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The comment you respond to states "more readily." This is undoubtedly true. Influenza virus is designed to recombine at every single replication cycle. Coron

The comment you respond to states "more readily." This is undoubtedly true. Influenza virus is designed to recombine at every single replication cycle. Coronaviruses as a whole do not do that. We have a lot of data on coronavirus mutation rates and they are dramatically lower (1000x) than influenza. The point is not that mutation/recombination can't happen (it can and will happen), it is just that this mutation/recombination is relatively rare and we will not get the standard twice-yearly seasonal flu effect where we have to tweak the vaccine every year.

f38zf5vdt 6y ago
Influenza undergoes recombination seemingly exclusively through reassortment whereas betacoronaviridae undergoes homologous recombination -- but to think of the latter as much less effective at producing genetic diversity may be incorrect. > In fact, there is evidence of at least seven potential regions of recombination in the SARS-CoV genome in the replicase- and Spike-coding regions, with possible recombination partners that include porcine epidemic diarrhea virus (PEDV), transmissible gastroenteritis virus (TGEV), bovine coronavirus (BCoV), HCoV-229E, MHV, and IBV [1] > Unlike other viruses that have emerged in the past two decades, coronaviruses are highly recombinogenic. ... For coronaviruses, however, recombination means that small genomic subregions can have independent origins, identifiable if sufficient sampling has been done in the animal reservoirs that support the endemic circulation, co-infection and recombination that appear to be common. [2] > Recombination seems to be rampant in HCoV-OC43 viruses and contributed to originate the A to E viral genotypes, as well as viruses that do not belong to these major genotypes. [3] Unfortunately, nature doesn't "design" anything, it's just the consequence of natural selection and fitness of new generations. While the mutation rate might low compared to influenza, the mutation rate is very high compared to something like a prokaryote, enough so that there's an article entitled "Why are RNA virus mutation rates so damn high?" We've already seen a gain of function mutation creating enhanced infectivity and a recombination event involving ferrets, so it's not a stretch that we might see a new more of this in the future. Whether or not it will impact the toxicity of the virus or whether or not its susceptible to a vaccine is up in the air, but once an effective vaccine exists strong selective pressure will be placed on versions of the viruses that evade it. [1] https://jvi.asm.org/content/84/7/3134 https://jvi.asm.org/content/84/7/3134 [2] https://www.nature.com/articles/s41564-020-0771-4 https://www.nature.com/articles/s41564-020-0771-4 [3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7111218/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7111218/
- hcknwscommenter 6y ago
  Check out Figure 1 of your cite [3]. Of course mutation rate is high compared to a prokaryote. The point is that coronaviruses (as proven by Fig. 1 of [3]) do not have a high mutation rate for an RNA virus. Indeed, the mutation rate is much lower than influenza.

f38zf5vdt 6y ago

Influenza undergoes recombination seemingly exclusively through reassortment whereas betacoronaviridae undergoes homologous recombination -- but to think of the latter as much less effective at producing genetic diversity may be incorrect. > In fact, there is evidence of at least seven potential regions of recombination in the SARS-CoV genome in the replicase- and Spike-coding regions, with possible recombination partners that include porcine epidemic diarrhea virus (PEDV), transmissible gastroenteritis virus (TGEV), bovine coronavirus (BCoV), HCoV-229E, MHV, and IBV [1] > Unlike other viruses that have emerged in the past two decades, coronaviruses are highly recombinogenic. ... For coronaviruses, however, recombination means that small genomic subregions can have independent origins, identifiable if sufficient sampling has been done in the animal reservoirs that support the endemic circulation, co-infection and recombination that appear to be common. [2] > Recombination seems to be rampant in HCoV-OC43 viruses and contributed to originate the A to E viral genotypes, as well as viruses that do not belong to these major genotypes. [3] Unfortunately, nature doesn't "design" anything, it's just the consequence of natural selection and fitness of new generations. While the mutation rate might low compared to influenza, the mutation rate is very high compared to something like a prokaryote, enough so that there's an article entitled "Why are RNA virus mutation rates so damn high?" We've already seen a gain of function mutation creating enhanced infectivity and a recombination event involving ferrets, so it's not a stretch that we might see a new more of this in the future. Whether or not it will impact the toxicity of the virus or whether or not its susceptible to a vaccine is up in the air, but once an effective vaccine exists strong selective pressure will be placed on versions of the viruses that evade it. [1] https://jvi.asm.org/content/84/7/3134 https://jvi.asm.org/content/84/7/3134 [2] https://www.nature.com/articles/s41564-020-0771-4 https://www.nature.com/articles/s41564-020-0771-4 [3] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7111218/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7111218/

hcknwscommenter 6y ago
Check out Figure 1 of your cite [3]. Of course mutation rate is high compared to a prokaryote. The point is that coronaviruses (as proven by Fig. 1 of [3]) do not have a high mutation rate for an RNA virus. Indeed, the mutation rate is much lower than influenza.