Coronavirus mutations - Politics Forum.org | PoFo

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By Atlantis
#15148207
Scientists have always claimed that SARS-CoV-2 is relatively stable and that it doesn't mutate much. But that doesn't mean that it doesn't mutate at all. In fact, the greater the number of cases, the more mutations there are going top be.

The original L and S strains from China were replaced by the G strain from Italy in the spring, probably because it is more contagious and also because China used stringent controls to stamp out the virus.

While previous mutations were minor, the mutations we have seen in recent months are greater and can alter the virus' properties such as mortality or transmissibility. The British variant B. 1.1.7, which was first detected in Kent on September 20th, has 18 mutations that occurred in the same host, possibly a patient who was ill for weeks in which the virus mutated to evade an antibody therapy.

if antibody therapy is administered after many weeks of chronic infection, the virus population may be unusually large and genetically diverse at the time that antibody-mediated selective pressure is applied, creating suitable circumstances for the rapid fixation of multiple virus genetic changes through direct selection and genetic hitchhiking


8 of the 18 mutations in the British variant are in the spike protein, which docks the virus to human cells and which is also targeted by the new mRNA vaccines and by a number of vector vaccines. The B.1.1.7 variant has made the virus more transmissible so that it is now the dominant strain in the UK, from where it has spread to more than 40 other countries. Even if virus mortality is not increased, it will kill many more people because it spreads so rapidly. Despite containment measures, daily new infections in the UK have grown 4.5 times in a single month from around 15k to 68k.

Biontech/Pfizer have said that their vaccine is still effective against the new variant, but they have only conducted a small lab test against one of the mutations.

Mutation in SARS-CoV-2 Variant Does Not Affect Vaccine: Study

While the British variant spreads across the globe, new variants keep on popping up almost on a daily basis. The Danish mink variant doesn't seem to have spread, but there is a lot of concern about the South African variant, which is also more transmissible. It's still not clear if it doesn't evade the vaccines. There are also new variants in Nigeria, Brazil and the US, about which little is known at this point.

The virus has become constantly more transmissible and therefor also kills more people. Even if current variants don't evade vaccines, we don't know if the vaccines will have the same efficacy. With the exponential growth we see across the globe, it's just a matter of time before it evades vaccines or leads to reinfections.

It's a miracle that we got vaccines in less than a year, but the rollout of the vaccines won't be fast enough to halt the current exponential growth. More countries need to apply hard lockdowns to prevent further deaths and the rapid mutations which are bound to evade the vaccines sooner or later.
#15148224
Atlantis wrote:Scientists have always claimed that SARS-CoV-2 is relatively stable and that it doesn't mutate much. But that doesn't mean that it doesn't mutate at all. In fact, the greater the number of cases, the more mutations there are going top be.

The original L and S strains from China were replaced by the G strain from Italy in the spring, probably because it is more contagious and also because China used stringent controls to stamp out the virus.

While previous mutations were minor, the mutations we have seen in recent months are greater and can alter the virus' properties such as mortality or transmissibility. The British variant B. 1.1.7, which was first detected in Kent on September 20th, has 18 mutations that occurred in the same host, possibly a patient who was ill for weeks in which the virus mutated to evade an antibody therapy.



8 of the 18 mutations in the British variant are in the spike protein, which docks the virus to human cells and which is also targeted by the new mRNA vaccines and by a number of vector vaccines. The B.1.1.7 variant has made the virus more transmissible so that it is now the dominant strain in the UK, from where it has spread to more than 40 other countries. Even if virus mortality is not increased, it will kill many more people because it spreads so rapidly. Despite containment measures, daily new infections in the UK have grown 4.5 times in a single month from around 15k to 68k.

Biontech/Pfizer have said that their vaccine is still effective against the new variant, but they have only conducted a small lab test against one of the mutations.

Mutation in SARS-CoV-2 Variant Does Not Affect Vaccine: Study

While the British variant spreads across the globe, new variants keep on popping up almost on a daily basis. The Danish mink variant doesn't seem to have spread, but there is a lot of concern about the South African variant, which is also more transmissible. It's still not clear if it doesn't evade the vaccines. There are also new variants in Nigeria, Brazil and the US, about which little is known at this point.

The virus has become constantly more transmissible and therefor also kills more people. Even if current variants don't evade vaccines, we don't know if the vaccines will have the same efficacy. With the exponential growth we see across the globe, it's just a matter of time before it evades vaccines or leads to reinfections.

It's a miracle that we got vaccines in less than a year, but the rollout of the vaccines won't be fast enough to halt the current exponential growth. More countries need to apply hard lockdowns to prevent further deaths and the rapid mutations which are bound to evade the vaccines sooner or later.


