Moderna vaccine appears to work against variants(bbc.co.uk)
bbc.co.uk
Moderna vaccine appears to work against variants
https://www.bbc.co.uk/news/health-55797312
118 comments
The headline is slightly misleading if only because it's so vague, which is why this is out today:
"Moderna says it’s working on Covid booster shot for variant in South Africa, says current vaccine provides some protection"
"The company’s researchers said its current coronavirus vaccine appears to work against the two highly transmissible strains found in the U.K. and South Africa, although it looks like it may be less effective against the latter."
https://www.cnbc.com/2021/01/25/covid-vaccine-moderna-workin...
"Moderna says it’s working on Covid booster shot for variant in South Africa, says current vaccine provides some protection"
"The company’s researchers said its current coronavirus vaccine appears to work against the two highly transmissible strains found in the U.K. and South Africa, although it looks like it may be less effective against the latter."
https://www.cnbc.com/2021/01/25/covid-vaccine-moderna-workin...
EK484K is a particular mutation, not a variant. It is common to a Brazilian variant and the SA variant referenced in the article.
Can you explain what is the difference between mutation, lineage, variant, strain, please?
The linked study names the 501.V2 / B.1.351 / South African (vulg.) variant. This variant also has the E484K found in the B.1.1.248 / Brazil (vulg.) variant.
That said based on the title you might assume the vaccine to be as effective, but that's not quite what the study says. In short it states:
>A six-fold reduction in neutralizing titers was observed with the B.1.351 variant relative to prior variants. Despite this reduction, neutralizing titer levels with B.1.351 remain above levels that are expected to be protective.
That said based on the title you might assume the vaccine to be as effective, but that's not quite what the study says. In short it states:
>A six-fold reduction in neutralizing titers was observed with the B.1.351 variant relative to prior variants. Despite this reduction, neutralizing titer levels with B.1.351 remain above levels that are expected to be protective.
Six fold reduction is extremely concerning!
As the vaccine becomes more widespread, it will be tested more widely by exposure to the virus and this will trigger faster evolutionary cycles by the virus to defeat the vaccine.
My forecast is we will have to get much faster at releasing updated vaccines and distributing them in order to stay ahead of this virus -- and that everyone will need to be vaccinated every 6 months until we hit sufficient heard immunity of the circulating strains such that is stops circulating so rapidly and the speed of mutation consequently reduces.
As the vaccine becomes more widespread, it will be tested more widely by exposure to the virus and this will trigger faster evolutionary cycles by the virus to defeat the vaccine.
My forecast is we will have to get much faster at releasing updated vaccines and distributing them in order to stay ahead of this virus -- and that everyone will need to be vaccinated every 6 months until we hit sufficient heard immunity of the circulating strains such that is stops circulating so rapidly and the speed of mutation consequently reduces.
I believe the same thing. We need a fast vaccine update cycle. We also need much faster production. It looks like the mRNA vaccines have the fastest turnover cycle. IMO the government should employ emergency measures to force Pfizer and Moderna to upgrade their production facilities to 10x what they are now. Get other companies involved. Pour as much money as necessary.
Fortunately, it seems there is openness from the FDA to have a faster approval cycle for vaccine tweaks. Moderna is already working on a "booster shot" to try and increase immunity to the South-African variant.
I wish that we also had other therapeutic tools to combat COVID. I wonder if we couldn't save people who are getting hospitalized by employing drugs that block the receptor the virus uses to enter cells. Similarly to the way HIV is kept under control. That could save lives and it would be more mutation-proof.
Fortunately, it seems there is openness from the FDA to have a faster approval cycle for vaccine tweaks. Moderna is already working on a "booster shot" to try and increase immunity to the South-African variant.
I wish that we also had other therapeutic tools to combat COVID. I wonder if we couldn't save people who are getting hospitalized by employing drugs that block the receptor the virus uses to enter cells. Similarly to the way HIV is kept under control. That could save lives and it would be more mutation-proof.
I hate suggestion like this - most of the government involvement so far has been negative - don't wear masks, do wear masks and cloth masks are fine (they probably are not). We're going to cancel doctors license who go out of order in vaccine distribution (so now when the 65 year old drives their 75 year old partner in they can't both be vaccinated).
If anyone actually cared about this there is an EXISTING mechanism to get business to produce pretty much any quantity of anything you want. You pay them money. Instead the government is constantly canceling contracts, seizing products, stopping the sale of products for more than 10% more than historic prices etc.
ALL these steps REDUCE confidence in making a big / high risk investment.
My guess - if we looked at even existing use of the DPA - probably most stuff got made by folks not expert in making it and sat in a warehouse. I'm serious - I want to know how many ventilators made under DPA by rando companies are actually in use?
I've worked in govt contracting - the govt does not get "the best" producers to produce, in situations like this the hands reach out from the experts playing the govt contracting game. Not end of world normally, but with lives on the line some more standard approaches would be refreshing.
If anyone actually cared about this there is an EXISTING mechanism to get business to produce pretty much any quantity of anything you want. You pay them money. Instead the government is constantly canceling contracts, seizing products, stopping the sale of products for more than 10% more than historic prices etc.
ALL these steps REDUCE confidence in making a big / high risk investment.
My guess - if we looked at even existing use of the DPA - probably most stuff got made by folks not expert in making it and sat in a warehouse. I'm serious - I want to know how many ventilators made under DPA by rando companies are actually in use?
I've worked in govt contracting - the govt does not get "the best" producers to produce, in situations like this the hands reach out from the experts playing the govt contracting game. Not end of world normally, but with lives on the line some more standard approaches would be refreshing.
Which high risk investment?
