Angiotensin converting enzyme 2 (ACE2)
“First, several reports have shown that hormonal and sex chromosomes contributed to the blood pressure variations between the sexes.[29,30] Second, there was a much great difference in the frequency of distribution of ACE2 variants among different racial and ethnic lines.[19,28] For instance, the T allele frequencies of rs2285666 were 40.1% in Chinese Han, 32.4% in Chinese Dongxiang, 22.0% in Anglo Celtic “
The researchers, led by Jason McLellan of the University of Texas at Austin, defined the structure of 2019-nCoV’s spike protein using a technique called cryogenic electron microscopy, or “Cryo-EM”. This involves cooling the protein to below -150℃, so that it crystallises and then its structure can be determined with near-atomic resolution.
They also identified the “keyhole”, the host cell receptor: it is a human protein called angiotensin converting enzyme 2 (ACE2). This is the same human receptor protein targeted by the earlier SARS coronavirus.
But, disturbingly, the researchers found that 2019-nCoV binds to ACE2 with much higher affinity (10-20 times higher!) than SARS. In other words, 2019-nCoV’s “key” is a lot “stickier” than the SARS one. It’s like a SARS “key” covered in superglue. This means that once it’s in the lock, it’s far less likely to be shaken loose and is therefore presumably more effective at invading our cells.