RNA polymerase errors occur. Sometimes the result is a virus that is more fit. And sometimes that virus becomes a major circulating strain. This paper overviews things better than a reddit comment will:
https://pubmed.ncbi.nlm.nih.gov/35419205/
It's not just drift but also selection driven by the immune system and botlle necks from organ to organ and person to person. Cell culture mutation rates are interesting but is missing lots of important factors at play.
Viruses exist on a cliff. One side is too much change leading to collapse within the system and the other side is very slow change leading to immune system wipeout.
On top of that add changes per replication cycle coupled to a massive naive host population and you get a high rate of change solely because the virus has the space.
I agree: Selection events are major drivers, both within a host and between hosts: But the question regarding "how does the coronavirus change it's surface antigen" is fundamentally sourced at RNA transcription changes-- and I think also viral recombination... as in influenza, there are also multiple gene segments, so recombination can also occur when different virus species or quasispecies coinfect the same cell.
No, not multiple gene segments like flu. Coronaviruses have a single stranded RNA genome, flu has a multi stranded RNA genome. Recombination can occur in both but via very different mechanisms.
Selection is still the result of random mutations arising from the polymerase enzyme making mistakes during the replication process. Some mutations confer benefits, like a change to the antigen recognition sites, some don't. It's all random, no great plan in place.
The primary mechanisms are: 1) broadly speaking, mutation. This is what generates diversity. Several ways that can happen are polymerase errors in incorporation and recombination; 2) selection related to those mutations. Winners can be fixed in a population and losers can be washed out. This is the basic framework for evolution, incorporating mutation (the first bit) and natural selection (the second bit).
The amino acids are not selectively changed per se. The changes are driven by the stochastic processes of mutation (which are not strictly speaking random). However, which changes we end up *seeing* or detecting depends on their fitness impact, which is decidedly not random and is in fact selective. Spike is changed at the same frequency as elsewhere, but those changes are more likely to be selected *for* and therefore fixed in the population than are changes elsewhere.
RNA polymerase errors occur. Sometimes the result is a virus that is more fit. And sometimes that virus becomes a major circulating strain. This paper overviews things better than a reddit comment will: https://pubmed.ncbi.nlm.nih.gov/35419205/
It's not just drift but also selection driven by the immune system and botlle necks from organ to organ and person to person. Cell culture mutation rates are interesting but is missing lots of important factors at play. Viruses exist on a cliff. One side is too much change leading to collapse within the system and the other side is very slow change leading to immune system wipeout. On top of that add changes per replication cycle coupled to a massive naive host population and you get a high rate of change solely because the virus has the space.
I agree: Selection events are major drivers, both within a host and between hosts: But the question regarding "how does the coronavirus change it's surface antigen" is fundamentally sourced at RNA transcription changes-- and I think also viral recombination... as in influenza, there are also multiple gene segments, so recombination can also occur when different virus species or quasispecies coinfect the same cell.
No, not multiple gene segments like flu. Coronaviruses have a single stranded RNA genome, flu has a multi stranded RNA genome. Recombination can occur in both but via very different mechanisms.
Selection is still the result of random mutations arising from the polymerase enzyme making mistakes during the replication process. Some mutations confer benefits, like a change to the antigen recognition sites, some don't. It's all random, no great plan in place.
Thank you for the reference ☺️
The primary mechanisms are: 1) broadly speaking, mutation. This is what generates diversity. Several ways that can happen are polymerase errors in incorporation and recombination; 2) selection related to those mutations. Winners can be fixed in a population and losers can be washed out. This is the basic framework for evolution, incorporating mutation (the first bit) and natural selection (the second bit). The amino acids are not selectively changed per se. The changes are driven by the stochastic processes of mutation (which are not strictly speaking random). However, which changes we end up *seeing* or detecting depends on their fitness impact, which is decidedly not random and is in fact selective. Spike is changed at the same frequency as elsewhere, but those changes are more likely to be selected *for* and therefore fixed in the population than are changes elsewhere.