The governments funded the research and buy pretty much any working vaccine. Just look at Oxford and AstraZeneca.
And it's not only about quantity but also about distribution. What do you think how much money is needed to vaccinate lots of people in a short period of time.
Money is the reason why so few companies produce vaccines in the first place. Long term treatment make more profit than one time shots.
This is an emergency situation. I don't know if we can count on individual companies to just do the right thing. They might be risk-averse, afraid of financial losses, but we need them to go full-steam ahead. Pfizer and Moderna should definitely be financially compensated for everything they produce. We could pay them above cost and basically guarantee their financial success in this operation.
It's possible that the current generation of vaccines could end up being outdated, and there could be some amount of waste, but the important thing is the production rate. When an updated vaccine becomes available, we want to be able to produce it and distribute it as fast as possible.
On another note, there's also research into oral vaccines. IMO that would be amazing if it could pan out. Imagine if we could just mail people capsules containing booster doses updated for the latest strain every month. We'd crush any pandemic in no time.
It's possible that the current generation of vaccines could end up being outdated, and there could be some amount of waste, but the important thing is the production rate. When an updated vaccine becomes available, we want to be able to produce it and distribute it as fast as possible.
On another note, there's also research into oral vaccines. IMO that would be amazing if it could pan out. Imagine if we could just mail people capsules containing booster doses updated for the latest strain every month. We'd crush any pandemic in no time.
The really wild vaccines use a self replicating viral vector. One of Merck's discontinued candidates used a live, replicating virus.
I guess if you really nail the science, you can make it infectious and vaccinate by breathing on people.
I guess if you really nail the science, you can make it infectious and vaccinate by breathing on people.
> I guess if you really nail the science, you can make it infectious and vaccinate by breathing on people.
I suppose that a government-funded infectious vaccine would be one way to get anti-maskers to reverse their stance on wearing cloth face coverings...
I suppose that a government-funded infectious vaccine would be one way to get anti-maskers to reverse their stance on wearing cloth face coverings...
Disagree completely.
This is war. Governments fight wars. It's one of the primary roles of government. In WW2 all sorts of prioritization and direction came from government. This should be the same.
This is war. Governments fight wars. It's one of the primary roles of government. In WW2 all sorts of prioritization and direction came from government. This should be the same.
You think the government are the ones manufacturing the vaccines?
We have many other therapeutic tools to combat COVID-19.
https://www.evms.edu/covid-19/covid_care_for_clinicians/#d.e...
https://www.evms.edu/covid-19/covid_care_for_clinicians/#d.e...
I wonder what would be the implications for being able to develop and deliver RNA vaccines on this shorter, more regular timeline? Specifically, does the infrastructure required to accomplish this goal also bring other vaccines or treatments in the realm of feasibility?
Of course, mRNA vaccines on their own open up a new category of vaccination. E.g. Biontech is working on a mRNA multiple sclerosis vaccine and cancer vaccines.
Aren't most antibodies at this point a result of infection?
That scenario only plays out if vaccinated people can be carriers. If not, virus that is exposed to the vaccine will not have a chance to evolve more quickly.
Even if they cant, for the period when there are lots of people vaccinated and also lots of people infected, that's lots of mutations happening in infected people and then trying to jump into vaccinated people, giving it more chances that one of those mutations would then spread from vaccinations people even if current mutations don't (which isn't known yet). If it spreads from vaccinated people already then that would be even worse.
B.1.1.7(UK) and B.1.351(SA) the article links to the source. They say "variants including", but I doubt they would leave out the Brazilian one if it was tested.
No reason to be afraid of new strains. Coronaviruses become less deadly as they evolve to become better at spreading.
A virus may become less deadly. There is no guarantee. It depends on what evolutionary options are available and what pressures are selecting mutations.
Pre-symptomatic infectiousness has about the same selection pressure as low mortality rate IMO. Low risk viruses circulate well because people don’t care about transmission very much. High risk infections cause people to take precaution and thus eliminates those stains. SARS-COV-1 and MERS were that way.
But pre-symptomatic infectiousness (SARS-COV-2) makes this calculus immaterial for most people; they transmit it without knowledge. This reduces the pressure on high mortality / morbidity strains / variants.
Pre-symptomatic infectiousness has about the same selection pressure as low mortality rate IMO. Low risk viruses circulate well because people don’t care about transmission very much. High risk infections cause people to take precaution and thus eliminates those stains. SARS-COV-1 and MERS were that way.
But pre-symptomatic infectiousness (SARS-COV-2) makes this calculus immaterial for most people; they transmit it without knowledge. This reduces the pressure on high mortality / morbidity strains / variants.
That is a dangerous misunderstanding of evolutionary pressure in viruses.
LONG TERM, less deadly viruses will tend to spread better because the more deadly a virus is, the more it raises stakes for the host population to remove it or prevent it , and the more it can make it apparent who has been infected. Ebola for instance justifies pretty almost any action you can imagine to contain it's spread, where we are still arguing if lockdowns or travel restrictions are the cost appropriate measure with COVID.
If the time of fatality is sufficiently delayed, or the time to implement other countermeasures or recognize the situation has changed is too long, it doesn't help anyone in the short, medium, or potentially even long term - you can have massive fatalities and huge spread.
The 1918 pandemic had multiple waves, with the second in particular having a much higher fatality rate than the first - 10x a typical flu season, which is what we're seeing now. This was almost certainly caused by variants, though lack of data makes it impossible to prove. [https://en.wikipedia.org/wiki/Spanish_flu]
A particularly nasty example [https://www.adn.com/alaska-news/science/2020/03/22/how-an-al...]
