A mutation, known as D614G, was discovered which affects the spike protein on the novel coronavirus' surface. The mutation is not new. It appears in low levels in samples taken from COVID-19 patients as far back as February.
Below diagram: Distribution of A23403G (D614G) Mutation and Other Mutations on an Approximate Phylogenetic Tree Using Parsimony
But this variation of the virus (nicknamed the "G" variation) seems to show up in more and more of the virus samples taken from people infected recently compared to early in the pandemic.
A new paper, published July 2 in the journal Cell, argues that the rise in the "G" variation of the new coronavirus is due to natural selection.
The study finds that virus particles with this mutation have an easier time making their way into cells, suggesting that it is out-competing other strains of the virus to become the dominant version of SARS-CoV-2.
Other, not-yet-published experiments have found similar results. However, some researchers are not yet convinced that the mutation has any real-world impact on coronavirus transmission at all. Instead, it's possible that the G variant's spread is due to chance, said Nathan Grubaugh, an epidemiologist at the Yale School of Medicine who co-authored a commentary accompanying the paper's publication.
G versus D
Original samples of the novel coronavirus out of Wuhan, China, were a variation that scientists now call the "D" clade.
Before March 1, more than 90% of viral samples taken from patients were from this D variation.
Over the course of March, G began to predominate.
This mutation is caused by the swapping of an adenine (A) nucleotide to a guanine (G) nucleotide at a particular spot in the coronavirus genome. It always appears alongside three other mutations that similarly swap one building block of RNA for another. (The letters in RNA help code for the proteins the virus makes once inside a cell.)
The G variant represented 67% of global samples taken in March, and 78% of those taken between April 1 and May 18. During this time, the locus of the outbreaks shifted away from China into Europe and the United States.
The mutation piqued interest because it seemed to take over even in areas were the D variation had initially held sway, said Bette Korber, the lead author of the new Cell paper and a computational biologist at Los Alamos National Laboratory in New Mexico. She and her colleagues at Duke University and the La Jolla Institute of Immunology in California inserted the G mutation and D mutations into pseudoviruses, which are viruses engineered to display the surface proteins of other viruses. Pseudoviruses are useful, Korber told Live Science, because they can't spread disease and because they contain molecular tags that researchers can use to track their movement into cells.
The researchers then exposed cell cultures to pseudoviruses with either the G or D variants of the coronavirus spike protein to track which was more infectious.
They found that the G variations led to much higher amounts of virus in the cell culture, indicating increased infection and replication. The viral loads found from G variations of the spike protein were 2.6 to 9.3 times larger than from the D variations of the spike protein.
The pseudoviruses and cells used in the experiment were neither real coronavirus nor human lung cells, but another study that used infectious SARS-CoV-2 virions reached similar findings. That study, which was published July 7 to the preprint server bioRxiv and has not yet been peer-reviewed, was spearheaded by biologist Neville Sanjana at New York University. He and his colleagues tested the G and D versions of SARS-CoV-2 in cell cultures, including human lung cells, and found that the G variant infected up to eight times more cells than the D variant.
Some clinical work has suggested that the G variant's apparent advantage might hold outside of the Petri dish. A study, posted May 26 to the pre-print database medRxiv, also not yet peer-reviewed, led by Northwestern University Feinberg School of Medicine researchers Dr. Egon Ozer, Judd Hultquist found three distinct versions of SARS-CoV-2 circulating in Chicago in mid-March.
Researchers in Washington state have released similar findings. If the results hold up, they could hint at increased transmission, because higher levels of virus in the upper airways might translate to more virus emitted when people breathe and talk, Ozer told Live Science.
But it's impossible to say for sure, he said. Scientists don't even know how many virions a person needs to come into contact with to get infected, so it's not clear if the extra viral load makes a difference.
The outbreak in New York seeded many of the outbreaks in the rest of the United States, including many places where the virus is now running essentially unchecked.
"What's going to be important now is to continue to monitor in these places," Grubaugh said. If the G variant continues to dominate even in places where both the G and D versions are present, that might be a sign that the G mutation does provide the virus a transmission advantage.