The variation ratio of covid 19 is equal to the flu where there are only one or more consequential variants per year
By Atlantis
#15148360
Brandenski wrote:The variation ratio of covid 19 is equal to the flu where there are only one or more consequential variants per year


I doubt that there is only one consequential flu variant a year. It's more like the manufacturers try go guess the dominant strains ahead of each flu season and than design a vaccine that'll work with most of the likely variants. Anyways, SARS-CoV-2 is different from flu viruses in a number of ways.

Firstly, it's more deadly. Therefore greater interventions are required.

Secondly, it is not as seasonal as flu viruses. It continued to spread all year round even during the summer. If you are worried about the flu in my part of world, you get a flu shot in November. That'll give you reasonable protection until about April. For the rest of the year you don't have to worry about the flu. That's going to be different with Covid19.

The good news is that the new mRNA vaccines can be redesigned in about 7 weeks to adapt to new mutations.
By Atlantis
#15148498
There has been the first case of reinfection with the new B.1.1.7 variant in the UK. A man who was first infected with the wild version of the virus on April 2nd, and who had tested negative multiple times after recovery, was infected with the new variant in December, eight months after the first infection.

England has reported the first confirmed case of reinfection with the “more contagious” coronavirus variant which was first discovered in the UK. According to David Harrington, who works at the NHS in London, the case involved a 78-year-old man with significant underlying health conditions, but with no history of immunosuppression.

The man presented with fever while undergoing haemodialysis on April 2 and tested positive for COVID-19, but was discharged home and had an uneventful recovery. He continued to be routinely tested while undergoing haemodialysis and tested negative 22 times between May 5 and December 1. Antibodies were detected on 6 occasions between May 5 and December 1 with no evidence of antibody waning.

The patient developed shortness of breath in mid-December and he was rushed to hospital on December 14 when his condition worsened. “He was brought in by ambulance in extremis, very short of breath and unable to talk, with severe hypoxia, leading to emergency intubation,” Harrington said. The man was admitted to ICU with severe pneumonia, which was complicated by a heart attack. The man’s current condition has not been released.

“The [whole genome sequencing] results confirm reinfection with a different lineage 8 months after initial infection in the absence of significant immunocompromise. The reinfection was with the ‘new variant’ VOC202012/01,” Harrington said. He noted that the variant has raised questions about possible immune escape and vaccine evasion, but emphasized that more research is needed. (Source)


VOC202012/01 was the initial designation given to the B.1.1.7 variant. VOC is short for Variant of Concern.

There is also a report about a reinfection with the South African variant in Brazil.

SA variant detected in reinfection case in Brazil, first such incidence in the world
By Atlantis
#15149495
Just as we are about to beat the pandemic with vaccines, the virus starts to mutate.

The UK strategy of delaying the 2nd shot by 12 weeks or more will result in numerous partially immune patients in which the virus can mutate to evade the vaccine. That could set us back to square one.

More infectious coronavirus variants will emerge, disease expert predicts

Highly contagious strains already detected in several countries including UK and South Africa

Highly contagious new variants of coronavirus will emerge more frequently and spur further infection waves such as those threatening to overwhelm hospitals in the UK and South Africa, one of the world’s leading infectious disease experts has warned.

Salim Abdool Karim, chairman of South Africa’s Covid-19 ministerial advisory committee, also said it was too early to know the extent to which existing vaccines would provide immunity to the new variants.

Scientists around the world have been alarmed by the rapid spread of the new 501.v2 variant first detected in South Africa and the equally infectious B.1.1.7 variant that has led to a recent surge in cases in the UK. Other variants have emerged recently in Brazil and Japan.

Prof Abdool Karim, the epidemiologist who led South Africa’s fight against HIV/Aids, explained that viruses evolved as they infected people with partial immunity in order to escape recognition by their antibodies.

We’re going to see this occur more commonly now than in 2020, as we vaccinate and as more people are infected,” he said in an interview with the Financial Times.

The epidemiological finding of increased transmissibility was supported by “biological evidence showing the 501.v2 variant binds more readily and more strongly to human cells”, added Prof Abdool Karim.

Image

The Sars-Cov-2 virus that causes Covid-19 has mutated once or twice a month on average since appearing in humans in late 2019. But the variants detected in South Africa and the UK carry about 20 mutations, where previous ones had been associated with one or two significant genetic changes.

Greater numbers of mutations can cause the behaviour of the virus to change more extensively. The variants that originated in the UK and South Africa are both about 50 per cent more infectious than previous forms of the virus, although neither is thought to cause more severe symptoms.

Another question is how the variants interact with the human immune system, in particular whether they reduce the effectiveness of Covid-19 vaccines. “We’ll have an answer within the next two weeks or so but we don’t know yet,” Prof Abdool Karim said of the 501.v2 variant.

Antibodies from people who have recovered from Covid-19 were less effective against the new variant, Prof Abdool Karim said, but “the way in which T-cells and the B-cells function is quite different in vaccine immunity. I wouldn’t extrapolate from natural immunity to vaccine immunity.”

