Originally Posted by
MickG0105
The mechanism by which coronaviruses replicate and mutate is very well understood - the RNA replication process that occurs after a coronavirus infects a cell is markedly less accurate than DNA replication. Each time a replication occurs the RNA creates a protein sequence and that protein sequence is then used to create a new strand of RNA - the protein sequence is a bit like a negative in photography or a mould in casting. Because of the inherent weakness in RNA replication there is a very small chance that the protein sequence could change slightly so you end up with a very, very slightly flawed negative or mould. Those changes result in the resulting next generation of RNA changing every so slightly. When you have many, many replications occurring many, many times as you would get in a large infected population, basic probability favors that the virus will adjust. It is straightforward evolution but on a very, very condensed timeline because of a) the relatively very short inter-generarional cycle time and b) the relatively poor accuracy of the replication process. Most of the time the small 'misprints' or 'miscasts' (mutations) that arise have no effect whatsoever on how the coronavirus interacts with its target hosts but every once in a while they do.
And you don't need to know how or what "caused" the original coronavirus to emerge, once you have mapped it genetically then you're on your way to dealing with it.
So stopping the spread is also the key to stopping mutations which spread faster, so stopping the spread is also key to stopping mutations which spread faster, so..................?