Antibodies mostly target the attachment heads of RNA viruses, which mutate very quickly to evade them. But that mutation also applies to its own reproductive mechanisms, like RNA polymerase, which degrades in the presence of evolutionary pressure from the immune system against the attachment proteins, so the latter strains become dormant because they lose reproductive integrity. It then takes conditions lacking an immune response to evolve back to a working polymerase and attachment head.
I think it is interesting to note that the immune system itself is largely responsible for spreading most RNA viruses: inflammation, coughing, sneezing etc. Is this us evolving population-level (probably more like Dunbar number than 8B) defense in response to the general threat of viruses, or is it a weakness that each individual virus evolves to exploit. It seems to me that this involuntary spreading behavior is much more pronounced in humans than other mammals.
So it's finally okay to say there's multiple strains with different infectiousness and (possibly) severity?
Back in February-ish (I forget exactly when), we had confirmed community spread in Washington (West-coast state in the US), with the belief that it had been spreading for weeks and no one noticed, because of how few cases there were, and no bump in hospitalizations. This was likely the Wuhan strain, which likewise had been spreading in Wuhan for at least a month and a half before it was detected.
On the flipside, when it reached Italy, it hit that country hard. It wasn't clear why, but I remember a report sometime during the summer that the most prevalent version of the virus in Italy was distinct from the Wuhan one, and could possibly be labeled a different strain because of its increased infectiousness, that mutation apparently occurring somewhere in Europe and spreading out from there (France was also hit hard at the same time IIRC, but Germany for example was not).
Not long after that I remember a cross-country comparison that said the primary version of the virus in New York (US East coast, also hit hard) matched the one in Italy, but not the Wuhan one, and that what we had in Chicago was a mix of the different strains with (at the time) no one winning out over the others.
Nice to finally see confirmation about there actually being different strains that are shifting over time, but unfortunately the timing makes it look like lockdowns may have selected for the more virulent version and caused the pandemic to be worse than it otherwise would have been (see the graphs in the "G strains take over" section, where the cases spike only after, well, the "G" strains take over and the Wuhan "L" strain has been pushed out).
No, according to the majority of experts, there's still no sound basis for claiming that the strains have different infectiousness and there's even less evidence for different severity.
The only thing known is that we can decode the genome across the world and that the virus, as it spreads, slowly gets some small changes which could be followed.
There's no sign that anything people did (especially "lockdowns") up to now had any evolutionary effect on the virus. Coronaviruses mutate much slower than a lot of viruses. The majority of experts believe that what we observe (these still minimal changes) could be attributed to the "founder effect."
Not an evolutionary biologist, but I think it's better to think of it as potentially killing off an earlier, less virulent strain.
Putting it in concrete terms, if you have two versions of the virus, X which for each infected person tends to infect 1.8 others, and Y which tends to infect 2.8 others, then after ten days there might be more people infected with Y than X, but X would still be around.
Now if everyone takes precautions, maybe those rates are cut in half. Now X only infects 0.9 people per infected person, and thus dies out, while Y is still infecting 1.4 people per infected person, and thus is still spreading, just slower.
> Putting it in concrete terms, if you have two versions of the virus, X which for each infected person tends to infect 1.8 others, and Y which tends to infect 2.8 others, then after ten days there might be more people infected with Y than X, but X would still be around.
This is actually an observed effect in many transmittable illnesses; over time, they become more transmittable, and less deadly. Extremely deadly forms kill their hosts, ending the ability to reproduce via transmission, and the more transmittable strains reproduce effectively. This type of optimization leads to things like the common cold and flu. The scary thing about COVID19 is that it has a very long lead time between infection and symptoms, if they develop at all, meaning it can circumvent some of those "normal" optimization peaks; it can be both very deadly, and very transmittable, because of the latency in the signal.
I'm mainly basing it on the graphs provided: The cases don't spike until after the "G" strain is present, no matter how long the "L" and "S" strains were present beforehand.
Actually I think I should have said "infective" rather than "virulent" there; basically lockdowns select for versions of the virus that can spread despite the lockdowns. It only looks more virulent because of the larger number of total infections.
