| Project/Area Number |
23890252
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | National Institute of Infectious Diseases |
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Principal Investigator |
ABE Masako 国立感染症研究所, ウイルス第三部, 研究員 (80613968)
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| Project Period (FY) |
2011 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
|
| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | TMPRSS2 / ウイルス性肺炎 / センダイウイルス / 開裂 / パラインフルエンザウイルス / ノックアウトマウス |
|---|
| Research Abstract |
We showed that human parainfluenza viruses and Sendai virus (murine parainfluenza virus type 1) use TMPRSS2 for their activation. TMPRSS2 knockout mouse model suggested the possibility that TMPRSS2 might not be critical for SeV spread in mice. Residues at the P3, P2 and P1 positions (QSR) of the cleavage site of virus membrane fusion proteins are highly conserved among many respiratory viruses, such as human parainfluenza viruses, SeV and human metapneumovirus, Finally, our data demonstrated importance of the P2 serine and P3 glutamine residues for SeV replication.
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