Study on the role of TMPRSS2 in respiratory virus spread
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 |
Research Field |
Pediatrics
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Research Institution | National Institute of Infectious Diseases |
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
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Project Status |
Completed (Fiscal Year 2012)
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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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Report
(3 results)
Research Products
(10 results)
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[Presentation] Importance of the P3 Glutamine residue for proteolytic activation of the fusion protein of parainfluenza virus by TMPRSS22012
Author(s)
Masako Abe, Atsushi Kato, Maino Tahara, Kouji Sakai, Kazuhiko Kanou, Kazuya Shirato, Masahiro Noda, Hirokazu Kimura, Yasushi Ami, Shutoku Matsuyama, Katsumi Mizuta, Makoto Takeda
Organizer
The 11^<th> Awaji International Forum on Infection and Immunity
Place of Presentation
淡路島
Related Report
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