The G614 mutation is part of a cluster of four mutations that appear together, Korber said, so more work needs to be done on what the other three mutations might do.
Another important line of work will be testing the genetic variants in animal models that better mimic human transmission. Scientists are working with a number of animals, from ferrets to Syrian hamsters to macaques, to study the coronavirus, but they haven't yet established which animals best represent how the disease spreads from human to human. (Hamsters and ferrets catch influenza much like humans, so scientists hope that they might also be a good animal model for coronavirus spread.)
The findings indicate that it's important for scientists to keep track of the virus' mutations as it spreads. As the virus interacts with more and more immune systems, it will experience more evolutionary pressure and may continue to change, Ozer said.
"We have seen that in the course of one month, a particular form of the virus can go from being very rare to the globally most common form," Korber said. "It could happen again."
"We can't even get a handle on testing, we don't have effective control measures really at all right now… If we keep allowing opportunities for the virus to have a new host, then it's going to keep on spreading, regardless of if it's a more fit variant or not," Grubaugh argued.
BEING INFECTED WITH TWO STRAINS SIMULTANEOUSLY CAN PROVE FATAL
Researchers from the UC Berkeley school of public health said variations of the pathogen circulating in Europe and the United States could be causing “serial infections” in some people, confusing the immune system and triggering an overreaction or even death.
“If one strain is still highly prevalent, the situation should be closely monitored, especially for severe disease occurrence, and social distancing should still be maintained to make sure the second strain doesn’t get introduced,” Lee Riley, professor and chair of the division of infectious disease and vaccinology at the school and lead author of the study, told the South China Morning Post on Thursday.
The D614G strain has further evolved into two major subgroups, one with one extra mutation (C14408T), and the other with two (C14408T, G2556T).
“[The finding] raises a disturbing possibility that people living in places with high prevalence of co-circulating strains may get serially infected with each variant,” the researchers said in the paper.
For example, Germany had low mortality at the early stage of the pandemic but the American strain arrived in March and quickly spread, accounting for as many as half of the cases at one point. Three to four weeks later, the death rates in Germany peaked.
The California city of San Francisco had a low death rate of 1.6 percent, and it has been dominated by the American strain. But Santa Clara county in the same state suffered a co-circulation with the European strain and recorded a death rate three times higher.
REMEMBER THAT LITTLE TONY FAUCI IS NOT A MEDICAL DOCTOR WHO TREATS PATIENTS.
CAN THERE BE ANY DOUBT HE DOESN'T?
THIS ARTICLE FROM THAILAND GIVES A MORE REALISTIC LOOK AT FAUCI's IGNORANCE.
For the Consumer. Applies to adenovirus vaccine:
Side effects include: Upper respiratory tract infection, headache, nasal congestion, pharyngolaryngeal pain (sore throat), cough, arthralgia (musculoskeletal pain), chills, GI effects (abdominal pain, nausea, diarrhea, vomiting).
Pyrexia (temperature of 100.5F or higher), pain in extremity.
SOUNDS SIMILAR TO COVID-19 SYMPTOMS, YES?
AstraZeneca’s Covid-19 vaccine, which made headlines recently when it was halted briefly due to an adverse event in a study volunteer, is built from a variation on a chimpanzee virus. (The Italian company ReiThera has its own vaccine candidate is made from a gorilla adenovirus.)
The leading "vaccine candidates" are viral vector vaccines, which means they use a bio-engineered version of another, milder virus—here it’s one that causes common colds, which is also a coronavirus—as a delivery system.
A new paper, published July 2 in the journal Cell, argues that the rise in the "G" variation of the new coronavirus is due to natural selection.
The study finds that virus particles with this mutation have an easier time making their way into cells, suggesting that it is out-competing other strains of the virus to become the dominant version of SARS-CoV-2.
Other, not-yet-published experiments have found similar results. However, some researchers are not yet convinced that the mutation has any real-world impact on coronavirus transmission at all. Instead, it's possible that the G variant's spread is due to chance, said Nathan Grubaugh, an epidemiologist at the Yale School of Medicine who co-authored a commentary accompanying the paper's publication.
