An excerpt from a 2004 paper on the evolution of t

An excerpt from a 2004 paper on the evolution of the original SARS virus.

A bit dense, but explains the propensity for RNA viruse to evolve. Each human host can have 10^12 viral copies ( a billion billion) with a high intrinsic rate of mutation.

Rhinovirus (another RNA virus) has similar capability to mutate, this we get a cold (or multiple colds) every year.

Eventually, I hope and expect that COVID-19 will join the
other four endemic human corona viruses as just a bad cold. Unfortunately, we’re like a few years at minimum from that point.

THE POPULATION GENETICS AND EVOLUTIONARY EPIDEMIOLOGY OF RNA VIRUSES

https://www.researchgate.net/profile/Fernando...ion_detail

“ Mechanisms of viral evolution
Processes of evolutionary change. Central to population genetics is understanding how the five main forces of evolutionary change — mutation, recombination, nat- ural selection, GENETIC DRIFT and migration — interact to shape the genetic structure of populations. These same forces are also central to understanding RNA virus evolution, although their relative strengths differ to those observed for DNA-based organisms.
For RNA viruses, most attention has been directed towards mutation, selection and genetic drift. We can understand their importance and interaction by consid- ering four basic properties of RNA virus populations. First, RNA viruses often have very large population sizes, such that the number of viral particles in a given organism might be as high as 10^12. Second, such immense population sizes, which are several orders of
magnitude larger than those observed for cellular organisms, are a product of explosive replication. For example, a single infectious particle can produce an average of 100,000 viral copies in 10 hours. As natural selection is most efficient with large populations, it is no surprise that experiments using RNA viruses have shown that selection is of fundamental importance in controlling their evolutionary dynamics, such that new mutants with increased FITNESS (as measured by their selection coefficient, s) continually appear and out-compete older, inferior alleles4. Third, owing to the lack of proofreading activity in their polymerase proteins, RNA viruses exhibit the highest mutation rates of any group of organisms, approximately one mutation per genome, per replication 5,6. Finally, the genome sizes of RNA viruses are typically small, rang- ing from only 3 kb to ~30 kb, with a median size of ~9 kb. These last two properties are intimately related because high-mutation rates are theoretically expected to limit genome size. In particular, a muta- tion rate that exceeds a notional ERROR THRESHOLD (set at approximately the reciprocal of the genome size) generates so many deleterious mutations in each replication cycle that even the fittest viral genomes are unable to reproduce, and population size decreases to extinction7,8. However, RNA viruses that exist close to (but below) the error threshold are also able to produce many beneficial mutations in a short time, thereby enhancing adaptability, provided that their populations are sufficiently large.”