Less is known about the new variant of Sars-Cov-2 detected in Brazil after scientists sequenced 180 viral genomes from the state of Rio de Janeiro.

Researchers from Brazil’s national genomic surveillance network identified a “significant increase” in cases of the variant that “raise concerns about public health management” in a country with more than 200,000 Covid-19 deaths, the second-highest number of fatalities after the US.

Carolina Voloch of the Federal University of Rio de Janeiro, lead author of a preprint paper about the variant, said that samples taken from Rio state showed it increased in frequency from zero in September to 20 per cent by November.

“For now we can’t say it’s more contagious. What we can say is there’s an increase in the frequency of this lineage,” said Dr Voloch.

Japanese authorities also detected a new variant in four passengers who arrived from Brazil on January 2. It is related to the B.1.1.248 variant of the virus circulating in Brazil, and shares some of the same mutations as the UK and South African variants, according to Japan’s National Institute of Infectious Diseases.

But Emma Hodcroft, a viral geneticist at the University of Bern who monitors the evolution of Sars-Cov-2, said: “It doesn’t look as though these four cases from Japan are part of the larger Brazilian cluster.”

She agreed that conditions in 2021 were likely to favour the evolution of more variants with multiple mutations, as a larger proportion of people were infected and evolutionary pressure on the virus increased.

A modelling study by scientists at Emory and Penn State, published in Science journal on Tuesday, suggested the evolutionary path for Sars-Cov-2 would eventually lead to a less virulent “endemic” virus, joining the ranks of other mild cold-causing coronaviruses that currently circulate in humans.

“We’re in uncharted territory but . . . immunological indicators suggest that fatality rates and the critical need for broad-scale vaccination may wane in the near term, so maximum effort should be on weathering this pandemic,” said Ottar Bjornstad, a Penn State professor.

Prof Abdool Karim also made the point that the selective pressure for all viruses was to “become more transmissible and less pathogenic over time”.
By Atlantis
#15150208
In Brazil the pandemic is about to take a turn for the worse. The new Brazilian virus variant B1128/P1 is driving a new wave of infections like the British variant B117 in the UK. In addition, the Brazilian variant has the E484K mutation that can evade antibodies.

By Atlantis
#15150218
Some of the most worrisome mutations have occurred in the UK, Brazil, the US and South Africa, all countries in which governments have failed to a lesser or greater degree in controlling the spread of the pandemic.

A worrying coronavirus mutation is discovered in Washington state

Three COVID-19 infections diagnosed in Washington in October were caused by virus with a mutation that might boost the respiratory bug’s ability to dodge immune defenses.

The mutation, called E484K, is also present in two of the worrisome new viral variants spreading around the globe — those that originated in South Africa and Brazil. But the virus detected in Washington did not have any of the other mutations that characterize those variants, said researchers at the UW Medicine Virology Lab.

No other infections with the mutation have been detected since October, though surveillance is limited in the state.

“Based on what we have right now, it hasn’t taken off,” said computational biologist Pavitra Roychoudhury, part of a team that sequenced the three genomes. “We definitely want to keep an eye on it.”

The mutation has been spotted sporadically in the U.S. since spring, said Trevor Bedford, a computational biologist at the Fred Hutchinson Cancer Research Center who has been tracking genetic changes in the virus since the start of the pandemic.

Those isolated sightings haven’t sparked major outbreaks. “It appears that just having the (E484K) mutation isn’t enough to make a huge difference to the virus,” he wrote in an email. However, in combination with the 10 or more other mutations in the South Africa and Brazil variants, it is spreading rapidly.

The mutation is located at a specific site on what’s called the “receptor binding domain” — the part of the viral spike protein that latches on to human cells.

A research team at The Hutch recently identified that site as the most concerning, because changes there seem to make the virus more difficult for some people’s antibodies to neutralize.

However, laboratory experiments showed that while the mutations might dampen immunity, they don’t wipe it out, said Fred Hutch virologist Jesse Bloom, who collaborated with graduate student Allison Greaney and others on the work.

Genetic changes in the virus are raising alarms because several new variants have emerged recently around the world, some of which spread more easily. None of the new variants have yet been detected in Washington, though the variant now dominant in the U.K. has popped up in several other states.

One of the biggest worries is that the virus will morph to the point where it can evade the body’s immune response, either natural or vaccine-induced. At least one person in Brazil who had recovered from COVID-19 was reinfected by the variant with the E484K mutation.

It’s probably inevitable that the virus will someday outwit vaccines, Bloom said. But that will take several years, giving pharmaceutical companies time to tweak their formulas, as they do every year for the flu vaccine.

“It’s not something that the average person needs to get really worried about every time they hear about another of these mutations,” he said. “It’s not going to cause catastrophic failure of immunity.”