G versus D
Original samples of the novel coronavirus out of Wuhan, China, were a variation that scientists now call the "D" clade.
Before March 1, more than 90% of viral samples taken from patients were from this D variation.
Over the course of March, G began to predominate.
This mutation is caused by the swapping of an adenine (A) nucleotide to a guanine (G) nucleotide at a particular spot in the coronavirus genome. It always appears alongside three other mutations that similarly swap one building block of RNA for another. (The letters in RNA help code for the proteins the virus makes once inside a cell.)
The G variant represented 67% of global samples taken in March, and 78% of those taken between April 1 and May 18. During this time, the locus of the outbreaks shifted away from China into Europe and the United States.
The mutation piqued interest because it seemed to take over even in areas were the D variation had initially held sway, said Bette Korber, the lead author of the new Cell paper and a computational biologist at Los Alamos National Laboratory in New Mexico. She and her colleagues at Duke University and the La Jolla Institute of Immunology in California inserted the G mutation and D mutations into pseudoviruses, which are viruses engineered to display the surface proteins of other viruses. Pseudoviruses are useful, Korber told Live Science, because they can't spread disease and because they contain molecular tags that researchers can use to track their movement into cells.
The researchers then exposed cell cultures to pseudoviruses with either the G or D variants of the coronavirus spike protein to track which was more infectious.
They found that the G variations led to much higher amounts of virus in the cell culture, indicating increased infection and replication. The viral loads found from G variations of the spike protein were 2.6 to 9.3 times larger than from the D variations of the spike protein.
The pseudoviruses and cells used in the experiment were neither real coronavirus nor human lung cells, but another study that used infectious SARS-CoV-2 virions reached similar findings. That study, which was published July 7 to the preprint server bioRxiv and has not yet been peer-reviewed, was spearheaded by biologist Neville Sanjana at New York University. He and his colleagues tested the G and D versions of SARS-CoV-2 in cell cultures, including human lung cells, and found that the G variant infected up to eight times more cells than the D variant.
Some clinical work has suggested that the G variant's apparent advantage might hold outside of the Petri dish. A study, posted May 26 to the pre-print database medRxiv, also not yet peer-reviewed, led by Northwestern University Feinberg School of Medicine researchers Dr. Egon Ozer, Judd Hultquist found three distinct versions of SARS-CoV-2 circulating in Chicago in mid-March.
Some matched the dominant version circulating in New York City, some matched the predominant version from the West Coast, and some seemed most closely related to the original samples from China.
"The virus kind of came both ways around the globe and smacked into Chicago and we got virus originally from China, we think, thanks to O'Hare being such a transportation hub," Hultquist told Live Science.
The New York clade, which contained the G mutation, was linked to a higher viral load in the upper airways than the virus that was closer to the original China strain, the researchers found.
"The virus kind of came both ways around the globe and smacked into Chicago and we got virus originally from China, we think, thanks to O'Hare being such a transportation hub," Hultquist told Live Science.
The New York clade, which contained the G mutation, was linked to a higher viral load in the upper airways than the virus that was closer to the original China strain, the researchers found.
Researchers in Washington state have released similar findings. If the results hold up, they could hint at increased transmission, because higher levels of virus in the upper airways might translate to more virus emitted when people breathe and talk, Ozer told Live Science.
But it's impossible to say for sure, he said. Scientists don't even know how many virions a person needs to come into contact with to get infected, so it's not clear if the extra viral load makes a difference.
The outbreak in New York seeded many of the outbreaks in the rest of the United States, including many places where the virus is now running essentially unchecked.
"What's going to be important now is to continue to monitor in these places," Grubaugh said. If the G variant continues to dominate even in places where both the G and D versions are present, that might be a sign that the G mutation does provide the virus a transmission advantage.
The G614 mutation is part of a cluster of four mutations that appear together, Korber said, so more work needs to be done on what the other three mutations might do.
Another important line of work will be testing the genetic variants in animal models that better mimic human transmission. Scientists are working with a number of animals, from ferrets to Syrian hamsters to macaques, to study the coronavirus, but they haven't yet established which animals best represent how the disease spreads from human to human. (Hamsters and ferrets catch influenza much like humans, so scientists hope that they might also be a good animal model for coronavirus spread.)