The more infections, the more likely we'll get more variants, and the more likely we'll get some that cause terrible, terrible problems - and may still be quite infectious.
Long term, will the most terrible ones die out? Very likely. However, smallpox was a scourage on humanity since likely 300 BCE and up until eradication by a massive global effort in 1975, it still had fatality rates around 25-35%. So don't just assume COVID will 'evolve to harmlessness', or if it does that it would happen on a timeframe convenient for society [https://www.cdc.gov/smallpox/history/history.html]
LONG TERM, less deadly viruses will tend to spread better because the more deadly a virus is, the more it raises stakes for the host population to remove it or prevent it , and the more it can make it apparent who has been infected. Ebola for instance justifies pretty almost any action you can imagine to contain it's spread, where we are still arguing if lockdowns or travel restrictions are the cost appropriate measure with COVID.
If the time of fatality is sufficiently delayed, or the time to implement other countermeasures or recognize the situation has changed is too long, it doesn't help anyone in the short, medium, or potentially even long term - you can have massive fatalities and huge spread.
The 1918 pandemic had multiple waves, with the second in particular having a much higher fatality rate than the first - 10x a typical flu season, which is what we're seeing now. This was almost certainly caused by variants, though lack of data makes it impossible to prove. [https://en.wikipedia.org/wiki/Spanish_flu]
A particularly nasty example [https://www.adn.com/alaska-news/science/2020/03/22/how-an-al...]
The more infections, the more likely we'll get more variants, and the more likely we'll get some that cause terrible, terrible problems - and may still be quite infectious.
Long term, will the most terrible ones die out? Very likely. However, smallpox was a scourage on humanity since likely 300 BCE and up until eradication by a massive global effort in 1975, it still had fatality rates around 25-35%. So don't just assume COVID will 'evolve to harmlessness', or if it does that it would happen on a timeframe convenient for society [https://www.cdc.gov/smallpox/history/history.html]
Trench warfare is responsible for evolving a deadly 1918 Spanish Flu virus.
Soldiers with minor symptoms remained where they were, not coming in contact with many other people.
The very sickest soldiers were transported by train, where the infected many other people, to hospitals, where they continued infecting many other people. It was our own attempts to care for the soldiers that caused the deadliest strains to spread and continue evolving.
Soldiers with minor symptoms remained where they were, not coming in contact with many other people.
The very sickest soldiers were transported by train, where the infected many other people, to hospitals, where they continued infecting many other people. It was our own attempts to care for the soldiers that caused the deadliest strains to spread and continue evolving.
Those conditions allowed more infections to happen, and eventually one of them was more deadly. ANY situation that results in more infections will result in more mutations (as it is a property of the viral replication mechanism), and increase the odds that one of them will be more successful in infecting and spreading - with the possible side effect of host death.
What some folks are proposing in this thread (uncontrolled community spread so it will 'mellow out') is an even more massive expansion of that due to the quite visible ability for COVID to be infectious in patients with no symptoms for long periods of time, which Influenza has not been able to pull off.
What some folks are proposing in this thread (uncontrolled community spread so it will 'mellow out') is an even more massive expansion of that due to the quite visible ability for COVID to be infectious in patients with no symptoms for long periods of time, which Influenza has not been able to pull off.
Viruses are believed to become less deadly over time when being less deadly offers an evolutionary advantage in ability to spread. If being more deadly and more spreadable have the same mechanism (e.g., avoiding spike protein-inhibiting antibodies), you can expect that old adage not to hold true over the short-term.
I think this is kind of not representing the reality. _Some_ viruses _have become_ less deadly over time. Not all viruses go through this process and the selection pressure that promotes this kind of evolution is _death._
So we have no reason to believe this will occur with covid19.
So we have no reason to believe this will occur with covid19.
> the selection pressure that promotes this kind of evolution is _death._
Not necessarily. Assume that people try to self-quarantine as soon as they notice symptoms. (They don't need to be 100% effective at this.) Consider "mutations that affect how quickly it spreads within your body". Those that increase said efficiency would presumably increase the likelihood of death; but they would also probably shorten the "asymptomatic spreading" period, which means they'd get selected against; this selection happens even among those that aren't dying.
(Author background disclaimer: No biology beyond 9th grade.)
Not necessarily. Assume that people try to self-quarantine as soon as they notice symptoms. (They don't need to be 100% effective at this.) Consider "mutations that affect how quickly it spreads within your body". Those that increase said efficiency would presumably increase the likelihood of death; but they would also probably shorten the "asymptomatic spreading" period, which means they'd get selected against; this selection happens even among those that aren't dying.
(Author background disclaimer: No biology beyond 9th grade.)
If anything, this is an argument against lockdowns and masking. Letting asymptomatic and barely-symptomatic people spread more-contagious but less-deadly strains would evolve the virus into a minor nuisance in short order.
That is wildly wrong. As long as the virus is spreading, there are no evolutionary pressures on it to become less deadly.
No it won't - it increases the chances for mutations and variants to form, randomly, increasing the odds that one of them will be more deadly AND more infectious.
A strain that spreads more while not being significantly less deadly is much scarier than a more deadly strain that spreads less. Do the math if you don't believe me.
UK's Pandemic Team says the new strain appears to be more deadly. https://www.webmd.com/lung/news/20210125/uk-variant-may-be-m...
That's a mixed bag, as on one hand sure the number of dead goes down per 100, but then the number of folks infected goes up, thereby meaning the same number of dead possibly, or more people infected in hospitals.
At some point the virus will run out of people to infect.
It actually will just continue to mutate and start reinfecting people as immunity wanes.
