Please note, that neutralization by antibodies is only one of the many possible ways how our immune system can take action. Antibody recognition is still possible with the found mutant:
"To determine whether 501Y.V2 is still recognized by non-neutralizing antibodies, the binding of polyclonal sera (from Fig.2a) to a recombinant 501Y.V2 RBD+SBD1 protein and an RBD+SBD1 from the original lineage was assessed by ELISA (Fig.2b). These data revealed that binding of polyclonal plasma to 501Y.V2 RBD+SBD1 was only substantially affected in a minority of cases (14 of 44 with ≥five-fold reduction, 32%). Most of the convalescent plasma/serum suffered less than four-fold reductions in total binding activity (as measured by area under the curve), suggesting a considerable non-neutralizing antibody component are still able to bind the 501Y.V2 spike antigen"
Its also worth to note that only 44 plasma samples were used from individuals out of a population where the virus probably originated.
Looks like this was posted again, so I'll post my response here as well:
This is correct, but just want to add that many may interpret this as a positive sign, it is not necessarily. In many cases, binding antibodies increase cell infectivity. Also, there is some research that indicates the presence of non-neutralizing antibodies without the corresponding neutralizing antibodies and humoral response may be a factor in the development of antibody dependent enhancement. As far as we know, it is the neutralization potency that strongly correlates with disease severity.
Everything you've written is speculation or assertion, whereas the OP's comment is a factual statement about the limitation of the work. They're showing that this mutation escapes a few particular antibodies. That's all.
At the very least, the current headline "strongly resistant to past immunity" is editorialized and completely misleading, and should be changed to the title of the paper.
> In many cases, binding antibodies increase cell infectivity.
Citation absolutely required. I am unaware of an example of this, let alone "many cases".
Was just hoping to point out for those who aren't as close to this space that the fact that non-neutralizing antibodies can bind is neither a positive nor negative signal.
Neither of these papers supports the claim you made. The first one explicitly says that antibody-dependent enhancement has not been observed for this virus:
> There is no evidence that ADE facilitates the spread of SARS-CoV in infected hosts. In fact, infection of macrophages through ADE does not result in productive viral replication and shedding
"suboptimal antibody responses" are indeed...suboptimal...but the paper here is not showing that. As the OP noted, the concerning result is limited to a few examples of monoclonal antibodies. The human immune response is much more complicated.
You edited your comment after I had responded, so hopefully I can address those concerns. I'm not sure the "claim" you think I am making.
As for increased infectivity, that is at the core of what is understood to occur in ADE. And in general, cases where the Fc mediated response is utilized to gain entry to immune cells. I believe Dengue is the typical example spoken to, but this pattern has been observed in Zika, HIV, RSV off the top of my head.
Lots of editing! Also, did not state that ADE occurs for SARS-CoV2. The fact that studies indicate it does not replicate or shed after phagocytosis is a positive signal.
The current headline (“strongly resistant to past immunity”) is editorialized and not what the research here shows. It’s resistant to donor antibodies, which is definitely unfortunate and concerning, but there’s more to immunity than just antibodies, and even more to antibodies than just the ones donated. Preliminary research [1] shows that vaccines are still effective, at least, and likely that implies natural immunity is still effective too.
I agree, the headline is definetly not what the research shows. See my other comment on non-neutralizing antibodies. Please change the title to the original one.
The paper you cited actually states that existing vaccines are less effective: “However, neutralization by 14 of the 17 most potent mAbs tested was reduced or abolished by either K417N, or E484K, or N501Y mutations.”
Yep. It's an irresponsible headline, like so many others, renewing panic even amongst the crowd here.
I hope your comment and others like it are not lost amongst all the others so quick to call for a doubling-down of imposed quarantines and lock downs without regard for collateral damage, based on their partial knowledge of the immune system and lack of perspective.
