Thread: Corona Virus

It should be obvious that in a disease such as this, if a mutation enables the virus to spread more easily or rapidly, this will be the one that will become dominant, simply because it will, over time replace other variants that spread less rapidly. The changes that enable it to spread more rapidly will tend to be the same even if they originate from a different mutation.

This is simply the working of evolution by natural selection, as outlined by Charles Darwin about 160 years ago, and is exactly what we should expect to happen.

Perhaps worth noting that selection for a strain with higher mortality rate is unlikely, as the host dying removes the opportunity for spread, so there is this comfort when contemplating the likely evolution of the virus.

Originally Posted by JDNSW

It should be obvious that in a disease such as this, if a mutation enables the virus to spread more easily or rapidly, this will be the one that will become dominant, simply because it will, over time replace other variants that spread less rapidly. The changes that enable it to spread more rapidly will tend to be the same even if they originate from a different mutation.

This is simply the working of evolution by natural selection, as outlined by Charles Darwin about 160 years ago, and is exactly what we should expect to happen.

Perhaps worth noting that selection for a strain with higher mortality rate is unlikely, as the host dying removes the opportunity for spread, so there is this comfort when contemplating the likely evolution of the virus.

Then how do you explain this? " convergent evolution. "

He walked upstairs, to the office of South Africa’s corollary to Anthony Fauci, an epidemiologist named Salim Abdool Karim, to tell him the news. Days later, they alerted the World Health Organization. Now on the lookout, scientists in the United Kingdom soon discovered one of those mutations spreading in the southeast part of Britain. A few weeks later, an eerily similar cluster of genetic changes surfaced among travelers from Brazil. But neither was a case of jet-setters seeding a single new strain around the world. Analyses of global coronavirus genome databases showed that these were in fact three distinct versions of the virus—three distantly related branches of the SARS-CoV-2 family tree that had independently acquired some of the same mutations despite emerging on three different continents.



That pattern is what scientists refer to as “convergent evolution,” and it’s a sign of trouble ahead.

And then there is another mutation in California

• All viruses change over time. The more people a virus infects, the more chances it has to mutate into a new variant.
• So countries in which the coronavirus is spreading more widely are more likely to see problems like this, experts say.

More than 1 million people in Los Angeles County have gotten COVID-19 since the start of the pandemic. Two-thirds of those cases were reported in the last two months.
According to a preliminary study, one factor driving the area's recent coronavirus surge may be a new variant called CAL.20C. The variant, which is different than the more infectious strains first detected in the UK (B.1.1.7) and South Africa (B.1.351), has become one of the prominent versions of the virus in LA county.

The more a virus spreads, the more it replicates, which raises the likelihood of mutations. So in places where transmission is high, we are more likely to see variants emerge.
The more infectious variants that vaccine developers and public-health experts are keeping their eyes on around the world have similar mutations in the genetic codes for their spike protein, which is what the coronavirus uses to invade cells. Tweaks in the spike protein may make it easier for variants to infect people.
CAL.20C has mutations in that part of its genetic code as well, though it lacks two key mutations that the South Africa and UK variants share. The Cedars-Sinai researchers said additional studies are needed to find out whether CAL.20C spreads more easily than other existing strains, or if it can evade the antibodies our bodies develop in response to infection with the original virus or existing vaccines.




Researchers say a new coronavirus variant found in California may have contributed to Los Angeles' case surge (msn.com)

Originally Posted by bob10

Then how do you explain this? " convergent evolution. "

He walked upstairs, to the office of South Africa’s corollary to Anthony Fauci, an epidemiologist named Salim Abdool Karim, to tell him the news. Days later, they alerted the World Health Organization. Now on the lookout, scientists in the United Kingdom soon discovered one of those mutations spreading in the southeast part of Britain. A few weeks later, an eerily similar cluster of genetic changes surfaced among travelers from Brazil. But neither was a case of jet-setters seeding a single new strain around the world. Analyses of global coronavirus genome databases showed that these were in fact three distinct versions of the virus—three distantly related branches of the SARS-CoV-2 family tree that had independently acquired some of the same mutations despite emerging on three different continents.



That pattern is what scientists refer to as “convergent evolution,” and it’s a sign of trouble ahead.

The three variants came from mutations in three separate areas and only acquired SOME of the same mutations.

The virus will mutate more with the more new infections and some of those mutations are going to be similar in different places just because of the sheer number of cases.

DL

Edit: I see you've partly answered your question while I wrote this.

Originally Posted by 350RRC

The three variants came from mutations in three separate areas and only acquired SOME of the same mutations.

The virus will mutate more with the more new infections and some of those mutations are going to be similar in different places just because of the sheer number of cases.

DL

Edit: I see you've partly answered your question while I wrote this.