The findings indicate that it's important for scientists to keep track of the virus' mutations as it spreads. As the virus interacts with more and more immune systems, it will experience more evolutionary pressure and may continue to change, Ozer said.
"We have seen that in the course of one month, a particular form of the virus can go from being very rare to the globally most common form," Korber said. "It could happen again."
"We can't even get a handle on testing, we don't have effective control measures really at all right now… If we keep allowing opportunities for the virus to have a new host, then it's going to keep on spreading, regardless of if it's a more fit variant or not," Grubaugh argued.
“It has been thought that there are at least six different strain types and this is the dominant one that has taken over," Dr. Ravina Kullar, an epidemiologist, told Fox News.
A virus typically starts out very virulent and deadly and slowly mutates so the host survives, Kullar said.
“This allows it to live in a dormant state in the host and potentially reappear at a later point," she explained.
Dr. Paul Tambyah, an infectious disease expert, told Reuters that data suggests the D614G mutation proliferation has coincided with a drop in death rates in some parts of the world.
“Maybe that’s a good thing to have a virus that is more infectious but less deadly," told Tambyah, also the president-elect of the International Society of Infectious Diseases and a senior consultant at the National University of Singapore, to the news outlet.
MAYBE IT ISN'T.
THAT MIGHT MEAN THOSE WHO HAD THE FIRST STRAIN OUT OF CHINA CAN NOW BE INFECTED BY THIS MUTATION, OR OTHER MUTATIONS.
CHINESE RESEARCHERS ARE SAYING THAT IS HIGHLY LIKELY.
THAT WOULD MEAN THAT EACH MUTATION CAN REINFECT THOSE WHO HAD THE OLDER STRAINS.
THERE IS ALREADY A WARNING ABOUT THE V483G MUTATION BEING ANTIBODY RESISTANT AND EVEN MORE INFECTIOUS.
MEDICAL 'EXPERTS' HAVE ALSO WARNED THAT ONCE VACCINES AND ANTIBODIES ARE USED HEAVILY THAT NEWER MORE RESISTANT STRAINS OF SARS-CoV2 WILL EMERGE.
IT'S THE ABILITY OF VIRUSES TO MUTATE QUICKLY AND OFTEN THAT MAKE THEM ALMOST IMPOSSIBLE TO STOP.
MUTATION N439K INITIALLY APPEARS TO BE ONE OF THOSE TROUBLESOME MUTANTS THAT CAN EVADE HUMAN IMMUNE RESPONSE.
BEING INFECTED WITH TWO STRAINS SIMULTANEOUSLY CAN PROVE FATAL
Researchers from the UC Berkeley school of public health said variations of the pathogen circulating in Europe and the United States could be causing “serial infections” in some people, confusing the immune system and triggering an overreaction or even death.
“If one strain is still highly prevalent, the situation should be closely monitored, especially for severe disease occurrence, and social distancing should still be maintained to make sure the second strain doesn’t get introduced,” Lee Riley, professor and chair of the division of infectious disease and vaccinology at the school and lead author of the study, told the South China Morning Post on Thursday.
The D614G strain has further evolved into two major subgroups, one with one extra mutation (C14408T), and the other with two (C14408T, G2556T).
“[The finding] raises a disturbing possibility that people living in places with high prevalence of co-circulating strains may get serially infected with each variant,” the researchers said in the paper.
For example, Germany had low mortality at the early stage of the pandemic but the American strain arrived in March and quickly spread, accounting for as many as half of the cases at one point. Three to four weeks later, the death rates in Germany peaked.
The California city of San Francisco had a low death rate of 1.6 percent, and it has been dominated by the American strain. But Santa Clara county in the same state suffered a co-circulation with the European strain and recorded a death rate three times higher.
YOU CAN DOWNLOAD THE FULL PDF OF THE BERKELEY STUDY <HERE>.
Fauci: Early COVID-19 vaccines will only prevent symptoms, not block the virus.
October 26, 2020
“The primary thing you want to do is that if people get infected, prevent them from getting sick, and if you prevent them from getting sick, you will ultimately prevent them from getting seriously ill,” Fauci said at Yahoo Finance’s All Markets Summit Monday.
