| Budget Amount *help |
¥49,530,000 (Direct Cost: ¥38,100,000、Indirect Cost: ¥11,430,000)
Fiscal Year 2013: ¥9,360,000 (Direct Cost: ¥7,200,000、Indirect Cost: ¥2,160,000)
Fiscal Year 2012: ¥9,360,000 (Direct Cost: ¥7,200,000、Indirect Cost: ¥2,160,000)
Fiscal Year 2011: ¥30,810,000 (Direct Cost: ¥23,700,000、Indirect Cost: ¥7,110,000)
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| Research Abstract |
Invading viral RNA is sensed by RIG-I-like receptor (RLR) in the cytoplasm and antiviral innate immunity, including production of interferon, is induced. It was unclear where RLR senses viral RNA. We found that viral infection induces RNA-protein aggregates, in which RLR is recruited and acts as a platform for viral RNS sensing. We termed this aggregate as antiviral stress granule (avSG). We also found that several viruses actively inhibit avSG to facilitate their replication. Our findings also include that the double-stranded RNA sensors, PKR and DHX36 play critical roles in the formation of avSG.
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