library by using the RNA-dependent RNA polymerase (RdRp) assay system derived from H5N1 IAV including a drug-resistant PA mutant (I38T) and a viral polymerase activity enhancing PB2 mutant (T271A). Upon screening, we found vidofludimus can be served as a potential inhibitor for IAV. Vidofludimus an orally active inhibitor for dihydroorotate dehydrogenase (DHODH), a key enzyme for the cellular de novo pyrimidine biosynthesis pathway. We found that vidofludimus exerted antiviral activity against wild-type and drug-resistant mutant IAV, with effective concentrations (EC50) of 2.10 and 2.11 μM, respectively. The anti-IAV activity of vidofludimus was canceled by the treatment of uridine or cytidine through pyrimidine salvage synthesis pathway, or orotic acid through pyrimidine de novo synthesis pathway. This indicated that the main target of vidofludimus is DHODH in IAV RdRp expressing cells. We also produced recombinant seasonal IAV H1N1 virion and influenza B virus (IBV) RdRp assay system and confirmed vidofludimus also carried highly antiviral activity against seasonal IAV and IBV. Vidofludimus is a candidate drug for the future threat of IAV H5N1 infection among humans as well as seasonal influenza virus infection.

    DOI： 10.1002/jmv.29372

    Scopus

    PubMed

  • Masaaki Toyama, Norikazu Sakakibara, Midori Takeda, Mika Okamoto, Koichi Watashi, Takaji Wakita, Masaya Sugiyama, Masashi Mizokami, Masanori Ikeda, Masanori Baba .  Pyrimidotriazine derivatives as selective inhibitors of HBV capsid assembly .  Virus Research   2019年10月査読

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

  • Midori Takeda, Masanori Ikeda, Shinya Satoh, Hiromichi Dansako, Takaji Wakita, Nobuyuki Kato .  Rab13 Is Involved in the Entry Step of Hepatitis C Virus Infection .  Acta Medica Okayama   2016年4月査読

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    担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

  • Hiroki Hiramoto, Hiromichi Dansako, Midori Takeda, Shinya Satoh, Takaji Wakita, Masanori Ikeda, Nobuyuki Kato .  Annexin A1 negatively regulates viral RNA replication of hepatitis C virus .  Acta Medica Okayama   2015年4月査読

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

  • Youki Ueda, Midori Takeda, Kyoko Mori, Hiromichi Dansako, Takaji Wakita, Hye-Sook Kim, Akira Sato, Yusuke Wataya, Masanori Ikeda, Nobuyuki Kato .  New Preclinical Antimalarial Drugs Potently Inhibit Hepatitis C Virus Genotype 1b RNA Replication .  PLOS ONE   2013年8月査読

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

  • Midori Takeda, Masanori Ikeda, Kyoko Mori, Masahiko Yano, Yasuo Ariumi, Hiromichi Dansako, Takaji Wakita, Nobuyuki Kato .  Raloxifene inhibits hepatitis C virus infection and replication .  FEBS Open Bio   2012年8月査読

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    担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

  • Midori Takeda, Masanori Ikeda, Yasuo Ariumi, Takaji Wakita, Nobuyuki Kato .  Development of hepatitis C virus production reporter assay systems using two different hepatoma cell lines .  Journal of General Virology   2012年7月査読

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    担当区分：筆頭著者   記述言語：英語   掲載種別：研究論文（学術雑誌）  

▼全件表示

MISC

  • 肝炎治療剤の新しい知見

    池田 正徳, 武田 緑, 濱田 智仁, 池内 秀幸, 稲生 佳菜子, 小林 勉, 岸川 洋介

    Medical Science Digest   45 ( 1 )   38 - 39   2019年1月

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    記述言語：日本語   出版者・発行元：(株)ニュー・サイエンス社