This is not correct. SARS-CoV-2 is nothing like influenza virus from a virological or evolutionary standpoint.

A short thread on some big differences: https://twitter.com/drtomfrieden/status/1353020200757686276

Mutation drives evolution. All RNA viruses, including both orthomyxoviruses (flu) and coronaviruses, have a high mutation rate because the enzyme (RNA-dependent RNA polymerase or RdRp) that copies the genome during replication can’t proofread.

(Incidentally our enzymes that copy our genomes when our cells divide, called DNA polymerase, does have proofreading capabilities, so we have fewer mutations. That, along with our much lower reproduction rate, is why evolution occurs over a much longer time scale for us)

So if the RdRp makes an error, or a typo, when copying the genome, that’s a mutation, a normal occurrence for RNA viruses. However, coronaviruses have another enzyme that DOES proofread, like a partial spell checker. So CoVs have a lower mutation rate than influenza viruses.

Influenza also has a segmented genome. CoV genomes are one big piece of RNA, while flu genomes are divided into 8 pieces. That means if a bird, a pig, or a human is infected with 2 different influenza viruses at once, they can mix and match genome segments, called reassortment.

Reassortment can result in new influenza viruses with unpredictable properties. Reassortant viruses can have different host range, different transmissibility, & different pathogenicity. This can result in rapid emergence of completely new strains.

Coronaviruses can’t reassort because they don’t have segmented genomes. They can recombine but there’s no evidence that recombination is occurring, particularly with regard to these new variants.

Finally, influenza and coronaviruses are subject to different selection pressures driving evolution. Flu evolution occurs in humans, but also in wild and domestic birds and pigs. Cross-species transmission is common due to agricultural practices like factory farming.

Any time a virus crosses species it will adapt to the new host. This can also have unpredictable effects. There are many flu viruses circulating in animals and going back and forth between species. This is not the case for SARS-CoV-2.

While there has been some cross-species transmission of SARS-CoV-2 between humans and farmed mink, this is much less common than for influenza. There are also not multiple sarbecoviruses (SARS-like beta coronaviruses) circulating in domestic animals the way there is for flu.

So the selection pressures driving SARS-CoV-2 are mainly from human hosts, not from a combination of humans + multiple species of birds + pigs. No reassortment is occurring to rapidly create new emergent strains. Mutation is occurring at a slower rate.

While the emergence of new variants with increased transmissibility, different immune properties, and *maybe* increased virulence (I’m not convinced) is indeed ominous, it’s nothing like influenza and we should be glad that it’s not.