HUH? WHAT THE HELL IS HE SAYING?
“What I would settle for, and all of my colleagues would settle for, is the primary endpoint to prevent clinically recognizable disease,” he said.
That level of protection would be the ultimate goal to diffusing the crisis, but is hard to do with companies facing an immediate demand for some sort of solution. While no vaccine is 100% effective, having a majority of the population inoculated and higher percentages of efficacy is the best to hope for."
The U.K. is looking at challenge trials, which intentionally infect a smaller group of participants with the virus in an effort to test a vaccine’s or treatment’s efficacy.
Fauci said the U.S. is not anticipating such a move because the rate of spread is so high in the [U.S.] that it’s sufficient enough of an environment to test the vaccine. The daily case count for the U.S. in the past few days has reached a new record of more than 80,000 cases.
“So although you can get some good information from a challenge trial, the real-world information that you want is out in the field when someone is actually being exposed to natural infection, and to determine if the vaccine prevents against that,” Fauci said.
“So right now we're not planning any challenge studies because we have so much infection going on.”
October 26, 2020
“The primary thing you want to do is that if people get infected, prevent them from getting sick, and if you prevent them from getting sick, you will ultimately prevent them from getting seriously ill,” Fauci said at Yahoo Finance’s All Markets Summit Monday.
HUH? WHAT THE HELL IS HE SAYING?
“What I would settle for, and all of my colleagues would settle for, is the primary endpoint to prevent clinically recognizable disease,” he said.
That level of protection would be the ultimate goal to diffusing the crisis, but is hard to do with companies facing an immediate demand for some sort of solution. While no vaccine is 100% effective, having a majority of the population inoculated and higher percentages of efficacy is the best to hope for."
The U.K. is looking at challenge trials, which intentionally infect a smaller group of participants with the virus in an effort to test a vaccine’s or treatment’s efficacy.
Fauci said the U.S. is not anticipating such a move because the rate of spread is so high in the [U.S.] that it’s sufficient enough of an environment to test the vaccine. The daily case count for the U.S. in the past few days has reached a new record of more than 80,000 cases.
“So although you can get some good information from a challenge trial, the real-world information that you want is out in the field when someone is actually being exposed to natural infection, and to determine if the vaccine prevents against that,” Fauci said.
“So right now we're not planning any challenge studies because we have so much infection going on.”
FAUCI MADE FULL DISPLAY OF HIS IGNORANCE.
WHO WRITES HIS MATERIAL, MICKEY MOUSE?
HE WANTS A VACCINE THAT SIMPLY MASKS ("PREVENTS") THE SYMPTOMS?
"The primary thing you want to do is that if people get infected, prevent them from getting sick..." ???
WHAT DOES HE MEAN?
INFECTED IS INFECTED, WHETHER THEY FEEL SICK OR NOT!
"The primary thing you want to do is that if people get infected, prevent them from getting sick..." ???
WHAT DOES HE MEAN?
INFECTED IS INFECTED, WHETHER THEY FEEL SICK OR NOT!
REMEMBER THAT LITTLE TONY FAUCI IS NOT A MEDICAL DOCTOR WHO TREATS PATIENTS.
CAN THERE BE ANY DOUBT HE DOESN'T?
THIS ARTICLE FROM THAILAND GIVES A MORE REALISTIC LOOK AT FAUCI's IGNORANCE.
NO SILVER BULLET' AGAINST CORONAVIRUS, WARNS WORLD HEALTH ORGANIZATION CHIEF
"There is no magic cure for this virus at this time.
There is no silver bullet at the moment and there might never be."
RESEARCHERS FROM UNIVERSITY OF CALIFORNIA-BERKLEY HAVE FOUND THAT PEOPLE INFECTED WITH TWO STRAINS OF THE VIRUS SIMULTANEOUSLY SENDS A HUMAN IMMUNE SYSTEM INTO OVERDRIVE, MAY RENDER VACCINES AND TREATMENT USELESS AND PRESENTS A MORE DEADLY OUTCOME.