Influenza certainly hasn't. It will mutate past defenses, and survive, just as seasonal coronaviruses have - unless a concerted effort occurs to completely eradicate it, and that effort is successful.
SARS-CoV-2, by best estimates (0.3% mortality), is roughly 3x as deadly as the seasonal flu.
The common cold is a coronavirus. It is significantly less deadly than the seasonal flu. We have every reason to believe that a more contagious but less deadly version will resemble the common cold.
The common cold is a coronavirus. It is significantly less deadly than the seasonal flu. We have every reason to believe that a more contagious but less deadly version will resemble the common cold.
SARS1 was also a coronavirus, and it had more than 50% mortality for those infected. The virus strain tells you nothing about its mortality.
SARS-CoV-2 is also only ~3x as deadly as the flu WITH UNPRECEDENTED MEASURES TO CONTAIN IT. In areas where it wasn't contain, such as the initial outbreak in Italy that overwhelmed hospitals, it was 10x or more as deadly as the flu.
SARS-CoV-2 is also only ~3x as deadly as the flu WITH UNPRECEDENTED MEASURES TO CONTAIN IT. In areas where it wasn't contain, such as the initial outbreak in Italy that overwhelmed hospitals, it was 10x or more as deadly as the flu.
Common cold is caused by a variety of viruses, only a small subset of which is coronaviruses. Look it up.
The mortality rate is higher than .3%.
.3% of New York City has already died.
Unless the vast majority of New Yorkers have already contracted the virus, the mortality rate has to be substantially higher than .3%.
.3% of New York City has already died.
Unless the vast majority of New Yorkers have already contracted the virus, the mortality rate has to be substantially higher than .3%.
I'm not surprised. These new variants started taking over months ago before many people were vaccinated, so there was no pressure to adapt to the vaccines.
My theory is that what they are adapting to is all the other mitigation measures that we've been doing for a while--think masks and social distancing.
My theory is that what they are adapting to is all the other mitigation measures that we've been doing for a while--think masks and social distancing.
Viruses can't really "adapt" to "not being spread". It's not quite zero, I suppose we could hypothesize some superior ability to survive on a surface for some period of time or something, but there's not much they can do about it.
Bacteria would have more options, since they're so much more complex. Viruses just don't have much they can do.
Bacteria would have more options, since they're so much more complex. Viruses just don't have much they can do.
> Viruses can't really "adapt" to "not being spread".
Of course they can. We have this pandemic because a coronavirus became highly transmissible.
Of course they can. We have this pandemic because a coronavirus became highly transmissible.
Perhaps I was not clear. A virus can't "adapt" to not being physically presented to its potential host. It can't "adapt" to "being blocked by a mask" or "the person I infected intelligently self-isolating and thus I can't spread any farther". Even if you could hypothetically draw out genetic changes that would permit it, it would require substantial changes to evolve all at once.
Not really, no. There is a 99.999% chance that the virus was just as infective if not more in bats or pangolins or whatever, and simply adapted to humans.
These mutations are the virus finishing its adaptation to humans. It will eventually end up at a local maxima, just like, say, measles did.
These mutations are the virus finishing its adaptation to humans. It will eventually end up at a local maxima, just like, say, measles did.
It most likely jumped the species barrier.
They mutate, and mutations more successful in causing infections cause more infections and become dominant.
There are many ways for this to happen, some of which covered in this thread - changes in the surface presented to the host, more viral load produced and expelled by an infected host earlier being some obvious ones.
Some potential methods that have occurred with other diseases in the past include additional methods of infecting hosts (from prior versions), such as viral envelopes that can insert against additional types of cells, or changes to the way the virus hijacks cell replication machinery to produce products that are better at hiding what is going on to the immune system.
There are many ways for this to happen, some of which covered in this thread - changes in the surface presented to the host, more viral load produced and expelled by an infected host earlier being some obvious ones.
Some potential methods that have occurred with other diseases in the past include additional methods of infecting hosts (from prior versions), such as viral envelopes that can insert against additional types of cells, or changes to the way the virus hijacks cell replication machinery to produce products that are better at hiding what is going on to the immune system.
Those all involve the virus reaching the host.
The virus can't "evolve" its way around not reaching the host very well. Evolution isn't magic. The virus can't "evolve" teleportation or an immunity to high-energy electromagnetic radiation just because it would be really useful to it if it could. It can't just "evolve" its way around masks very well.
As I said, bacteria have at least more options, though they face the same physical constraints everything else in the universe does. Viruses don't really have many options. They are very simple.
The virus can't "evolve" its way around not reaching the host very well. Evolution isn't magic. The virus can't "evolve" teleportation or an immunity to high-energy electromagnetic radiation just because it would be really useful to it if it could. It can't just "evolve" its way around masks very well.
As I said, bacteria have at least more options, though they face the same physical constraints everything else in the universe does. Viruses don't really have many options. They are very simple.
> The virus can't "evolve" its way around not reaching the host very well.
That's what "becoming more contagious" is. Obviously, no one in a submarine is getting it until it docks, but when you're dealing with 95% effective masks, tests that have a 20% false negative rate, and surfaces not being an effective vector, there are still plenty of opportunities to reach the host, and we're selecting for viruses that were able to. Someone else mentioned measles; sars-cov2 is nowhere near that contagious, but it means there's room for it to get worse.
That's what "becoming more contagious" is. Obviously, no one in a submarine is getting it until it docks, but when you're dealing with 95% effective masks, tests that have a 20% false negative rate, and surfaces not being an effective vector, there are still plenty of opportunities to reach the host, and we're selecting for viruses that were able to. Someone else mentioned measles; sars-cov2 is nowhere near that contagious, but it means there's room for it to get worse.
