By ‘effective’ I was going with ‘reliably able to exclude infectious people’. There were fever-screeners in American airports who never caught anyone with a fever, but got infected by someone they screened without a fever.
People seem to be infectious for days before they get a fever, and about a third of people probably never develop fevers in the first place. And this is a function of the particular individual infection, not ‘strains’ - there is not enough generations and selection and genetic diversity for the strains to be meaningfully different yet.
But in the context of the question as to whether it might exert selective pressure, even a ~10% reduction in R₀ would be quite relevant, when compounded over one or two dozen generations of the virus.
You overestimate the rate of emergence of relevant mutations. In the explosive range-expansion phase most lineages have zero functional difference from each other and almost all expansion of particular lineages comes from chance invasions of large vulnerable populations.
There is a reason that when a species suddenly has a range-expansion event, you actually see a relaxation of selection and a buildup of deleterious mutations...
It’s worth noting here that coronaviruses are less vulnerable to selective pressure than most RNA viruses given that that they unusually encode proofreading activity, limiting genetic diversity. This article ( https://www.sciencemag.org/news/2020/03/mutations-can-reveal-how-coronavirus-moves-they-re-easy-overinterpret# ) claims that SARS-CoV-2 accumulates 1-2 mutations per month (its genome has 30,000 bases), which is...enormously inadequate to make even the smallest dent anytime this year in the monumental task that is modulating host immunity to modify onset of fever.
By ‘effective’ I was going with ‘reliably able to exclude infectious people’. There were fever-screeners in American airports who never caught anyone with a fever, but got infected by someone they screened without a fever.
People seem to be infectious for days before they get a fever, and about a third of people probably never develop fevers in the first place. And this is a function of the particular individual infection, not ‘strains’ - there is not enough generations and selection and genetic diversity for the strains to be meaningfully different yet.
But in the context of the question as to whether it might exert selective pressure, even a ~10% reduction in R₀ would be quite relevant, when compounded over one or two dozen generations of the virus.
You overestimate the rate of emergence of relevant mutations. In the explosive range-expansion phase most lineages have zero functional difference from each other and almost all expansion of particular lineages comes from chance invasions of large vulnerable populations.
There is a reason that when a species suddenly has a range-expansion event, you actually see a relaxation of selection and a buildup of deleterious mutations...
It’s worth noting here that coronaviruses are less vulnerable to selective pressure than most RNA viruses given that that they unusually encode proofreading activity, limiting genetic diversity. This article ( https://www.sciencemag.org/news/2020/03/mutations-can-reveal-how-coronavirus-moves-they-re-easy-overinterpret# ) claims that SARS-CoV-2 accumulates 1-2 mutations per month (its genome has 30,000 bases), which is...enormously inadequate to make even the smallest dent anytime this year in the monumental task that is modulating host immunity to modify onset of fever.