Competition between viruses and intracellular antiviral immunity

2016 Fiscal Year Final Research Report

• Project Area: Molecular basis of host cell competency in virus infection
• Project/Area Number: 24115004
• Research Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
• Allocation Type: Single-year Grants
• Review Section: Biological Sciences
• Research Institution: Kyoto University
• Principal Investigator: Fujita Takashi 京都大学, ウイルス・再生医科学研究所, 教授 (10156870)
• Co-Investigator(Kenkyū-buntansha): 高折 晃史 京都大学, 医学(系)研究科(研究院), 教授 (20324626)
• Co-Investigator(Renkei-kenkyūsha): KATO Hiroki 京都大学, ウイルス・再生医科学研究所, 准教授 (10597173) ; SHINDO Keisuke 京都大学, 医学研究科, 助教 (10602344)
• Project Period (FY): 2012-06-28 – 2017-03-31
• Keywords: 自然免疫 / インターフェロン / ウイルス / 感染症 / RIG-I / ストレス顆粒 / イメージング / 複製複合体

Outline of Final Research Achievements

Fujita has elucidated that DHX36 and Pumilio play critical role in recognition of viral RNA in antiviral stress granule (avSG) by RIG-I-Like Receptor (RLR). They discovered that Picornaviruses evade RLR function by cleaving G3BP, an important component of avSG, to evade immune response. They discovered that viral poly A+ RNA is recognized in avSG to enhance host immune responses. IPS-1 is a critical adaptor for RLR signaling. They discovered that aggregation of TRAF binding domain is sufficient for signaling.
Takaori-Kondo has elucidated that the upregulation of intracellular level of HIV-1 Vif by CBF-β is mainly caused by suppressing MDM2-mediated proteasomal degradation and that expression of APOBEC3B is augmented by activation of the classical NF-κB pathways.

Free Research Field

抗ウイルス自然免疫学