This is the article I read which says the strains of the SARS-CoV-2 coronavirus found in the US are generally milder than the more deadly strains found in Europe. The exception seems to be New York, which has the more deadly European strains.
There might be some better articles on this subject, but I have not actually Googled it.
I saw the phylogenetic tree, had a wtf moment, and then did some research. Still have a lot of doubts personally, let me tell you.
The coronavirus family actually have what is called an mRNA proofreader mechanism, which makes it less prone to phylogenetic drift. The mutations you are seeing, and the "two main strains" you might have heard of are typically benign or useless mutations, that have no selective pressures, don't make it more infectious or deadly, and don't contribute rapidly to the error catastrophe—the extinction of an organism as a result of excessive mutations.
This is something that actually happened with the 1918 subtype, losing much of its lethality.
In this paper, we examine an alternative point of view regarding mutation accumulation within H1N1. We suggest that, while specific adaptive mutations commonly occur within the H1N1 virus, many more deleterious mutations are accumulating than beneficial mutations, even when there is strong selection. Consequently, H1N1 appears to have been in very gradual error catastrophe throughout its history.
Our results strongly confirm the widely recognized fact that all past and present human and swine H1N1 influenza strains derive from the 1918 strain. By extension, this applies to other human influenza strains, including H3N2 and H2N2 [1].
It seems unlikely this new coronavirus will mutate itself to death sadly. And I haven't seen any evidence to support the idea that the mutations out there already have had a huge effect on infectivity or lethality.
End game
Some researchers hope that the virus will weaken over time through a series of mutations that adapt it to persist in humans. By this logic, it would become less deadly and have more chances to spread. But researchers have not yet found any sign of such weakening, probably because of the virus’s efficient genetic repair mechanism. “The genome of COVID-19 virus is very stable, and I don’t see any change of pathogenicity that is caused by virus mutation,” says Guo Deyin, who researches coronaviruses at Sun Yat-sen University in Guangzhou.
Rambaut, too, doubts that the virus will become milder over time and spare its host. “It doesn’t work that way,” he says. As long as it can successfully infect new cells, reproduce and transmit to new ones, it doesn’t matter whether it harms the host, he says.
But others think there is a chance for a better outcome. It might give people antibodies that will offer at least partial protection, says Klaus Stöhr, who headed the World Health Organization’s SARS research and epidemiology division. Stöhr says that immunity will not be perfect — people who are reinfected will still develop minor symptoms, the way they do now from the common cold, and there will be rare examples of severe disease. But the virus’s proofreading mechanism means it will not mutate quickly, and people who were infected will retain robust protection, he says.
“By far the most likely scenario is that the virus will continue to spread and infect most of the world population in a relatively short period of time,” says Stöhr, meaning one to two years. “Afterwards, the virus will continue to spread in the human population, likely forever.” Like the four generally mild human coronaviruses, SARS-CoV-2 would then circulate constantly and cause mainly mild upper respiratory tract infections, says Stöhr. For that reason, he adds, vaccines won’t be necessary.
Some previous studies support this argument. One10 showed that when people were inoculated with the common-cold coronavirus 229E, their antibody levels peaked two weeks later and were only slightly raised after a year. That did not prevent infections a year later, but subsequent infections led to few, if any, symptoms and a shorter period of viral shedding.
The OC43 coronavirus offers a model for where this pandemic might go. That virus also gives humans common colds, but genetic research from the University of Leuven in Belgium suggests that OC43 might have been a killer in the past11. That study indicates that OC43 spilled over to humans in around 1890 from cows, which got it from mice. The scientists suggest that OC43 was responsible for a pandemic that killed more than one million people worldwide in 1889–90 — an outbreak previously blamed on influenza. Today, OC43 continues to circulate widely and it might be that continual exposure to the virus keeps the great majority of people immune to it.
But even if that process made OC43 less deadly, it is not yet clear whether something similar would happen with SARS-CoV-2. A study in monkeys showed that they retained antibodies to SARS-CoV-2, but the researchers only reported on the first 28 days after infection, so it is unclear how long the immunity lasted12. Concentrations of antibodies against SARS-CoV also dropped significantly over a two- to three-year period13. Whether those lowered levels would be enough to prevent infection or reduce severity has not been tested. Cats, cows, dogs and chickens do not seem to become immune to the sometimes deadly coronaviruses that infect them, leaving veterinarians over the years to scramble for vaccines. Despite all the questions about whether people retain any immunity to SARS-CoV-2, some countries are promoting the idea of giving survivors ‘immunity passports’ to allow them to venture out without fear of being infected or infecting others.
Many scientists are reserving judgement on whether the tamer coronaviruses were once as virulent as SARS-CoV-2. People like to think that “the other coronaviruses were terrible and became mild”, says Perlman. “That’s an optimistic way to think about what’s going on now, but we don’t have evidence.”
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