The submitted title ("New mutation of COVID19 strongly resistant to past immunity") broke the site guidelines by editorializing, and probably also by being misleading. Please don't do that. If you want to contribute your interpretation, that's fine, but do so in a comment—then your interpretation is on a level playing field with everyone else's. On HN, being the user to submit an article doesn't come with any special rights about how to frame it for others.
"Please use the original title, unless it is misleading or linkbait; don't editorialize."
This is the one headline I’m constantly afraid of reading... do any HN biotech experts have any comments or feedback? Is this a serious cause for concern?
Please note, that neutralization by antibodies is only one of the many possible ways how our immune system can take action. Antibody recognition is still possible with the found mutant:
"To determine whether 501Y.V2 is still recognized by non-neutralizing antibodies, the binding of polyclonal sera (from Fig.2a) to a recombinant 501Y.V2 RBD+SBD1 protein and an RBD+SBD1 from the original lineage was assessed by ELISA (Fig.2b). These data revealed that binding of polyclonal plasma to 501Y.V2 RBD+SBD1 was only substantially affected in a minority of cases (14 of 44 with ≥five-fold reduction, 32%). Most of the convalescent plasma/serum suffered less than four-fold reductions in total binding activity (as measured by area under the curve), suggesting a considerable non-neutralizing antibody component are still able to bind the 501Y.V2 spike antigen"
This is correct, but just want to add that many may interpret this as a positive sign, it is not necessarily. In many cases, binding antibodies increase cell infectivity. Also, there is some research that indicates the presence of non-neutralizing antibodies without the corresponding neutralizing antibodies and humoral response may be a factor in the development of antibody dependent enhancement. As far as we know, it is the neutralization potency that strongly correlates with disease severity.
"On 7 January 2021 it was reported that Pfizer researchers had found the Pfizer and BioNTech COVID-19 vaccine in tests involving 20 blood assays to be capable of affording protection against one of the 501.V2 variant mutations (N501Y, shared with variant B1.1.7). Further investigation was to be undertaken to ascertain the level of protection involved."
The next section in the article is what's important here:
E484K mutation
The E484K amino acid change, a receptor-binding-domain (RBD) mutation, was reported to be "associated with escape from neutralising antibodies" which could adversely affect the efficacy of spike protein-dependent COVID vaccines.[50][51] The E484K spike mutation was linked to a case of reinfection with the 501.V2 variant of SARS-CoV-2 in Brazil, believed by researchers to be the first such case of reinfection involving this mutation.[29] The possibility of an alteration in antigenicity was referred to as an "escape mutation" from a monoclonal antibody with the capability of neutralising the spike protein variants of SARS-CoV-2.[52][53]
I read that. They're only speculating that this could impact vaccines that rely on the spike protein. They didn't actually test for that.
The links I posted show that testing with current mRNA vaccines against this exact variant are under way. Pfizer's (very small) initial tests results seem positive.
1) it's in the spike protein. I think it's in the area that typically elicits antigen response. That's super bad news. If you look carefully, it's near the cleft of a representative antibody (fig 1a), and the buried surface area is high across the board on (clinically?) sampled antibodies (fig 1e), suggesting its importance.
2) it's a mutation that changes the charge state of one of the amino acid residues. E->K, changes a negative charge to a positive charge, potentially very bad if typically antibodies have a positive surface charge to interact with it, now they will be repelled. Since individual humans make random antibodies, even if there is no charge interaction, K amino acid is bigger than E, and so there is likely a shape interaction that could get disrupted by the "new bump" in the spike.
Is it a serious cause for concern? Yeah, almost certainly. The current round of vaccinations will probably be rendered inactive.
IMO the fastest way around this is to quickly approve a reformulation of the moderna/pfizer vaccines that encode for the new amino acid, or better yet, a cocktail of both.
For the more traditional protein-based vaccines, it could be more challenging, because the gut feeling is that an amino acid change like this could pose more of a risk to the effectiveness of the formulation for delivery of the vaccine (mrna is more "neutral" information medium that typically exerts less of a chemical change to the delivered product when altered).