Most of the masks people are wearing are also nowhere near 95% effective - cloth masks are more like 70%. Helpful, yes! Solid protection? Far from it.
COVID-19 had a measured replication rate before measures were taken in NYC of ~ 6. Measles is ~ 11 (and the most infectious known airborne virus). New variants are supposed to be between 50-70% more infectious than 'baseline' COVID, though it isn't clear how solid that data is, or how exactly it is being computed.
That could put it at a 'with no social changes/baseline behaviour in manhattan' at a replication rate of ~9 to ~10. Which is damn close to measles.
Lockdowns, social distancing, face masks will reduce this quite a bit in reality (and have - the measured R value is in the 1.1-1.2ish range in most areas now) - but increases in infectivity will require stepping up countermeasures to contain it, or a massive rollout in vaccines to stamp it out before a variant that the vaccine doesn't prevent against exists.
COVID-19 had a measured replication rate before measures were taken in NYC of ~ 6. Measles is ~ 11 (and the most infectious known airborne virus). New variants are supposed to be between 50-70% more infectious than 'baseline' COVID, though it isn't clear how solid that data is, or how exactly it is being computed.
That could put it at a 'with no social changes/baseline behaviour in manhattan' at a replication rate of ~9 to ~10. Which is damn close to measles.
Lockdowns, social distancing, face masks will reduce this quite a bit in reality (and have - the measured R value is in the 1.1-1.2ish range in most areas now) - but increases in infectivity will require stepping up countermeasures to contain it, or a massive rollout in vaccines to stamp it out before a variant that the vaccine doesn't prevent against exists.
Since there are probably specialists out there, can you answer me a question?
Since these vaccines are targeting spike proteins, shouldn't they work with every variant? Is there (big) risk of a mutation actually changing the spike protein?
Since these vaccines are targeting spike proteins, shouldn't they work with every variant? Is there (big) risk of a mutation actually changing the spike protein?
Yes there is a big risk that the vaccines won't work if the viral spike protein has sufficiently diverged from the one encoded by the vaccine's mRNA template. Viral proteins are constantly changing. They accumulate sequence mutations both naturally and due to selective pressure. There's a limited landscape of acceptable changes but we don't know what those are and how they relate to each other. All we can do is generate new mRNA templates to the more popular strains and revaccinate. This means that we will most likely we will end up taking a cocktail of mRNA vaccines and yearly boosters.. with new mRNA templates.
"Won't work" in this case is defined on a spectrum. Moderna's vaccine is currently about 90% efficacious. Newer variants could reduce that down to say 60% or more. At some point the current vaccine could become useless.
"Won't work" in this case is defined on a spectrum. Moderna's vaccine is currently about 90% efficacious. Newer variants could reduce that down to say 60% or more. At some point the current vaccine could become useless.
But could they become useless before we "solve" this pandemic? Is actually my fear and other "noobs" in this matters.
yep.
When the immune system creates antibodies, they basically hug the spike protein and build antibodies on every nook and cranny they can find a way to bind an antibody. These regions are called epitopes, and the immune system creates many antibodies for each invader.
If the spike protein mutates, it means that the structure of the spike is different. Obviously the spike can't change too much, because it needs to still be able to latch onto cells, and many changes would be irrelevant. Even if one antibody suddenly stops working because of a slight shift in the protein, there are other antibodies targeting different parts of the protein that would still be effective.
Only if the spike changes so dramatically that literally none of the antibodies you had before are relevant anymore. That's why it's not super expected that we'll get a version of the virus that these vaccines won't at least produce some antibodies against.
If the spike protein mutates, it means that the structure of the spike is different. Obviously the spike can't change too much, because it needs to still be able to latch onto cells, and many changes would be irrelevant. Even if one antibody suddenly stops working because of a slight shift in the protein, there are other antibodies targeting different parts of the protein that would still be effective.
Only if the spike changes so dramatically that literally none of the antibodies you had before are relevant anymore. That's why it's not super expected that we'll get a version of the virus that these vaccines won't at least produce some antibodies against.
Thank you. Basically they could just change the actual vaccine a bit to cover all those variants right?
I'm not a specialist, but I can link you to the answer: [1]
Key quote: "B.1.1.7 is defined by 23 mutations from the original Wuhan strain, 8 of which are in the spike protein. The 3 mutations hypothesized to have the largest potential biological effect are N501Y, spike deletion 69-70del and P681H."
The B.1.351 (South Africa) variant has N501Y but not the 69-70 deletion. We're still learning, but virologists I follow are concerned that N501Y may be a driver of higher transmission. But it's likely that multiple mutations contribute.
[1]: https://asm.org/Articles/2021/January/B-1-1-7-What-We-Know-A...
Key quote: "B.1.1.7 is defined by 23 mutations from the original Wuhan strain, 8 of which are in the spike protein. The 3 mutations hypothesized to have the largest potential biological effect are N501Y, spike deletion 69-70del and P681H."
The B.1.351 (South Africa) variant has N501Y but not the 69-70 deletion. We're still learning, but virologists I follow are concerned that N501Y may be a driver of higher transmission. But it's likely that multiple mutations contribute.
[1]: https://asm.org/Articles/2021/January/B-1-1-7-What-We-Know-A...
ELI5: The spike protein itself is changing on the virus.
Unpublished, non-peer reviewed, and sample size of 8... is there a well known name for opposite of FUD?
This seems like an unreasonable assessment. The preprint is available (https://www.biorxiv.org/content/10.1101/2021.01.25.427948v1), submitted for peer review, and the article is pretty clear from the start that this is a preliminary finding.
Where was it submitted? I couldn't see that anywhere.