But more contagious forms of the virus, like the U.K. variant, are likely to have major impacts in terms of surging numbers of infection and deaths.

To understand how viral evolution can affect immunity, Bloom and his team examined all 4,000 possible mutations in the receptor binding domain. In lab experiments, they tested each mutation to see how it affected the virus’ ability to bind to human cells. They also exposed the mutated spike proteins to blood serum from 11 people who had been infected by the virus and recovered.

In most cases, the mix of antibodies in the patients’ blood was able to attack and neutralize the mutants. The main exception was E484K and related mutations, which reduced the potency of some patients’ antibodies by a factor of 10. But other patients’ sera had no trouble fighting the mutant form, Bloom said.

The results were posted recently but have not yet been peer-reviewed or published in a scientific journal. Bloom and his team are now working to evaluate the mutations’ impact on vaccine-induced immunity.

The three Washington cases with the E484K mutation were discovered during routine genome sequencing as part of a surveillance system for new variants, Roychoudhury explained. The sequences were submitted to a repository called GISAID, where a researcher flagged the mutations.

The team at the UW Virology Lab works with randomly selected leftover specimens from positive coronavirus tests. All of the identifying information is stripped away, so they don’t know anything about the cases, including where they occurred, how they may have been related, or how the patients fared, Roychoudhury said.

The absence of related cases suggests the infections may have been dead ends, said Alex Greninger, assistant director of the virology lab.

“These viruses are not omnipotent,” he said. “If someone has a variant virus, but they’re not interacting with other people, it’s not going to transmit.”
By Atlantis
#15150225
Molecular dynamic simulation reveals E484K mutation enhances spike RBD-ACE2 affinity and the combination of E484K, K417N and N501Y mutations (501Y.V2 variant) induces conformational change greater than N501Y mutant alone, potentially resulting in an escape mutant

Rapidly spreading SARS-CoV-2 variants present not only an increased threat to human health due to the confirmed greater transmissibility of several of these new strains but, due to conformational changes induced by the mutations, may render first-wave SARS-CoV-2 convalescent sera, vaccine-induced antibodies, or recombinant neutralizing antibodies (nAbs) ineffective.
#15150420
not that I want to evade the forum practice about forbidden linking to other e-forums, but in case of this concerning thread and the urgency that have emerged from the sars-2 pandemics, I would suggest we should also comment here the mutation topic posts from avianflutalk forum ...

► Show Spoiler


I notice they said they really didn't know a lot about how these mutations were going to affect the virus....with that said, how can they be so sure the vaccination will work? I am not anti-vaccine by any means, but from a medical perspective, it seems weird to say in one sentence "we don't know enough about this new strain" and then in another "the vaccine will still work"
________________________________
NOW is the Season to Know that Everything you Do is Sacred


As i said in another thread.....
We are enhancing mutations by international travel....
In a few weeks we will see another mutation/varient/evolution.....
Call it what you will, Trouble is it's already here.....
Lurking in some backwater waiting, waiting........
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Everything we hear is an opinion, not a fact. Everything we see is a perspective, not the truth.
Marcus Aurelius


To be clear, the article is saying the UK variant is not 40-70% more transmissible, but 231% more, yes?
________________________________
"Every thing looks great, until you think." Dr. Al Bartlett


in my case of dull observer on this pandemic hype, and with the little knowledge that I have on epidemiology and virology, what I can point is first of all stay healthy through healthy lifestyle ... this approach is utmost logical first defense because until we awake to the fact that updating vaccines is not easy job many will suffer and die, but how can governments push for antijunkfood mentally, when there is poverty deadend, aside that also their economies depend from such consumerist glitch!?

... must say I am not antivacer, even less conspi prone about this pandemic, although I've made unnecessary joke while trying to defend China indirectly [1] yet I am furious how there is no joint effort at least through who and un to address this pandemic with mutual vaccine response, its almost ridiculous how they relay individually on with vaccine hype although they are too late in case of these new mutations ...
By Atlantis
#15150426
Odiseizam wrote:I am furious how there is no joint effort at least through who and un to address this pandemic with mutual vaccine response,


There is an international joint vaccine procurement initiated by the EU, which is now known as Covax, and which is to provide 2 billion doses of vaccines to poor countries by the end of the year. The imperialist powers: US, China and Russia did not joint the international cooperation. Instead they are trying to use their vaccines to expand their global hegemonic influence.

The EU has also opted for a joint vaccine procurement to provide vaccines to poor and rich member alike.
#15150443
@Atlantis still that dont pardon europeans why they didnt done more to overcome the differences with russians and encourage them on collaboration eg. with proposal for lifting of sanctions or chinese eg. with new trade deal ... as if they hope that this pandemic is similar to the previous, hm as in case of economic crises every next is more deadly and more difficult to manage ...
By Atlantis
#15150524
In short: researches studied the combination of mutations that would make SARS-CoV-2 more dangerous. They found that changing 0.6% of the virus genome at S477N, E484K, and N501Y would make the virus bind to the human ACE2 receptors 600 times more tightly than the original virus.