In any case this emergent phenomenon will be certainly challenging to the regulatory landscape around vaccination.
But CAN you safely reformulate vaccines to include this new protein and introduce it widely into the population without knowing if this protein's antigen is already present in the body and might cause severe side effects?
I think you can't. It's famously difficult to anticipate off-target effects of any novel antigen target. This can't be tested in-vitro. You have to repeat the full range of clinical trials with each reformulation that targets a new antigen.
> You have to repeat the full range of clinical trials with each reformulation that targets a new antigen.
Are you sure? I don't think we do this with the seasonal flu vaccine in general. It certainly wasn't a consideration in the CDC pandemic flu response fire drill (sequence antigen -> manufactured vaccine in ~2 weeks) that I got a sideline seat on.
A new mutation of COVID19 has been discovered in an South African donor. With this mutation, the spike protein changed which might render all existing vaccinations less effective or even ineffective.
"These data highlight the prospect of reinfection with antigenically distinct variants and may foreshadow reduced efficacy of current spike-based vaccines."
So it suggests that only spike-based vaccines may have reduced efficacy against it. I suppose the inactivated-virus vaccines should be fine. Which would put China and India at huge advantage (https://www.nytimes.com/interactive/2020/science/coronavirus...).
I think you have it backwards - If it is resistant to past immunity it will certainly knock out live virus vaccines, the statement is saying it will probably affect mRNA as well.
Worth noting that peer review is also a bit (or a lot slow) and not perfect, and that all peer-reviewed studies have in the past been not peer reviewed.
Today Biontech also announced results showing induces a similarly strong immune response against the new variants, although I haven't read the details. .
It is a different variant, but both the 501Y.V2 ("South African lineage" tested in OP) and B.1.1.7 ("UK lineage" tested in the Pfizer study you linked) have the N501Y spike mutation, which (I gather) is the residue of particular concern.
Interesting... the common cold and the flu also tend to mutate to be resistant to past immunity. I wonder if we’re on a the cusp of finally finding cures for these types of rapidly mutating viruses.
The common cold isn't just one virus. Many different viruses cause cold symptoms, including several coronaviruses. In particular HCoV-OC43 is quite similar to SARS-CoV-2. If you're exposed to one of those common cold viruses then it generally won't give you immunity to any of the others.
The issue with the flu isn't that it rapidly mutates but that we can't quite predict which mutations will happen each season. Developing a vaccine for a new strain of the flu is pretty mechanical at this point but each seasonal flu vaccine is really a combination of three different strains that World Health Organization scientists predict will be the dominant strains causing the most damage (it gets reevaluated twice a year). The way that most people take the vaccine (a live but weakened version of the virus) it's impractical, even dangerous, to give them all of the strains at once so an educated guess of three strains is our chosen sweet spot.
The common cold is an even more extreme version of that process but we haven't figured out an economic way of developing rapid vaccine candidates for rhino/coronavirus strains like we have for the flu. Moderna's RNA method might be a game changer here but it'll take a while for their method to be approved as a platform instead of a single drug candidate.
>The issue with the flu isn't that it rapidly mutates but that we can't quite predict which mutations will happen each season.
This doesn't make sense. Of course we cannot predict what mutation will happen. Are you trying to say we don't know which mutation take off? Even then the issue that we don't know what future mutation might take off is a problem.
> each seasonal flu vaccine is really a combination of three different strains
This year it was 4 different strains.
> it's impractical, even dangerous, to give them all of the strains at once
I've never heard this before. Can you provide a citation so I can verify it?
>The common cold is an even more extreme version of that process
There are a lot of different viruses for the common cold. There have been vaccines for them, but the odds of catching any one strain are so low that a vaccine against one isn't really significant.