I'm not sure; the Moderna release mentions submission but doesn't specify.
Well, in your analysis, what's the minimum sample size and why?
"Peer review" is not a suicide pact. In the middle of a pandemic, where days matter, you publish information as you get it, and act with that understanding.
I disagree. In a pandemic it's important to get solid and clear information to the population. If you start saying things that don't go through the proper channels to be verified as reasonably true, then you create massive confusion when you potentially have to go back on that information. Scientists can and do make mistakes. A lay person might not understand what "preprint" or "not peer reviewed" mean yet this article is on the BBC which the average lay person does trust as a source for reasonably true information.
Last week the media in the uk ran headlines saying that covid was spreading like wildfire, despite the evidence from the number of cases showing the opposite (halving every 2 weeks)
The day later they ran headlines sayign that covid wasn't spreading like wildfire.
The source of the first scaremongering inaccurate dangerous headline was a study which said:
"Covid-19 cases have increased more quickly since lockdown started in England, study finds"
(Lockdown started on Jan 5th - when about 60,000 cases were being identified each day. The headline was Jan 21st, when about 30,000 cases were identified)
https://inews.co.uk/news/covid-19-cases-england-increase-sin...
The 7 day cases identified from Jan 6th to 15th dropped from 55,885/day to 40,242/day
That either means the number of unidentified cases balooned, or the REACT study was too small to identify changes over the course of a week (it's not designed to). In the former case we'd expect fewer tests were being done, but tests throughout January have remained averaging about 550,000 a day.
The media will print whatever they can, so it's important to give headlines which make it clear the data is inconclusive. "appears" is a weasel-word that is well used in this case, and far better than misreporting a scientific paper
The day later they ran headlines sayign that covid wasn't spreading like wildfire.
The source of the first scaremongering inaccurate dangerous headline was a study which said:
During the period 6 January to 15 January, SARS-CoV-2 virus was circulating with a higher prevalence than between 25 November to 3 December with 158 in 10,000 infected. There was no strong evidence for either growth or decay in prevalence averaged across the period 6 January to 15 January.
"Covid-19 cases have increased more quickly since lockdown started in England, study finds"
(Lockdown started on Jan 5th - when about 60,000 cases were being identified each day. The headline was Jan 21st, when about 30,000 cases were identified)
https://inews.co.uk/news/covid-19-cases-england-increase-sin...
The 7 day cases identified from Jan 6th to 15th dropped from 55,885/day to 40,242/day
That either means the number of unidentified cases balooned, or the REACT study was too small to identify changes over the course of a week (it's not designed to). In the former case we'd expect fewer tests were being done, but tests throughout January have remained averaging about 550,000 a day.
The media will print whatever they can, so it's important to give headlines which make it clear the data is inconclusive. "appears" is a weasel-word that is well used in this case, and far better than misreporting a scientific paper
I think that if "the other side" sticks to the rules and doesn't publish things like :https://www.theguardian.com/society/2021/jan/20/covid-vaccin... using small sample sizes and various assertions about how the immune system works then you are right!
On the other hand, if you are in a situation where no holds bared screaming to get attention is the norm then it may be good to share information quickly and transparently.
On the other hand, if you are in a situation where no holds bared screaming to get attention is the norm then it may be good to share information quickly and transparently.
> is there a well known name for opposite of FUD?
False hope
False hope
hype
Hubris
This result is the absence of bad news. No more, no less.
Regardless of what this early result is, the only thing most of us can do is try to keep social distancing, use masks, and get vaccinated to protect ourselves as best as possible.
If the vaccine doesn't actually protect us against the newer strains, we should still take it because we need protection from the more widely strain regardless. The only difference is whether we'll need to take a second vaccine in another year.
Regardless of what this early result is, the only thing most of us can do is try to keep social distancing, use masks, and get vaccinated to protect ourselves as best as possible.
If the vaccine doesn't actually protect us against the newer strains, we should still take it because we need protection from the more widely strain regardless. The only difference is whether we'll need to take a second vaccine in another year.
The more guessing and conjecture I hear about the effectiveness of current vaccines on mutations, the angrier I get. Are there any clinical trials going on right now to determine how well various strains respond to the current vaccines? Until Pfizer or Moderna puts out a press release saying their products cover the top 4 major strains, I'm not believing anything.
There are two ways to do clinical trials on vaccine effectiveness. One is to vaccinate someone and then deliberately infect them; this gives you good data quickly, but due to the deadliness of COVID-19, this is generally regarded to not be an option. Another is to vaccinate a very large number of people and wait to see if they get sick with the virus from natural exposure. This is ongoing right now on a very large scale; millions of people have been vaccinated, and sooner or later people will come in contact with these new variants. However, it takes time to collect enough data with this approach to provide useful results, and in this case it can be confounded by the lack of a control group (you don't know how many exposure events happened that did not lead to infections).
Regardless, the current vaccination campaign is highly effective against the original - still very widespread and deadly - virus, so it's worth getting it, and as people get vaccinated with it, it will eventually be apparent whether it works against various variants as well. If it doesn't, it's likely that a booster vaccination can be developed for these variants (and indeed, Moderna has begun work, as an insurance policy, on a booster for the south african variant).
Regardless, the current vaccination campaign is highly effective against the original - still very widespread and deadly - virus, so it's worth getting it, and as people get vaccinated with it, it will eventually be apparent whether it works against various variants as well. If it doesn't, it's likely that a booster vaccination can be developed for these variants (and indeed, Moderna has begun work, as an insurance policy, on a booster for the south african variant).