It's worth bearing in mind that the graphs in the article are quite distorted. Testing was not widely available until months into the pandemic, making the early spikes look much smaller than they were.
Later strains may indeed turn out to be more infectious, but I don't think we have the evidence for that yet.
As long as the epidemic doesn't run close to saturation (and given the multiple effective vaccines it likely won't, ever), NPI-induced relative spread advantages of one strain over another don't make a difference unless they are also absolute advantages compared to non-NPI-scenario. And given the strength of pre- and asymptomatic spread of this particular virus, it's almost immune to selective pressure for weaker symptoms anyways (scarcity of PCR and deep connect tracing can cause some pressure).
a lockdown would select for a more communicable strain, not a more virulent strain. the big problem is this virus has morbidity latent to infection incubation and transmission.
these conditions mean that the virus can be 100% lethal and not succuum to the usual dynamics
Imagine the original strain had a mortality rate of zero, but later strains had high mortality rates.
The original strain would effectively be a vaccine. The lockdown would be the equivalent of the anti-vaxxers.
There’s no evidence the mortality rate has actually increased; this was just a thought experiment.
In prior pandemics (1918 flu), future strains were more deadly than earlier strains.
The nightmare scenario now is that a COVID-20 emerges with a 5% mortality rate instead of 0.5%. If catching COVID-19 gives you immunity to COVID-20 (and all the vaccines fail), then the lockdown would increase the death toll by 10x.
These are all hypotheticals that looked somewhat plausible in April, and implausible today.
Hard to believe, but true - because it didn't outcompete other alleles, it was just in the right place at the right time, as has been carefully documented:
The founder effect doesn't seem capable of explaining the spread of D614G given that it has replaced other varients in every place it has been introduced to, and that it has even doubled back and outcompeted other variants even when those variants were introduced far before D614G. I'll read this paper, though, to get a better idea of what they're claiming; thanks for the link.
You have assumed I'm ignorant when you could have attempted to understand why I believe the things I do which seems at least as big a mistake as the one you accused me of making.
the D614G strain has a loose binding domain in its spike.
this modifies what was a specific key into a lockpick.
this allows the virus to bind to a number of allelic versions of ACE2 rather than one or few specifics. thus promiscuous binding.
Interesting premise. But why doesn’t anyone look at the bigger elephant in the room?
Sometime in April 2019, reports of a mysterious illness started surfacing. They thought it was related to vaping products. [1]
Then in July 2019, a respiratory illness hit a retirement home in Virginia, and killed a bunch of old people. [2]
Then the Wuhan military games was in mid October 2019.
Then China reported of an unknown pneumonia in early December. They thought it came from a seafood market, which was proven incorrect.
The western world harassed them and accused them of eating bats, and transmitting the disease, which is also proven to be incorrect.
China then back-traced the earliest case to mid November. Which happens to coincide a few weeks after the Wuhan military games. Just the right amount of time for the virus to incubate and wreck havoc.
New evidence is suggesting that the virus was in Italy before it was in China. [3]
But the interesting thing, is that when they took MRI scans of the vaping outbreak patients, they saw white orbs in the picture in their lungs. Coincidentally, Covid-19 victims also had these white orbs in their lungs.
The whole origin of this virus was always very mysterious. Something just never seemed right about it.
The vaping thing just came and disappeared. Nobody really knows what caused it, just a few random theories about contaminated cartridges. But here’s the strange thing. Those vaping pens, are all made in China. And are sold all over the world. People in China uses those vaping pens everywhere, but there were no reports of a mysterious illness from it in China. Only in the United States and a few in Canada. Not even Europe reported any issues.
Why was it reported only in the United States? Then soon after, all the other pieces began to fall into place, one after the other.
To get down to the true origin of this virus, then they need to check those vaping people. Check them for the Covid-19 antibodies.
Then check the nursing home people from Virginia, for those that survived, for Covid-19 antibodies.
Then check the people that went to the Wuhan military games for Covid-19 antibodies.
Or not. And just conveniently blame China for being the origin of the virus, just because they were the first ones to detect it, and report it.