The combination of these three mutations hasn't yet appeared in any new variant; however,

- the British B.1.1.7 variant has the N501Y mutation,
- the South African B.1.358 variant has the E484K and N501Y mutations, and
- the Brazilian B.1.1.28 variant has the E484K, K417T and N501Y mutations.

The Brazilian variant is the closest to what the researches found to be the most dangerous mutation. RT-PCR test samples show that this variant represented almost half of positive cases in Manaus, Brazil, by the 2nd half of December.

Can SARS-CoV-2 Become Even More Troublesome Than The UK And South African Variants?

We are rapidly learning how SARS-CoV-2 mutates to create variants with new characteristics. Some of these new variants, such as those found in the UK and South Africa, may affect our ability to control the pandemic, including contagion mitigation, diagnosis, and vaccination.

Over the past few weeks, reports show that some variants of SARS-CoV-2 are more contagious than earlier strains. Sequence analysis of these variants reveals that their genome and proteins differ subtly from their less infectious origins. The viral protein studied in most detail is the spike protein. Multiple independent isolates harbor changes in the spike protein that account, at least partially, for their increased transmissibility.

In a preprint published on January 11, scientists from the Weizmann Institute of Science describe an experiment in which they attempt to mimic what occurs naturally. They looked for laboratory-created variants that stick more tightly to a structure on the cell’s surface that the virus uses to gain entry into our bodies. They were successful. The absolute winner bound the cell surface receptor, the ACE2 protein, 600 times more tightly than the original virus.

The shocking result was that their lab experiment reproduced almost exactly changes in naturally occurring strains in the UK and South Africa, and elsewhere. The lab-generated variants include precisely the same variants, specifically the changes designated S477N, E484K, and N501Y. The variants convey the same advantage in the test tube as they do in populations.

The winning laboratory-created variant contains seven amino acid substitutions in the spike protein's receptor-binding domain. Studies of the structure of the protein reveal their function. Four of the seven stabilize the spike protein structure, and three tighten the intimate contacts the spike makes with the ACE receptor.

These were not the only laboratory-created variants the researchers found. Some convey only a slight binding advantage. However, when combined with the ensemble of three winners, S477N, E484K, and N501Y, they create a spike protein that binds 600 times more tightly to the receptor than the original. This particular combination of variants has not yet been observed in nature. Given the rapid rate of change, it seems such a variant may appear soon. We may then be dealing with a more infectious virus than either the UK or South African strains. The public health implications of such an event are profound.

Detailed analysis of the variants reveals how they improve the virus's ability to bind the ACE2 receptor. Four of the seven changes stabilize the spike protein structure, while three tighten the spike's intimate contacts with ACE2.

In contemplating these observations' significance, consider that the scientists modified no more the 0.6% of the total genome and only about 12% of the spike protein. Analysis of many of the new variants that appear to be more infectious and seem to escape immune pressure reveals other spike locations and other viral proteins of interest. A similar study of the entire genome will likely reveal other tricks the virus deploys to increase infectivity and avoid immune detection.

Last spring SARS-CoV-2 variant that contained the spike mutation D614G spread more rapidly. This strain was so successful it has now displaced all others. All of the newly discovered more infectious variants contain the D614G. In other words, these new mutations ratchet up virus infectivity still further. The laboratory experiments described here suggest that naturally occurring variants have not yet reached the peak of infectivity.

It may be helpful to picture SARS-CoV-2 variants as a rapidly growing tree. At the base of the tree, a single strain of the virus provide the trunk. Ascending the tree branches appear, variants that contain all the earlier changes and still more of their own. Each is more fit to survive in its environment, the human population, than is its immediate ancestor. As we climb higher, the variants become more numerous, different from one another, even more fit to survive and flourish. What began as a few variants soon become many thousands, bedeviling our attempts to mitigate infection and disease.

We must prune the tree. We need to reduce the number of branches, stunt the tree. How? With methods advocated all along. We must administer vaccines as quickly as possible; we need to reinforce public health measures — social distancing, mask-wearing, and social isolation. As needed appropriate, we must incentivize and, if necessary, enforce the isolation of those exposed and contagious.

However dangerous we thought our foe, until a few weeks go we were confident we knew its form. We now realize that SARS-CoV-2 is a shape changer. Like Proteus, it changes even as we hold it in our grasp. As Hercules prevailed, separating Anteus from his mother earth, we must clear the ever-growing forest of virus variants by reducing the numbers of people infected, not only in our country but everywhere it has taken root.