I mean, if flu vaccines are any indication, what is more likely is we never cure it, but we end up with yearly covid shots to gain immunity to each year's strain(s)
The flu mutates a lot faster than COVID. There is still hope we can vaccinate against it and be done. This depends on speed of getting the vaccines out, and preventing it from jumping to something else and then getting a foothold there where mutations can jump back.
We will know in a couple years how successful we are.
These are necessarily temporary measures. Life cannot go on forever with these restrictions in place. Either medical science will find a way to limit the danger or people will adapt to their new, more dangerous world. I am not an anti-masker, but asking for permanent social distancing is not realistic.
Asia has absolutely not been social distancing, avoiding indoor gatherings and universally wearing masks for decades. After SARS, the social acceptability of wearing a mask, especially when sick increased. It was by no means the standard for everyone. I know you said "some people". Some people in the west also have germ pobia.
Every few years? My experience is more like every 6 weeks in the winter. Even with lock down I have caught the second cold of the season. I am guessing you don't have kids
While those are certainly measures to take, they're a non answer. We need to return to some amount of noalcy, and none of those measures are up to snuff. Literally everyone where I live wears a mask and distances, yet cases are sky high. Somehow my grandfather caught the virus despite his assisted living home despite them being so locked down that we haven't been able to see him in person besides through a glass window. Masks and distancing just spread the deaths out over time, but they aren't a solution.
Believe it or not, some of us don't like social distancing and mandatory masks in perpetuity. If we had spent more money on developing these kinds of vaccines years ago, we might not be in the situation we are in now. If you like being isolated then be my guest, but don't be on a high horse about "just" wearing masks, and so forth at this point. We all get it. Yet people continue to get sick and die.
I don't think we really know for sure. My guess is that it's both, but that even if masks/distancing were 100% effective on their own, it's not practical to expect enough people to take them seriously enough. This isn't an engineering problem, but a human one. This is why I take issue with those here who just blame everyone not participating for why the virus has spread. By the law of averages, you will never get everyone to comply. You need virtually everyone to comply for the virus to be stopped, and all it takes is a small number of people to allow a virus to spread, which keeps happening when you keep enough healthy people from even beginning to build an immunity. These social measures are stop gaps, and anyone suggesting "or we can just social distance" as if that's an alternative to vaccines needs to get a clue. It doesn't take a rocket scientist to look at the numbers before and after lockdowns and other restrictions are put in place to realize that they aren't impactful enough to be considered a solution.
Is this just one of the hundreds of variants that have been found so far but do not spread widely, or is there some reason to believe this variant is more easily spread and will become common?
This is one of the first variants that avoids our current plan of defense: antibody plasma.
At a minimum, it means that treating COVDID19 may require further tests to see if we have COVID19, or... what probably will be called COVID20 or COVID21 (for 2020 or 2021, depending on when we want to pin the "origin date" of this virus variant). I'm assuming COVID20 in my ignorance...
If COVID19 treatment doesn't work, doctors will then have to try COVID20 treatment.
--------------
It really depends on how much COVID20 has mutated compared to COVID19, as well as how effective Pfizer, Moderna, AstraZenica, and Johnson & Johnson's vaccines are against COVID20.
They've only been tested against COVID19 (the 2019 variant). We'll have to run tests to see if our defenses are good enough for COVID20, or if we have to start the vaccine race all over again.
> . In South Africa, genomic data highlighted that the 501Y.V2 variant rapidly displaced other lineages circulating, and preliminary studies suggest the variant is associated with a higher viral load, which may suggest potential for increased transmissibility; however, this, as well as other factors that influence transmissibility, are subject of further investigation.
> As of 30 December, the 501Y.V2 variant from South Africa has been reported from four other countries to date.
This one is spreading more widely in South Africa and has also been found in other countries already. It has an advantage in populations that have prior immunity from natural infection.