Dangers of using adeno-associated virus vectors for Covid-19 vaccines.
"There is no magic cure for this virus at this time.
There is no silver bullet at the moment and there might never be."
RESEARCHERS FROM UNIVERSITY OF CALIFORNIA-BERKLEY HAVE FOUND THAT PEOPLE INFECTED WITH TWO STRAINS OF THE VIRUS SIMULTANEOUSLY SENDS A HUMAN IMMUNE SYSTEM INTO OVERDRIVE, MAY RENDER VACCINES AND TREATMENT USELESS AND PRESENTS A MORE DEADLY OUTCOME.
Dangers of using adeno-associated virus vectors for Covid-19 vaccines.
For the Consumer. Applies to adenovirus vaccine:
Side effects include: Upper respiratory tract infection, headache, nasal congestion, pharyngolaryngeal pain (sore throat), cough, arthralgia (musculoskeletal pain), chills, GI effects (abdominal pain, nausea, diarrhea, vomiting).
Pyrexia (temperature of 100.5F or higher), pain in extremity.
SOUNDS SIMILAR TO COVID-19 SYMPTOMS, YES?
AstraZeneca’s Covid-19 vaccine, which made headlines recently when it was halted briefly due to an adverse event in a study volunteer, is built from a variation on a chimpanzee virus. (The Italian company ReiThera has its own vaccine candidate is made from a gorilla adenovirus.)
The leading "vaccine candidates" are viral vector vaccines, which means they use a bio-engineered version of another, milder virus—here it’s one that causes common colds, which is also a coronavirus—as a delivery system.
But some people who could end up getting these vaccines will have immunity to the vector.
If that’s the case—if their bodies have fought off the relevant cold virus in the past—then their preexisting antibodies may end up hampering (or even neutralizing) the new vaccines.
More concerning, this potential problem isn’t evenly spread across global populations: It’s much more common in the poorer nations of the developing world.
From Reuters, FDA FINALLY ADMITS RAPID-TEST ANTIGEN SWABS ARE INACCURATE.
The U.S. government has signed agreements with several companies including Becton Dickinson and Quidel Corp. to supply antigen tests to U.S. nursing homes in an attempt to identify outbreaks faster and stem the tide of the virus.
Antigen tests detect proteins on the surface of the virus. They require an uncomfortable nasal or throat swab, and can produce results more quickly than molecular tests - which detect genetic material in the virus - but are considered less accurate.
In September, Becton Dickinson, which is supplying 750,000 of its SARS-CoV-2 antigen test to the U.S. government, said it is investigating reports from U.S. nursing homes that its rapid coronavirus testing equipment is producing false-positive results.
SAVE $$$ ON TESTS THAT DON'T WORK AND THEN SEND THE CRAP TESTS TO NURSING HOMES?
WHAT A PLAN, RIGHT?
OUR CONFINED ELDERLY DON'T STAND A CHANCE IN AMERICA!
From Reuters, FDA FINALLY ADMITS RAPID-TEST ANTIGEN SWABS ARE INACCURATE.
The U.S. government has signed agreements with several companies including Becton Dickinson and Quidel Corp. to supply antigen tests to U.S. nursing homes in an attempt to identify outbreaks faster and stem the tide of the virus.
Antigen tests detect proteins on the surface of the virus. They require an uncomfortable nasal or throat swab, and can produce results more quickly than molecular tests - which detect genetic material in the virus - but are considered less accurate.
In September, Becton Dickinson, which is supplying 750,000 of its SARS-CoV-2 antigen test to the U.S. government, said it is investigating reports from U.S. nursing homes that its rapid coronavirus testing equipment is producing false-positive results.
SAVE $$$ ON TESTS THAT DON'T WORK AND THEN SEND THE CRAP TESTS TO NURSING HOMES?
WHAT A PLAN, RIGHT?
OUR CONFINED ELDERLY DON'T STAND A CHANCE IN AMERICA!
With rapid mutations, vaccines that were rushed into production, and poor dumb Fauci still in charge, what chance do any of us have in America?
Let's have another round of lockdowns...forever?
//WW
Let's have another round of lockdowns...forever?
//WW
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