Genomic characterisation of an emergent SARS-CoV-2 lineage in Manaus

We have detected a new variant circulating in December in Manaus, Amazonas state, north Brazil, where very high attack rates have been estimated previously. The new lineage, named P.1 (descendent of B.1.1.28), contains a unique constellation of lineage defining mutations, including several mutations of known biological importance such as E484K, K417T, and N501Y. Importantly, the P.1 lineage was identified in 42% (13 out of 31) RT-PCR positive samples collected between 15 to 23 December, but it was absent in 26 publicly available genome surveillance samples collected in Manaus between March to November 2020. These findings indicate local transmission and possibly recent increase in the frequency of a new lineage from the Amazon region. The higher diversity and the earlier sampling dates of P.1. in Manaus corroborates the travel info of recently detected cases in Japan, suggesting the direction of travel was Manaus to Japan. The recent emergence of variants with multiple shared mutations in spike raises concern about convergent evolution to a new phenotype, potentially associated with an increase in transmissibility or propensity for re-infection of individuals.
#15151856
how true or have ground this statement, was indeed the same case with sars-1 after vaccines

From an abundance of caution it should considered that not only will the vaccine suppress the original strain and thereby enhance the new variant's spread, but may also enhance the severity of a second infection. This is not an unknown risk, it happened with SARS.
By Atlantis
#15152272
That is where the gates to hell open

If the virus evades antibodies, neither prior infection nor vaccines will provide immunity.

The mutations of concern described in this paper are similar to those in the new variants from the UK, South Africa and Brazil.

To investigate the evolution of SARS-CoV-2 in the immune population, we co-incubated authentic virus with a highly neutralizing plasma from a COVID-19 convalescent patient. The plasma fully neutralized the virus for 7 passages, but after 45 days, the deletion of F140 in the spike N-terminal domain (NTD) N3 loop led to partial breakthrough. At day 73, an E484K substitution in the receptor-binding domain (RBD) occurred, followed at day 80 by an insertion in the NTD N5 loop containing a new glycan sequon, which generated a variant completely resistant to plasma neutralization. Computational modeling predicts that the deletion and insertion in loops N3 and N5 prevent binding of neutralizing antibodies. The recent emergence in the United Kingdom and South Africa of natural variants with similar changes suggests that SARS-CoV-2 has the potential to escape an effective immune response and that vaccines and antibodies able to control emerging variants should be developed.


SARS-CoV-2 escape in vitro from a highly neutralizing COVID-19 convalescent plasma
By Atlantis
#15152274
The problem is that the virus is always one step ahead of the science.

First, the new variant was ignored, than it was considered to be more transmissible after it spread like wildfire, and now it's considered more deadly since the hospitals are full.

Mr Johnson told a Downing Street briefing: "In addition to spreading more quickly, it also now appears that there is some evidence that the new variant - the variant that was first identified in London and the south east - may be associated with a higher degree of mortality.


Coronavirus: UK variant 'may be more deadly'
User avatar
By Drlee
#15152277
THE SKY IS FALLING! THE SKY IS FALLING!

The problem is that the virus is always one step ahead of the science


:roll: Tell that to Variola Major. It killed 300 million people in the 20th century. (And I lived through half of the 20th century and remember it well.) It was defeated by vaccination. Now you have probably never heard of it.

If you are concerned that it will not work please feel free to let your vaccination go to someone else. There's a good chap.
By Atlantis
#15154605
After saying for months that the virus is "stable", doesn't mutate much, won't evade vaccines and won't lead to reinfections, experts now have to admit that we are facing more and more mutations which have both higher transmissibility and fatality and allow reinfections and vaccine evasion.

The British variant has became the dominant variant in England in December, and is now becoming the dominant variant in Ireland, Portugal and The Netherlands, all countries with close ties to the UK. It has spread to more than 60 countries.

Since the spread of the British variant, Portugal has become the country with the highest Covid death rate in the world. ICUs are full, Germany is sending doctors and equipment while Austria has promised to take ICU patients.

The South African and Brazilian variants are even more dangerous since they have the E484K mutation at the spike protein which can evade antibodies. However, the E484K mutation has now also appeared in the UK.

A number of vaccines makers have tested their vaccines in South Africa. At least recent tests have been conducted while the South African variant had already spread in the country. The result is that Novavax reported 86% efficacy for its UK trial and only 49% for its South African trial. In vaccines with lower efficacy than Novavax, the loss in efficacy could be even greater.

Brazil, the UK and South Africa are accelerated breeding grounds for new variants because of a failed corona response or because of wide spread of HIV, as in South Africa.

In addition, British high risk strategies such as delaying the 2nd shot for 3 months risks to result in new variants which could lead to another wave, reinfections and vaccine evasion.