"SARS-CoV-2 501Y.V2, a novel lineage of the coronavirus causing COVID-19, contains multiple mutations within two immunodominant domains of the spike protein. Here we show that this lineage exhibits complete escape from three classes of therapeutically relevant monoclonal antibodies. Furthermore 501Y.V2 shows substantial or complete escape from neutralizing antibodies in COVID-19 convalescent plasma. These data highlight the prospect of reinfection with antigenically distinct variants and may foreshadow reduced efficacy of current spike-based vaccines."
Evolutionary paths for covid-19 that would normally be very unlikely become more and more likely as more people get infected with the virus, providing a large-scale, global playground for experimentation via random mutation. Random evolutionary events that would normally be rare become more and more likely as the numbers grow large enough.
Question: How would this affect severity? My basic understanding is because this is a new virus humans have very little existing immunity, which is the problem and why we don't die from colds. Over time our bodies get better at dealing with the virus and the virus gets better dealing with us.
I read a paper on hn to this effect a little while ago, I'll provide source if needed.
I think in general not causing death in the target host is a naturally selected trait in viruses. The least lethal viruses are the ones that spread the most.
This has been observed in herpes, which has evolved to infect nervous system cells but explicitly not nerve cells in the brain (which would cause death).
So considering that, perhaps future strains of COVID will reduce their lethality while increasing their ability to infect.
maybe. Measles was around for years and deadly. It (much like covid) could spread before it killed. Also like COVID it doesn't kill everyone it infects.
HIV/AIDS mutates a lot, but doesn't seem to be mutating in such a way as to not kill the host, you can be infected for 5-10 years before it kills you which is plenty of time to pass it on. It appears that a tiny number of people have a genetic immunity to HIV/AIDS, and so they could be the only survivors - which would mean that left unchecked humans will mutate to not be vulnerable to AIDS. (modern medical treatment has made significant progress on HIV/AIDS that I'm ignoring for this point)
1. The sera they tested this against obtained antibodies through natural infection. It's not clear whether vaccine-induced immunity is protective against this variant.
2. They only tested for neutralizing antibodies, but there is still T-Cell response which could provide protection.
I had assumed the vaccine was also intended/believed to induce T-cell response, is that not the case? Given that they disappear within a matter of months after a natural infection, how long are the antibodies from the vaccines believed to last?
Oh, it is. I meant that that is also part of 'natural' immunization. The distinction between the 'natural' exposure and the vaccine is that the natural exposure targets a number of epitopes, which may or may not include effective neutralizing antibodies against the spike protein; the vaccine, on the other hand, only offers the spike as an antigen, so you know you're generating neutralizing ab.
This is how the FDA's refusal to balance up-side risk is going to damage all of us. They're only interested in minimizing the risk from a treatment itself, and pay little to no attention to the risk from not having any treatment.
It's been a full year since the first vaccines were formulated, and it took the FDA 11 months to give the OK. That was a large streamlining of their normal processes, but not a meaningful balancing of risk, the standards remained the same.
In the meantime, the virus has had millions of opportunities to mutate like this. If we'd accepted a bit more risk, we could have significantly decreased its opportunities to mutate.
At least in this case, the virus can't mutate faster than our ability to formulate a new vaccine. Whether we can retool vaccine manufacturing I don't know. But so long as the FDA won't allow us to react quickly, the hole we're in keeps getting deeper.
On the flip side, you have a sizable portion of the population that feels even the Emergency Use Authorization (EUA) by the FDA was rushed (To be clear, I'm playing the Devil's Advocate here - I personally don't disagree with the FDA's decisions, and got my own shot weeks ago)
Genuine Q: which steps of the process do you see as superfluous? Pfizer announced the end of the phase 3 trials on November 18th, they submitted an application to the FDA for EUA on the 20th of November (or sometime shortly after), and the EUA was granted on the 11th of December.
