Laboratory for Infection Systems


Specially-appointed Professor Yumiko IMAI
Professor Mariko OKADA




Our laboratory aims to understand host responses to virus infection and pathogenesis formation as a system. In particular, we are focusing on the responses of the host nuclear system to viral infection, and the mechanism involved in the formation of lethal disease states. With the progress of recent genome analysis technology, mass spectrometry technology, bioinformatics analysis technology, etc., it has become possible to acquire huge quantitative life science data of multiple levels even in the research field of infection and immunity. While collaborating with domestic and overseas research groups, we comprehensively analyze the quantitative life science data such as host epigenome profiling, mRNA translation profiles, metabolome analysis, single cell transcriptome analysis, human microbiome analysis, and elucidate the networks involved in the molecular pathology and severity of infectious diseases.  By applying the genome synthesis and genome editing technology in mouse models, we conduct research aimed at establishing drug discovery, diagnostic methods and preemptive medical cares based on it. 

Current Research Programs

1) Dynamics of higher-order chromatin structural changes to viral infection and their roles in disease pathogenesis

2) Elucidation of host and virus mRNA translation mechanism to viral infection

3) Immune / neural organ interaction in the pathology of virus infection

4) Prediction of dynamic network responsible for the formation of severe pathology of virus infection and its application to preemptive therapy


  1. Fujiwara S, Hoshizaki M, Ichda Y, et al. Pulmonary phagocyte-derived NPY controls the pathology of severe influenza virus infection. Nature Microbiology. 2018 Nov19
  2. Yamaguchi T, Suzuki T, Sato T,et al. The CCR4-NOT deadenylase complex controls Atg7-dependent cell death and heart function. Sci Signal. 2018 Feb 6;11(516).
  3. Blank T, Detje CN, Spieß A, et al. Prinz M. Brain Endothelial- and Epithelial-Specific Interferon Receptor Chain 1 Drives Virus-Induced Sickness Behavior and Cognitive Impairment. Immunity. 2016 Apr 19;44(4):901-12.
  4. Katahira J, Dimitrova L, Imai Y, et al. NTF2-like domain of Tap plays a critical role in cargo mRNA recognition and export. Nucleic Acids Res. 2015 Feb 18;43(3):1894-904.
  5. Morita M, Kuba K, Ichikawa A, et al. The lipid mediator protectin D1 inhibits influenza virus replication and improves severe influenza. Cell. 2013 Mar 28;153(1):112-25.
  6. Ichikawa A, Kuba K, Morita M, et al. CXCL10-CXCR3 enhances the development of neutrophil-mediated fulminant lung injury of viral and nonviral origin. Am J Respir Crit Care Med. 2013 Jan 1;187(1):65-77.
  7. Neely G, Kuba K, Cammarato A, et al. A global in vivo Drosophila RNAi screen identifies NOT3 as a conserved regulator of heart function. Cell. 2010, 141(1):142-153.
  8. Imai Y, Kuba K, Neely GG, et al. Identification of oxidative stress and toll like receptor 4 signaling as a key pathway of acute lung injury. Cell. 2008, 18;133(2):235-49.
  9. Imai Y, Kuba K, Rao S, et al. Angiotensin-converting enzyme 2 protects from severe acute lung failure. Nature. 2005 Jul 7;436(7047):112-6.
  10. Kuba K, Imai Y, Rao S, et al. A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury. Nat Med. 2005 Aug;11(8):875-9.