The vaping issue was related to Vitamin E in THC vaping and was not related to vaping in general.
The Vitamin E was being vaporized and inhaled directly into the lungs, which caused the problems. Inhalation of Vitamin E into the lungs is a known cause of lung disease symptoms.
I know vitamine E acetate is a scourage in the vaping community, but I was under the impression that outbreak was a distincly different thing, at a different time.
Although the uninteresting answer is often true, I do dislike that people refuse to entertain anything remotely fringe. Some of the declassified CIA documents stated that they intentionally furthered this attitude as much as they could, as it allowed them to make many of thier projects dissappear.
What is the most promising theory of origin? A 5-10min search didn't help.
The lab theory is of course the most fun, but not the most probable. The fact that they were working on similar diseases, the lab was newish, and the country itself isn't exactly well known for IP security make me not discredit it as fast as I normally would.
The animal->human route via food (or less likely, bites/other contamination) seems to be most likely. It's happened plenty of times in the past, and given the SES level of the area and cultural norms, it could have definitely happened.
The rest of the ideas seem like a long tail where all of them have fairly obvious "gotchas" that make typing them out a waste, but I'd love to hear what other people think.
Looks like the CDC investigated the outbreak - if there was a virus responsible, wouldn't it have been found then? If it was related, it doesn't make sense that it would not have easily begun to spread at that time.
If it was SARS-CoV-2, the CDC could confirm that now retroactively with stored blood samples. I suggest it was probably not.
However, then, it does point to proto-pandemics happening as a regular occurrence. A fatal viral outbreak is contained within a care home rather than spreading - either by being slightly sub-exponential in the general population (R<=1), or perhaps just by pure luck.
That trope again. First, that's spilled milk, even it were true, and thus is a pointless discussion. Second, local Chinese authorities screwed up. That was followed by one of the quickest, strictest and most effective reactions. As for the international response, that could be based on cases in Korea and Japan, for example. Europe reacted quick enough in Spring, after Italy waited a couple of days to long. Which is now followed by a real screw up in Germany. So no, China didn't hide anything once central government took over. And no, even if they had that would not be an acceptable excuse for screwing up ones response.
It's not a "trope". Several papers ended up getting censored, and local samples getting destroyed. I was around and combing through the news stream at that time. Project Evidence was the group of people collating the circumstantial evidence around it, and I've seen a notable dearth of material that doesn't smell of some level of having been contrivance to put the field of virology squarely outside the crosshairs of the public's ire, or having been motivated by plausible geopolitical motivations or face saving measures.
If you look at the locality of happenstance, the lab escape is more than worth looking into. Just because search engines are bombing anything with regard to it to the bottom of search results, and press farms are working hard at propagating the zoonotic origin without touching on any of the impracticalities inherent to making that full set of connections feasible does not mean the information is not out there to be found.
I think you’re just engaging in conspiracies here.
It’s possible that China’s central CDC ordered the local samples to be destroyed, because the local facility was not authorized or equipped, to handle infectious diseases properly.
Think of it this way. Do you want junior high school kids, handling contaminated biowaste, where the probability or risk of infection is very high.
And this was at the very beginning, when the science behind this virus and disease was not fully known.
It’s safer to throw the samples into a fire furnace, than to risk transporting it or storing it, where its leakage could further infect more people.
There's truth in this, but you need to ask, why did local officials screw up? And it's probably related to the way mistakes are treated by central government. So, even if central government was not responsible for the individual actions early in the pandemic, they set the framework for how they interact with local governments, and thus still bear responsibility.
You want examples outside of China of more serious screw ups, once the real seriousness was known?
Ok, then. Bavaria had beer festivals in February and March, Austria kept Ischgl open and infected most of Europe. Other regions let the German carnival running. Leipzig had Champions League match. All in Feb and March. Just from top of my head.
At least local Chinese authorities still had the benefit of doubt. And did we already forget how fast they built hospitals and how many people the tested?
Yup, all screw ups. In my opinion, the scientific community should be held to a higher standard on this, but sure, you can judge them alongside the local beer festival I guess.