It didn't take 11 months for the FDA to give the OK. It took 11 months to design a vaccine from scratch, conduct phase I safety trials, phase 2 human safety and dosage trials, and a phase 3 trial to determine efficacy. This includes actual production of the mRNA & its vector in quantities sufficient for the trial, subject recruitment, shipping logistics worldwide to participants, administration of the test doses, data collection, analyses, and compiling results. Honestly, 11 months from start to finish seems like an amazingly short time to achieve so much.
It didn't take 11 months for the FDA to give the OK. It took 11 months to design a vaccine from scratch, conduct phase I safety trials, phase 2 human safety and dosage trials, and a phase 3 trial to determine efficacy.
The standards for the phase 1-3 trials are largely set by the FDA. Further, the whole idea that I can't weigh my own risks, and sign a paper saying "I acknowledge that this treatment is not fully tested, and choose to take my chances" is driven by the FDA. So yes, the time span before the public had access was driven by the FDA.
Sure, the timeline is driven by established protocols of safety & efficacy testing. So what should be done differently here? Are you advocating for mass availability to the general public on a caveat emptor basis, after say, animal safety trials?
From the FDA side, I suppose the issue is that in the absence of preliminary phase trial data, we don't know what we don't know. So it's less about not trusting the public to understand their individual risks, but that the drugs/vaccine offer risks that are unbounded. So perhaps the vaccine lipid nanoparticles are contaminated with toxic precursors that were not fully purified in the supply chain, or the lipids trigger an immune response to implants (something that did happen with cosmetic fillers), or they cross react with prescription statins in dangerous ways, or the encapsulated mRNAs trigger ANA antibodies, and so on. You may understand your own risk, but we were extremely ill equipped to understand the risks associated with the vaccines themselves till very recently.
You seem to be arguing that if FDA had begun widespread inoculation earlier with the current vaccines, variant COVID strains would not have arisen.
But that's wrong on several levels. Even if we had started producing vaccine en-masse in March, it would still take many more months (several years) to inoculate everyone on the planet. These novel strains would still have arisen within that time frame.
We would also have introduced additional problems that undertested therapies often suffer from and that the Chinese vaccine appears to have -- low efficacy. If quickly approved vaccines were no more than 50% efficacious on large fraction of the planet's peoples, herd immunity would take longer to accumulate and novel strains would still emerge.
Of course, toxicity is another likelier outcome from undertesting a new vaccine. Others can assess that risk better than I. In short, when it comes to combating pestilence, there's no free lunch.
You seem to be arguing that if FDA had begun widespread inoculation earlier with the current vaccines, variant COVID strains would not have arisen.
My statement isn't quite that strong. It MAY NOT have arisen; it's all probabilities. Every time the virus is passed to another person, there's another opportunity for a mutation. If we could have driven the infection rate down sooner via vaccine, then there's some chance that it wouldn't have happened.
Assuming ad arguendo that the new S. African strain is able to skirt the vaccines that are being distributed in America, what do we do? Wait another 11 months for a new formulation to be approved, and potentially for yet another slippery variant to arise? How do we get off that treadmill?
I sympathize. But vaccines are only one way to diminish the infection rate. Other options have not been employed to their maximum effect in the US, like distributing (and requiring) better masks, requiring mask wearing at all times when not at home, mandatory quarantine of infected people in encampments (as China and Singapore have done), and legal punishment of those who do not comply.
Employing medical procedures which are probably unsafe is not the only solution left to us.
This is an interesting take for sure that I hadn't heard before. Do you have more information on how they could have accelerated things?
If feels like the risk of shipping a vaccine that later is found to have adverse side effects would be so dangerous to the trust of the FDA that it would be really dangerous. Think of the shattered trust on both the FDA side and on vaccines in general, feels like maybe that would be too big a risk to take.
Given that most of the vaccines were produced "at risk" (i.e. before the trials showed that they were effective), I doubt that if the FDA had approved these vaccines on the day they were designed, we would have significantly more doses in people's arms today.
The FDA is slow? Compared to what? They approved the first vaccine 3 days after the NHS.