Actually the UK is performing a challenge trial with young adults. Sign up here to get infected: https://ukcovidchallenge.com/covid-19-volunteer-trials/
Sample size of 8 is not really a huge issue for this kind of analysis.
The hypothesis is that the Moderna vaccine produces antibodies against the new variant.
8/8 people sampled produced antibodies.
Can we confidently say that 100% of people will produce antibodies? No, not with a sample size of 8.
Can we say confidently that 50% of people will produce antibodies? That the vaccine gives you a coin toss's odds? If it's just a coin toss, this result would be the same probability as 8 "heads" in a row, or 1 in 256.
So, the result is hardly FUD or meaningless. They've also submitted to journals for the world to inspect the results.
The hypothesis is that the Moderna vaccine produces antibodies against the new variant.
8/8 people sampled produced antibodies.
Can we confidently say that 100% of people will produce antibodies? No, not with a sample size of 8.
Can we say confidently that 50% of people will produce antibodies? That the vaccine gives you a coin toss's odds? If it's just a coin toss, this result would be the same probability as 8 "heads" in a row, or 1 in 256.
So, the result is hardly FUD or meaningless. They've also submitted to journals for the world to inspect the results.
Here's a link to the actual study:
https://www.biorxiv.org/content/10.1101/2021.01.25.427948v1
I believe most of the vaccines approved or pending approval (Johnson and Johnson) target the spike protein, so I would expect their results to likely (hopefully) be similar.
I believe most of the vaccines approved or pending approval (Johnson and Johnson) target the spike protein, so I would expect their results to likely (hopefully) be similar.
Do not be so sure. The spike protein has two states, pre fusion and post fusion. It makes a difference what exactly the vaccine is targeting. My understanding of this is very limited though.
Is the efficacy still in the 94% range?
From the abstract of the paper linked in the article: No change for the UK variant, but lower efficacy for the South African variant (if my understanding of the abstract is correct):
No significant impact on neutralization against the B.1.1.7 variant was detected in either case, however reduced neutralization was measured against the mutations present in B.1.351.
Paper : https://www.biorxiv.org/content/10.1101/2021.01.25.427948v1
No significant impact on neutralization against the B.1.1.7 variant was detected in either case, however reduced neutralization was measured against the mutations present in B.1.351.
Paper : https://www.biorxiv.org/content/10.1101/2021.01.25.427948v1
This study was done in a laboratory based on blood samples and does not directly equate to a percentage effectiveness. Collecting data on actual effectiveness in the wild, as it were, will require a sufficient number of vaccinated people to come into contact with the variant strains in question, and will therefore take a few months, most likely.
They believe so ("neutralizing titer levels with B.1.351 remain above levels that are expected to be protective"), but this was a blood sample study that can't definitively demonstrate population efficacy.
The question should be can you get re-infected via SA variant. And what’s the mortality rate on re-infection? At this point, you have to assume vaccine rollout is too slow to catch up with the spread.
This is harder to answer as we don't have the data yet. There are case reports of patients who recovered from covid who have been reinfected and died. So, unfortunately, time will tell.
The P1 variant is specifically of interest.
https://www.npr.org/sections/goatsandsoda/2021/01/21/9589534...
If we fail to totally eradicate these strains of coronavirus from earth, like we have never ever in history managed, is lockdown forever right - the end of free life? Or was it just something required in 2020 for some reason?
> like we have never ever in history managed
Smallpox would like a word.
Polio, too, for the most part.
Smallpox would like a word.
Polio, too, for the most part.
Sorry if I could have worded it more clearly - I meant that we have never successfully eradicated a member of the coronavirus family. If we have, I appreciate a correction, preferably with a source. Reread my comment and I think this will be clear
> I meant that we have never successfully eradicated a member of the coronavirus family.
The last case of SARS-CoV-1 was in 2004 and the virus is considered eradicated.
https://en.wikipedia.org/wiki/Severe_acute_respiratory_syndr...
The last case of SARS-CoV-1 was in 2004 and the virus is considered eradicated.
https://en.wikipedia.org/wiki/Severe_acute_respiratory_syndr...
COVID is different in that it appears to have numerous animals it can live in. It's one thing to lock down people, but another entirely to lockdown animals.
Those two took decades to eradicate, we won't be able to keep the Earth's population on lockdown/no-lockdown cycles for that long.
We didn't keep the Earth's population on lockdown for the centuries/millenia before those diseases were brought under control.
That’s a goalpost move, and a matter of logistics, not outright impossibility.
A big change is that there is vaccine production capacity now, and the new vaccines can go through an approval process like is used for annual flu shots, meaning a new vaccine can start mass production in a few months vs the (very quick) year that it took this time.
A year ago there wasn't much more than experimental capacity to make mRNA vaccines. Now we are at tens of millions of doses a month and scaling up.
A year ago there wasn't much more than experimental capacity to make mRNA vaccines. Now we are at tens of millions of doses a month and scaling up.
Actually much faster than months. MRNA-based vaccines can be brewed up in days to weeks.
The approval of the update adds some time. I guess you can be manufacturing at the start of that.
Updates are likely to be fairly streamlined, though; we already do this for the annual flu shot.
Lockdown is required when there is a risk of more paitents from an infectious disease than there are beds. Lockdown isn't the purpose, the purpose is to stop the number of new paitents requiring hospital from outnumbering the number of paitents leaving hospital (either walking or in a bodybag)
When was the last last time we had a disease that spread this quickly and caused this many hospitalisations, on a global scale?
When was the last last time we had a disease that spread this quickly and caused this many hospitalisations, on a global scale?
even CA is lifting their stay at home order. I think the political costs of these hobby authoritarian regimes are finally getting too expensive.
The lockdowns are created by states and are political. If their goal has been archived, they can be lifted.