Vaccine makers are now in a race against the new variants. Luckily the new mRNA vaccine can be updates rapidly, but it'll be a challenge anyways. It could mean that we need a 3rd booster shot not long after the 2nd shot to immunize against the new variants.
By Atlantis
#15155125
This confirms what I said before, the mutations are starting to make vaccines and treatments less effective.

New mutations evading vaccines appear before we get done vaccinating.

New Study of Coronavirus Variants Predicts Virus Evolving to Escape Current Vaccines and Treatments

A new study of the U.K. and South Africa variants of SARS-CoV-2 predicts that current vaccines and certain monoclonal antibodies may be less effective at neutralizing these variants and that the new variants raise the specter that reinfections could be more likely.

The study’s predictions are now being borne out with the first reported results of the Novavax vaccine, says the study's lead author David Ho, MD. The company reported(link is external and opens in a new window) on Jan. 28 that the vaccine was nearly 90% effective in the company’s U.K. trial, but only 49.4% effective in its South Africa trial, where most cases of COVID-19 are caused by the B.1.351 variant.

"Our study and the new clinical trial data show that the virus is traveling in a direction that is causing it to escape from our current vaccines and therapies that are directed against the viral spike,” says Ho, the director of the Aaron Diamond AIDS Research Center and the Clyde’56 and Helen Wu Professor of Medicine at Columbia University Vagelos College of Physicians and Surgeons.

“If the rampant spread of the virus continues and more critical mutations accumulate, then we may be condemned to chasing after the evolving SARS-CoV-2 continually, as we have long done for influenza virus,” Ho says. “Such considerations require that we stop virus transmission as quickly as is feasible, by redoubling our mitigation measures and by expediting vaccine rollout.”

After vaccination, the immune system responds and makes antibodies that can neutralize the virus.

Ho and his team found that antibodies in blood samples taken from people inoculated with the Moderna or Pfizer vaccine were less effective at neutralizing the two variants, B.1.1.7, which emerged last September in England, and B.1.351, which emerged from South Africa in late 2020. Against the U.K. variant, neutralization dropped by roughly 2-fold, but against the South Africa variant, neutralization dropped by 6.5- to 8.5-fold.

“The approximately 2-fold loss of neutralizing activity against the U.K. variant is unlikely to have an adverse impact due to the large 'cushion' of residual neutralizing antibody activity,” Ho says, “and we see that reflected in the Novavax results where the vaccine was 85.6% effective against the U.K. variant.”

Data from Ho’s study about the loss in neutralizing activity against the South Africa variant are more worrisome.

“The drop in neutralizing activity against the South Africa variant is appreciable, and we’re now seeing, based on the Novavax results, that this is causing a reduction in protective efficacy,” Ho says.

The new study did not examine the more recent variant found in Brazil (B.1.1.28) but given the similar spike mutations between the Brazil and South Africa variants, Ho says the Brazil variant should behave similarly to the South Africa variant.

“We have to stop the virus from replicating and that means rolling out vaccine faster and sticking to our mitigation measures like masking and physical distancing. Stopping the spread of the virus will stop the development of further mutations,” Ho says.

The study also found that certain monoclonal antibodies used now to treat COVID patients may not work against the South Africa variant. And based on results with plasma from COVID patients who were infected earlier in the pandemic, the B.1.351 variant from South Africa has the potential to cause reinfection.

New study contains comprehensive analysis of variants
The new study conducted an extensive analysis of mutations in the two SARS-CoV-2 variants compared to other recent studies, which have reported similar findings.

The new study examined all mutations in the spike protein of the two variants. (Vaccines and monoclonal antibody treatments work by recognizing the SARS-CoV-2 spike protein.)

The researchers created SARS-CoV-2 pseudoviruses (viruses that produce the coronavirus spike protein but cannot cause infection) with the eight mutations found in the U.K. variant and the nine mutations found in the South African variant.

They then measured the sensitivity of these pseudoviruses to monoclonal antibodies developed to treat COVID patients, convalescent serum from patients who were infected earlier in the pandemic, and serum from patients who have been vaccinated with the Moderna or Pfizer vaccine.

Implications for monoclonal antibody treatments
The study measured the neutralizing activity of 18 different monoclonal antibodies—including the antibodies in two products authorized for use in the United States.

Against the U.K. variant, most antibodies were still potent, although the neutralizing activity of two antibodies in development was modestly impaired.

Against the South Africa variant, however, the neutralizing activity of four antibodies was completely or markedly abolished. Those antibodies include bamlanivimab (LY-CoV555, approved for use in the United States) that was completely inactive against the South Africa variant, and casirivimab, one of the two antibodies in an approved antibody cocktail (REGN-COV) that was 58-fold less effective at neutralizing the South Africa variant compared to the original virus. The second antibody in the cocktail, imdevimab, retained its neutralizing ability, as did the complete cocktail.

