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wjn0 | 6 years ago
Some background: viruses primarily contain the genetic material and a protein coat. The Spike (S) protein is one of the proteins in the coat, and plays a role in whether an infection will take root.
From the paper:
> we identified a peculiar furin-like cleavage site in the Spike protein of the 2019-nCoV, lacking in the other SARS-like CoVs
Furin is a protease that is present in healthy humans. Some proteins aren't "active" until they're cut (cleaved) at specific sites along their sequence, so furin's "job" is to cleave these proteins - activating them. Notably, furin is highly expressed in the lungs.
2019-nCoV apparently has a "furin-like site" in its Spike protein - a sequence that furin can bind to and cleave. Notably, furin is the protease that cleaves one of the proteins in the protein coat of HIV, which then allows for viral replication [1]. The authors therefore hypothesize that this mutation which creates the furin-like cleavage site accounts for some of the pathogenicity of 2019-nCoV. They further hypothesize that furin inhibitors may be effective agents in combating the virus (which have shown some promise in combating other viruses, tumours, etc.).
Disclaimer: not a virologist, just a computational biologist with a bit of interest in structural biology. Also, the authors emphasize that further experimentation needs to be done to validate this claim.
[1] doi:10.1038/360358a0
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