Setting aside the idea of intentional coverup, China is still the most likely area origin.
Normalized working/eating close to all animals, wet markets, pollution, lack of food care (incl refridgeration), unclean water, and more all make for a hotbed of potential disease.
Only for the record/FYI, there is growing evidence that the virus (cannot say which strain) was present in Italy months before, possibly since September 2019.
"Some people had antibodies that react with SARS-CoV2 prior to January 2020" isn't great evidence that the virus itself was present prior to 2020. There's some amount of cross-reactivity between antibodies to other human coronaviruses and SARS-CoV2.
What does everyone think of the idea that there is an 80/20 rule in play for Coronavirus? Specifically, 80% of the infections come from 20% of the infected. I’ve heard some hearsay about it, but nothing conclusive; I was hoping someone knew either way.
I don't know either way about your question, but aren't these sort of power law dynamics common in everything? I don't think it would be surprising if that was the case with this "pandemic" nor would it make this virus special. Just like 90% of the content is created by 10% of the people in social media, or something like that.
> Some cases of superspreading conform to the 80/20 rule, where approximately 20% of infected individuals are responsible for 80% of transmissions, although superspreading can still be said to occur when superspreaders account for a higher or lower percentage of transmissions.
> "Coronavirus does not spread evenly. Most people who get the virus won’t pass it on to anyone at all. But a small number of people will spread it widely. Scientists estimate as few as 10% of infected people are responsible for 80% of infections."
Based on this, they go on to explain why, if it's true, it becomes worthwhile to do backward contact tracing to reduce R.
A colleague of mine was infected, became symptomatic and tested positive, and results took several days to come back. The whole time he was at home with his family waiting for results, he quarantined at home but had contact with his family. He tested positive, but they never did. More credence to the idea that some are super spreaders and some are not.
Meanwhile I met my family for 2 hours, I started having a fever and immediately quarantined myself to another location.
I told them to open all the windows of the flat, they didn't take me seriously.
They all got COVID-19 from me.
This also happened to me. I had minor symptoms, but they didn’t feel like anything worse than bad allergies. My wife is in health care and is tested twice a week so I figured if she doesn’t have it then I must not have it either. That was until I lost my sense of smell. At the time I got my positive result back from the lab I had been experiencing covid symptoms for 9 days. I was doing nothing to shield the other 3 members of my household and none of them got it either.
I read that is what the Japanese did from the start (backwards tracing), and it worked well at the time. Something like the 80/20 rule was mentioned, that a minority of infected people were responsible for the majority of the spread.
Probably true, but I think it's because most infections happen in certain dangerous situations (an infected person being in a badly ventilated room with others for a while), not because of some feature of that infected person.
> But what would be the point of further discussing it?
If you have a limited number of vaccines, you can vaccinate the propagators first and have 80% of the benefit of full population vaccination for 20% of the cost.
Did anyone else think that 80/20 sounds too neat, especially when you consider that the definition of superspreaders is subjective? It suggests confirmation bias and reminds me of when biologists etc assume normal distributions but when you did into the detail you find normal is actually not normal.
Power laws aren't rigid, domain-specific variables create local fluctuations even in models like population or wealth distribution. It's just a general baseline which we can use to model certain characteristics of a system.
Maybe. It's often easy to choose a model and squint to make it fit. You have to be very very careful when performing empirical method, it's extremely easy to taint data and end up fitting models that you shouldn't have. It's not enough to simply fit a power law and say "it works" - that's bad science.
It's more utilitarian than that. The power law is a tool for inquisition, you need to verify your assumptions when possible. If you can't, the power law is one of many models which you can apply to seek insight into a system.
A good heuristic for knowing which model to apply is tantamount in absence of a testable environment.
Since this will continue to be misunderstood, it's important to emphasise that the article explicitly mentions that there is
1. No evidence to support the idea of strains that have any impact on infection
2. No evidence to support the idea that the strains will resist the vaccines or weaken vaccine efficacy.
This is not a "strain" in the sense of the flu, COVID-19 hasn't fundamentally changed in any meaningful way that lets us do anything other than track the pandemic's spread.