If your window of success vs. failure is very small, you simply have to test before you push to prod. Especially when using a technique with a long history of failed attempts.
Interesting to see what this will mean for the vaccines currently in use. If they generate the spike protein and the spike protein is significantly altered in the new variant, we in the uk are fucked.
the government of my region has decide that instead of following normal vaccination procedures, they will spread the available vaccine (Pfizer) to just give 1 dose to as many people as possible as opposed to the 2 required to be effective as per the clinical trials and the manufacturers advice. This decision is purely political, defying all biological evidence.
Seems to me this is the perfect scenario to evolve vaccine resistant variants.
Probably not. The second dose of the vaccine is more about ensuring that you are covered for a long time. So long as everyone gets the second dose in a few months we are fine. If we wipe out COVID there is no reason to give second doses at all.
"Pfizer said in a statement that there are "no data" to demonstrate that a single dose of its coronavirus vaccine will provide protection from infection after 21 days."
We don't know how long protection lasts after the 21 days, but we have enough data from other vaccines to make educated guesses. I wouldn't go more then a couple months.
My guess is we will need to FDA approve the mRNA vaccine development platform so we can develop a cocktail of spike mRNA vaccines and you will take 1 or more of them. We will need some kind of rapid clinical trial procedure to get updated mRNAs tested.. I am not sure what they do with the yearly flu vaccine in this regard but a similar approach is necessary. Then we will need a rapid surveillance program as well.
We will also need to update / create more antibody treatments like Regeneron's.
But that's a lot of technology to solve the wear a mask and social distance problem.
We need to keep the fire from spreading because it will just come back and burn down the things it missed the first time.
I suspect we will be dealing with rolling covid lockdowns for the next 10+ years.
It would seem that the horse is already out of the barn. Flights would have needed to be curtailed much earlier. In addition, we're seeing similar mutations popping up independently in geographical areas - seems to be evolutionary pressure in these directions.
The rise of these variants shows that we have to do a much better job with genomic analysis and surveillance and we have to be willing to be more proactive about shutting down travel to/from regions where these variants show up. I'm just not sure we have the political will to do what the science would suggest - we didn't for the original covid-19 and as it spread around the world political leaders of all stripes were slow to listen to the scientists. I guess I'm not sure that's going to change.
I think you lost me. How can we have an unfettered economy, not limited by lockdowns AND contain mutations regionally? These two statements you have made seem to be at odds with one another. Or am I overthinking/underthinking this?
The local economy is the global economy. Things I make here get shipped there, unless my business is shut down because of local mandates. Then nothing gets shipped over there.
I think you're oversimplifying and I can't figure out how to explain myself.
Let’s say you produce wine in France. France has a new variant. We shut France down. You’re French and live there. You’re affected. I’m in Mauritania, I keep on working unaffected by your shutdown.
You’re saying it’s preferable to have your economy, my economy and everyone else’s economy because... it’s better for you if we all get shut down?
No, I'm saying a local shut down in the economy may/does have impacts further reaching than the local economy, and that your statement is flawed.
Shutting down local economies is exactly what shuts down global supply chains/economies. It's not like you can carve France out of the global economy and act like they don't exist for three months.
It's not as simple as you're saying, is what my point is.
Please stop repeating this. Repetition is tedious and lowers signal/noise ratio. HN is supposed to be for curiosity, and curiosity wants just the opposite.
Edit: also, can you please stop posting unsubstantive comments generally? It looks like you've been doing that a lot, and that's not what HN is for, for the same reason: it repels curiosity.
The issue is that repeating the same thing over and over is not cool. If the account hadn't posted it three times in a row I wouldn't have replied.
Since you ask, though: a comment saying "wearing masks is going to help us get out of this" and not adding anything interesting would be a bad HN comment. A good comment would add some information or new insight. Simply repeating what we've all heard a million times does nothing for curiosity.
