Study on the role of TMPRSS2 in respiratory virus spread

我们发现，人类副流感病毒和仙台病毒（鼠副流感病毒1型）使用TMPRSS 2激活。TMPRSS2基因敲除小鼠模型表明，TMPRSS2可能不是SeV在小鼠中传播的关键。病毒膜融合蛋白裂解位点的P3、P2和P1位（QSR）残基在许多呼吸道病毒中高度保守，如人副流感病毒、SeV和人偏肺病毒。最后，我们的数据证明了P2丝氨酸和P3谷氨酰胺残基对SeV复制的重要性。

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.