“Decisions of the use of these treatments will depend heavily on the local prevalence of the South Africa and Brazil variants,” Ho says, “highlighting the importance of viral genomic surveillance and proactive development of next-generation antibody therapeutics.”

Reinfection implications
Serum from most patients who had recovered from COVID earlier in the pandemic had 11-fold less neutralizing activity against the South Africa variant and 4-fold less neutralizing activity against the U.K. variant.

“The concern here is that reinfection might be more likely if one is confronted with these variants, particularly the South Africa one,” Ho says.
By Atlantis
#15155354
I have already described how the virus mutates in immunocompromised patients. Here is an example of a patient in which the emergence of a new variant was actually observed by regular gene sequencing of the virus.

Extraordinary Patient Offers Surprising Clues To Origins Of Coronavirus Variants

Michaeleen Doucleff

Back in the spring last year, a 45-year-old man went to the Brigham and Women’s Hospital in Boston because of a COVID-19 infection. Doctors treated him with steroids and discharged him five days later.

But the COVID infection never went away — for 154 days. “He was readmitted to the hospital several times over the subsequent five months for recurrence of his COVID-19 infection and severe pneumonia,” says infectious disease doctor Jonathan Li at Harvard Medical School who helped to treat the man.

“So this is an extraordinary individual,” Li says.

So extraordinary in fact, that this man’s case is offering scientists surprising clues about where the new coronavirus virus variants emerged, and why they’re causing explosive outbreaks on three continents.

To be clear here, the man wasn’t what doctors call a “long hauler,” or a person who clears a COVID infection and then continues to have health problems for months. This man had living, growing virus in body for five months, Li says. The same infection lasted for five months.

“That is one of the remarkable aspects of this case,” Li says. “In fact, he was highly infectious even five months after the initial diagnosis.”

This man had a severe autoimmune disease, which required him to take drugs to suppress his immune system. So his body couldn’t fight off the COVID infection as well as a healthy person. He would get better for a while and then the virus would counterattack. He would fall sick again. Eventually, he ended up in the ICU. He passed away five months after the initial diagnosis.

Throughout the man’s infection, Li and his colleagues ran an illuminating experiment. Every few weeks, the team extracted coronavirus from the man’s body and sequenced the virus’ genome.

Li couldn’t believe what they found. “I was shocked,” he says. “When I saw the virus sequences, I knew that we were dealing with something completely different and potentially very important.”

The sequences showed Li and his team that the virus was changing very quickly inside the man’s body. The virus wasn’t picking up just one or two mutations at a time. But rather, it acquired a whole cluster of more than 20 mutations. Scientists had never seen SARS-Cov-2 mutate so quickly during the whole pandemic.

Furthermore, laboratory experiments have shown that some of those mutations help the virus bypass detection by antibodies.

“Toward the very end of his life, he was treated with monoclonal antibodies, from Regeneron,” Li says. “And shortly thereafter, we saw evidence that suggested the virus was developing resistance or escaping from these antibodies as well.”

Li and his colleagues published their findings in the New England Journal of Medicine back in early November 2020 with little fanfare. Then about a month later, the pandemic took a surprising turn — and this peculiar case in Boston took on a new importance.

Scientists in the U.K. and South Africa announced they had detected new variants of the coronavirus. These variants were causing huge surges of COVID-19 in these countries.

When researchers looked at the genes of these variants, guess what they found? A cluster of mutations that looked remarkably similar to the mutations found in the virus from the Boston patient.
The set of mutations weren’t exactly identical, but they shared important characteristics. They both have about 20 mutations and they share several key ones, including a mutation (N501Y) known to help the virus bind more tightly to human cells and a mutation (E484K) known to help the virus evade antibody detection.

Since Li and his colleagues published their findings, several other teams reported similar cases in which the virus evolved rapidly inside an immunocompromised person with a chronic COVID infection.

“So we have a number of examples, around the planet, in which patients’ viruses suddenly have a whole mess of new mutations all at once,” says virologist Jeremy Luban at the University of Massachusetts Medical School. And other cases have likely gone undetected, he says.

So scientists are starting to think the two phenomena could be related. That perhaps, the new variants arose inside people similar to the man in Boston – that is, people who are immunocompromised and have long-term COVID infections.

“I think that’s the leading theory,” Luban says.

In other words, perhaps, the coronavirus virus uses long-term infections as a mutational testing ground. While inside one person, they can try out all these different combinations of mutations and figure out, through trial and error, which ones are best at evading the immune system or helping the virus become more infectious.

Most of these viral versions probably don’t spread beyond the chronically infected patient. But every once in a while, as the theory goes, a variant gets lucky, infects a large number of people and launches a new whole stage of the pandemic.

And this process is likely happening again right now, worldwide, in other immunocompromised patients. Eventually, these new variants could mutate again and create even more dangerous forms of the virus.
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