Getting everyone to work in harmony is basically impossible. If a politician goes on the news and say you need to stay home for 2 weeks starting next Friday, what do you thinks going to happen? Mass panic buying and looting? People refusing to do it because it's a conspiracy? Mass protest events encouraging super spreading? By the time this is all over, 2 weeks has passed...
I'm curious, is this headline (which differs significantly from the one on the paper itself) making the common mistake of conflating "immunity" with "antibodies"? Just wondering if there is a difference between showing that the new strain is resistant to the antibodies as opposed to showing that it is likely to reinfect people who recovered from a previous strain.
> Here we show that this lineage exhibits complete escape from three classes of therapeutically relevant monoclonal antibodies. Furthermore 501Y.V2 shows substantial or complete escape from neutralizing antibodies in COVID-19 convalescent plasma. These data highlight the prospect of reinfection with antigenically distinct variants and may foreshadow reduced efficacy of current spike-based vaccines.
Ugh; this hurts to read.
The callouts there are "complete escape [from] convalescent plasma" (prior exposure won't help you), and "reduced efficacy of current spike-based vaccines" (which is all of the ones deployed, I believe).
> The callouts there are "complete escape [from] convalescent plasma" (prior exposure won't help you)
Whether prior exposure helps also depends on T-cell response. At this point it's well established that immunity lasts for some unknown period of time past when most antibodies have left the bloodstream.
Yeah, this is not great news. I hope the vaccine makers are looking at adding coverage for these variants to the existing vaccines. That should be relatively easy to do for the mRNA vaccines, but possibly harder for the adenovirus based vaccines like the Oxford/AZ and the J&J. The question is whether they would have to go through a full phase 3 trial for this kind of addition or would this be more like how we add coverage to different flu viruses to the annual flu vaccines?
> That should be relatively easy to do for the mRNA vaccines
That isn't super obvious to me anymore, after it was pointed out to me that the current mRNA vaccines rely on a modified sequence for the spike protein, designed to make the protein stable enough to be usable in the vaccine process (described here [1] as "antigen S-2P" - "S" for "Spike" and "2P" for the two proline substitutions in the sequence). It's my understanding that this work dates to 2017 [2], and that it might not be quick or easy to replicate for new spike protein variants.
[2] Pallesen, J. et al. Immunogenicity and structures of a rationally designed prefusion MERS-CoV spike antigen. Proc. Natl Acad. Sci. USA 114, E7348–E7357 (2017).
I for one am not concerned. The true mortality rate appears to be <1% and of that 90% are >65. What does that mean?
To put it into perspective you may only know one person in your friend group which knows one person who dies.
Your friends / family are more likely to die of cancer.
How often do you know someone die of cancer?
It's definitely unfortunate; we should all socially distance & wear N95's where possible. All of us can decide if we want to stay locked down or not. Probably half the population will, so the spread will be much lower than otherwise. The rest of the population can keep working, making money and feeding their children.
It is important to note that the current mortality rate is the mortality rate with treatment, and with varying degrees of spread mitigation measures. If hospitalization rates exceed the available beds, the mortality rate will rise.
That depends on how many smokers and ex-smokers you know. It makes it all the sadder because the death was preventable. Which puts it into a similar headspace with Covid.
"To determine whether 501Y.V2 is still recognized by non-neutralizing antibodies, the binding of polyclonal sera (from Fig.2a) to a recombinant 501Y.V2 RBD+SBD1 protein and an RBD+SBD1 from the original lineage was assessed by ELISA (Fig.2b). These data revealed that binding of polyclonal plasma to 501Y.V2 RBD+SBD1 was only substantially affected in a minority of cases (14 of 44 with ≥five-fold reduction, 32%). Most of the convalescent plasma/serum suffered less than four-fold reductions in total binding activity (as measured by area under the curve), suggesting a considerable non-neutralizing antibody component are still able to bind the 501Y.V2 spike antigen"
Its also worth to note that only 44 plasma samples were used from individuals out of a population where the virus probably originated.