| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Outline of Final Research Achievements |
Many environmental and physiological factors, such as infection of DNA viruses, can directly induce genome DNA damages and activate DNA damage response (DDR) pathways. Unlike DNA viruses, infection in the nucleus is uncommon for RNA viruses. Therefore, interaction between RNA virus and DDR pathways has been largely unknown.
Borna disease virus (BDV), a non-segmented, negative strand RNA virus, can establish persistent infection in the nucleus. BDV generates viral speckles of transcripts (vSPOTs) in the nucleus as the viral replication compartment. In this study, we found that γH2AX co-localizes with vSPOTs. On the other hand, neither acute nor persistent infection of BDV could activate DDR in infected cells. Furthermore, the inhibition of DDR altered the balance between BDV transcription and replication in the infected cells. These observations suggested that BDV may locate preferably at the DDR focus to regulate its balance between replication and transcritption.
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