It's far more involved than that. From the NYT.;

Like any virologist, Goldstein is hesitant to anthropomorphize his subjects. Viruses don’t have dreams and desires. They’re intelligent micromachines programmed to make as many copies of themselves as possible. But one way to do that is to increase their odds of invading new hosts. SARS-CoV-2 does that by guiding the array of spike proteins that coat its exterior toward a protein called ACE2 that sits on the outside of some human cells. The spike is encrusted in sugars which camouflage the virus from the human immune system, except for the very tip, known as the receptor binding domain, or RBD for short. This exposed section is the part that latches onto ACE2, changing the receptor’s shape—like a key rearranging the tumblers inside a lock—and allowing the virus to enter the cell and start replicating.
The mutations that have scientists so worried all occur in that little exposed bit of spike. And now researchers are racing to figure out how each of them might be giving SARS-CoV-2 some new tricks.

There’s N501Y, a mutation that occurs in all three variants, which replaces the coronavirus’s 501st amino acid, asparagine, with tyrosine. Studies in cells and animal models suggest that the change makes it easier for SARS-CoV-2 to grab onto ACE2, which is one hypothesis for why the variant has been, at this point, pretty convincingly associated with increased transmission. The best evidence for that so far has come out of the UK, which is doing more genomic sequencing than any other country in the world. Scientists there estimate that the UK variant, alternatively known as B.1.1.7, is between 30 and 50 percent more infectious than other circulating strains.

A Brazilian variant, also called P1, and the South African one, sometimes called B.1.351, also have a second and third mutation in common: K417T and E484K. At this moment, scientists know more about the latter. It changes an amino acid that was negatively charged to one that’s positively charged. In variants without this mutation, that section of the RBD sits across from a negatively charged stretch of ACE2, so they repel away from each other. But the E484K mutation reverses that charge, making them snap tightly together instead.

Scientists at the Fred Hutchinson Cancer Research Center found that E484K might be the most important alteration when it comes to enhancing the virus’s ability to evade immune defenses. In lab experiments, they observed that antibodies in the blood of recovered Covid-19 patients were 10 times less effective at neutralizing variants possessing the E484K mutation. In a separate study, some of De Oliveira’s colleagues tested the blood from Covid-19 patients who fell ill in South Africa’s first wave, and they found that 90 percent of them had some reduced immunity to the new E484K-containing variant. In nearly half of the samples, the new variant escaped the preexisting antibodies completely. Another study by another South African colleague, this time using live virus, found similar results. (All are being shared as preprints—neither has yet been peer-reviewed, as has become common in the age of Covid.)

All the evidence is starting to point in the same direction,” says de Oliveira. “We have a virus that is much less neutralized by convalescent plasma.” It’s still too soon to tell what that means in the real world. True reinfections are notoriously difficult to pin down. Scientists have to sequence samples taken from the first bout of illness and the second, and then compare the genetic signatures to determine if a different viral variant is responsible for each infection. De Oliveira says his group is in the process of doing that right now, and they’re finding many instances of what appear to be real reinfections with the South African variant. That data is not yet published. And until they sequence more samples, they can’t say whether B.1.351 is causing more reinfections than previous versions of the virus, which would be a sign that herd immunity might be much farther off than previously thought.

Originally Posted by bob10

It's far more involved than that. From the NYT.;

................... Viruses don’t have dreams and desires. They’re intelligent micromachines programmed to make as many copies of themselves as possible. ............

Seems like a bit of contradictory journo speak there. There is no way a virus consciously mutates, it just happens by the sheer number of replications.

Sure there is a lot of concern about what may happen with some of mutant strains. It seems really strange that some countries still don't take serious measures to minimise infection rates, and therefore replication, to reduce the chance of mutation.

Vaccinations are not going to stop new infections apparently.

In the unlikely event an Australian variant emerged I wonder what the consequences might be? ()

17 1/2 % more infectious while on holidays?

Maybe a NZ variant might cross over to sheep? It'd be hard to keep out of Oz in any case.

DL

Originally Posted by 350RRC

Seems like a bit of contradictory journo speak there. There is no way a virus consciously mutates, it just happens by the sheer number of replications.



DL

They are actually the words of Stephen Goldstein, an evolutionary virologist [ and that's a new one for me] who studies coronaviruses at the University of Utah, so I think he might know what he is talking about.

"All viruses mutate. They are, after all, just autonomous bits of protein-encased, self-replicating strings of code equipped with imperfect internal spell-checkers. Make enough copies and there are bound to be mistakes. Coronaviruses actually make fewer mistakes than most. This one, SARS-CoV-2, evolves at a rate of about 1,100 changes per location in the genome annually—or about one substitution every 11 days."

And, it's all about the money.

• Sweden had a contract to buy the Pfizer-BioNTech vaccine at five doses a vial.
• But Pfizer increased the dose size to six on January 8 and started charging Sweden for six doses per vial.
• Sweden is pausing payments to Pfizer until it gets clarity on why it's being charged for more than agreed

At least 192,700 vaccinations have been completed in Sweden as of Tuesday, Tegnell said, according to The Local.
In the early stages of the pandemic, Sweden was the focus of the world for its decision not to impose a lockdown and instead pursue herd immunity.
However, after suffering a high death rate per capita following a second wave this winter, the Swedish government passed a law in early January allowing it to close restaurants, bars, shops, and public transport in effort to stop the virus from spreading further.







Sweden is withholding vaccine payments to Pfizer as it suspects it is being overcharged (msn.com)