So I'd be cautious with this interpretation. The paper (bit.ly/2vd7mJV) models the structural interactions between the spike of #nCoV2019 & human ACE2, the receptor for SARS. They conclude that it is likely the new virus can use hACE2. They haven't yet proven it, yet.
In our own structural modeling, we came to a similar conclusion. While not proven, hACE2 is the betting favorite for #nCoV2019 receptor.
Yeah, not good, especially considering the history of SARS-CoV.
The silver lining: the quality and location of ACE2 binding matters.
Yeah, not good, especially considering the history of SARS-CoV.
The silver lining: the quality and location of ACE2 binding matters.
HCoV-NL63 is a common cold CoV and also uses hACE2 as a receptor, but causes... the common cold, not SARS-like disease.
Why? We don't exactly know. HCoV-NL63 grows well in the upper airways; SARS-CoV does not. NL63 may also have lower affinity for receptor.
Why? We don't exactly know. HCoV-NL63 grows well in the upper airways; SARS-CoV does not. NL63 may also have lower affinity for receptor.
Take away: Just cause the new virus uses the same receptor doesn't mean it SARS... yet.
From mouse studies we know receptor affinity is important. H2H spread can improve affinity. If #nCoV2019 binds hACE2, improving that binding could increase transmission and/or virulence.
From mouse studies we know receptor affinity is important. H2H spread can improve affinity. If #nCoV2019 binds hACE2, improving that binding could increase transmission and/or virulence.
Knowing the receptor is helpful and treatments have been designed to target receptors to disrupt infection.
I'd still argue the most important thing is finding the zoonotic source of the virus. We can't stop the flood if we don't turn off the water.
I'd still argue the most important thing is finding the zoonotic source of the virus. We can't stop the flood if we don't turn off the water.