If you ignore places like Australia that locked down hard and early. Melbourne experienced a near total 3 month lockdown for example. The result? Pretty much zero local cases now and life back to normal, sans international travel.
Coronavirus will naturally evolve into the attraction basin for viruses of its type, which is the common cold: https://www.sacbee.com/news/coronavirus/article248455480.htm...
It's already well on its way, from what I can gather.
One frustrating aspect of the reporting for me is people talking about "more infectious" variants without describing whether or not they are more or less dangerous. In general, the virus putting more work into being infectious is good news; it generally comes at the cost of being less dangerous in other ways as it hyper-optimizes into replication rather than anything else. We should expect and want to hear about "more infectious" variants, which double as natural vaccines to some extent against other less infectious, more dangerous strains still using the same external protiens.
It's already well on its way, from what I can gather.
One frustrating aspect of the reporting for me is people talking about "more infectious" variants without describing whether or not they are more or less dangerous. In general, the virus putting more work into being infectious is good news; it generally comes at the cost of being less dangerous in other ways as it hyper-optimizes into replication rather than anything else. We should expect and want to hear about "more infectious" variants, which double as natural vaccines to some extent against other less infectious, more dangerous strains still using the same external protiens.
There's a substantial lag, though, between finding out how infectious a variant is and how deadly it is (AIUI the rough averages are 2 weeks from infection to hospitalization and another 2 weeks from hospitalization to deaths, but that might have changed). That means that the data on how infectious a variant is becomes available ~1month ahead of information about how dangerous it is. Have we even had confirmed spread of these variants for a month?
BBC’s _More or Less_ did a bit on this. 70% more deadly (per person) would actually be better than 70% more infectious. Deaths increase linearly with deadliness of virus, but they increase exponentially with infectiousness.
Say the current mortality rate is 2% and each infected person passes on the disease to one other after a week, then stops being infectious. If 100 people have the virus in week 0, after 10 weeks 1000 people will have had the virus and 20 will have died.
Increase the death rate by 70% and you’d have 34 deaths instead. Increase the transmission rate by 70%, and you’d have 170 people newly infected in week 1, then 289 in week 2, totalling 285,000 infected people, of which 2% die. That’s now 570 deaths.
Obviously the numbers can all be changed somewhat depending on treatment, or whether you expect everyone to be infected at some point anyway, but the takeaway is that more deadly is not necessarily worse than more infectious.
Say the current mortality rate is 2% and each infected person passes on the disease to one other after a week, then stops being infectious. If 100 people have the virus in week 0, after 10 weeks 1000 people will have had the virus and 20 will have died.
Increase the death rate by 70% and you’d have 34 deaths instead. Increase the transmission rate by 70%, and you’d have 170 people newly infected in week 1, then 289 in week 2, totalling 285,000 infected people, of which 2% die. That’s now 570 deaths.
Obviously the numbers can all be changed somewhat depending on treatment, or whether you expect everyone to be infected at some point anyway, but the takeaway is that more deadly is not necessarily worse than more infectious.
Factor of 10 failure: 28,500 infections, 57 deaths
There is some talk that it also _is_ deadly.
https://www.theguardian.com/world/2021/jan/22/new-uk-covid-v...
It may be, but that article is also hedging quite a bit.
People have a hard time with this intuitively, because we probably live under the weakest selection pressure in the history of planet Earth, but it's vicious down there. Viruses are to a large extent playing a zero-sum game. If they get better at one thing, it almost has to come at the cost of something else, because they've already got all the knobs cranked up as high as they will go just to survive and they don't have a spare energy budget just lying around to put into other things without taking away from something else.
It's not impossible that some mutation was made that made it more infectious and more deadly... but it's a long enough shot that I'd consider the likelihood of incomplete early information and incentives that some parties have to amp up the danger in the presence of such uncertainty higher. Viruses do not routinely become more infectious and more deadly. If they did, we'd all be long dead. The evolution gradient tilts strongly away from that.
People have a hard time with this intuitively, because we probably live under the weakest selection pressure in the history of planet Earth, but it's vicious down there. Viruses are to a large extent playing a zero-sum game. If they get better at one thing, it almost has to come at the cost of something else, because they've already got all the knobs cranked up as high as they will go just to survive and they don't have a spare energy budget just lying around to put into other things without taking away from something else.
It's not impossible that some mutation was made that made it more infectious and more deadly... but it's a long enough shot that I'd consider the likelihood of incomplete early information and incentives that some parties have to amp up the danger in the presence of such uncertainty higher. Viruses do not routinely become more infectious and more deadly. If they did, we'd all be long dead. The evolution gradient tilts strongly away from that.
Very true, especially when you consider that a more deadly variant is highly likely to be associated with things like higher viral load, worse symptoms, and faster symptom onset. A virus that kills twice as many people will likely be harmful for twice as many people -- giving the virus fewer asymptomatic hosts that go around spreading without even knowing it.
It's more likely to go the other way; some derpy mutation that reduces viral load, slows incubation, reduces symptoms, makes more super-spreaders.
It's more likely to go the other way; some derpy mutation that reduces viral load, slows incubation, reduces symptoms, makes more super-spreaders.
The virus exists in multiple species. It may be perfectly fine in bats and reproduce without killing the bat. In humans, however, it kills.
People need to stop reading these articles and start exercising. If this virus hit 40 years ago when hardly no one was obese this virus wouldn't even be a thing.
"30% more deadly" means that only 99.6% of people survive it rather than 99.7%. Still not ebolapocalypse.
For example the E484K variant identified in Brazil that is supposed to be antibody resistant is quite terrifying.