The problem with "any" is its usually wrong. Here's an "old" paper from July:
Toyoshima, Y., Nemoto, K., Matsumoto, S. et al. SARS-CoV-2 genomic variations associated with mortality rate of COVID-19. J Hum Genet 65, 1075–1082 (2020). https://doi.org/10.1038/s10038-020-0808-9
The measured variation between the now extinct L strain and the new current G strain is the G strain was about 2% higher correlation between strain and fatality rate. The actual fatality rate was not 2% higher which would be huge, but the % of L in a population vs population fatality rate correlated 2% higher based on euro country data in the spring.
Certainly there's only two real impacts on fatality rate right now, both incredibly politically incorrect to discuss, there's an enormous staggering stunning huge disparity in fatality rate by age, and a merely giant disparity in fatality rate by comorbidity rate. The medical science seems clear, but the political impact makes it impossible to discuss quarantine policies that would minimize total death rates. Hundreds of thousands of lives could be saved by locking up everyone over 60 and everyone over 300 pounds and a couple other pre-existing conditions, but AARP is one of the strongest PACs out there and even if it saves her life, grandma will vote out anyone who "locks her up for a year for her own good".
Personally I'm old enough that I'm working very hard to max out my cardio health for when I inevitably get it.
Well, that's _mostly_ true, but the very fact that one virus variant displaces another over the course of a month or two, while by no means definitive proof of anything, is at the very least suggestive that for one reason or another it is better able to spread.
It _could_ be a neutral mutation that just spread due to a "founder affect" or something, but it would not be in any way surprising if a virus which is brand new in humans, evolved in the direction of adapting better to that new environment. What spreads better in bats, may not be the same as what spreads better in humans, and there is no particular reason to expect that this virus wouldn't be mutating in the direction that allows it to adapt to its new host.
Now, that could even be a good thing, if it was adapting in the direction of not triggering the host's immune system as strongly, since it is largely an immune system overreaction that kills the host. But, while by no means definitive, I don't think we can say that there is _no_ evidence to support the idea that strains have any impact on infection. the very fact that the initial strain has been largely displaced by others, suggests at least the possibility that it has.
Not questioning anything you wrote, but it would be interesting to know the strains of virus in people who acquired COVID in the mRNA vaccine trials. I imagine this is in the trial data but haven't seen it.
Is there any real concrete — or at least scientifically backed — reasons why we’re continuing to see numbers rise, in spite of more lockdowns in place and more people (supposedly?) wearing masks vs. in previous waves where the spread and deaths seem lower than now?
This is especially baffling considering how much more prepared we are (or should be?) and how much more we (should) know about the virus now vs. before.
It seems like one or more of the following is happening:
- Actually fewer people are wearing masks, or are wearing them less vs. previously
- Even though lockdown mandates/recommendations are increasing, they’re not being followed/enforced as much
- Masks aren’t as effective as we think
- It’s spreading in other ways that we’re unaware of
I’d love an ELI5 of why we’re continuing to see record numbers of positive test rates + deaths + hospitalizations, in spite of (again, supposedly) more diligence with masks and lockdowns.
To be clear, I’m a strong believer in wearing masks and staying home (I almost never leave my house, and when I do, I’m wearing a mask), but it’s baffling and a bit frustrating to see the numbers continue to rise without anyone seeming to have answers as to why.
I have no credentials or scientific evidence, but I never questioned the rising cases with each wave since I assume its just a property of the exponential nature of the virus spread: in march, say you had 5 people unknowingly carrying corona-virus arrive in your city and each of them spreads it to 5 more people in a two week period, your outbreak is 50 people (seems small now). But now in December, your city has about 350 people spreading the virus but only to 1.5 close contacts in a two week period, you'd expect the next outbreak to be 500 people.
I think hospitalizations are still a somewhat consistent percentage of cases, and will increase as the number of cases go up.
> Is there any real concrete — or at least scientifically backed — reasons why we’re continuing to see numbers rise, in spite of more lockdowns in place
Anthony Fauci summed this up pretty well a few days ago in a press release. He basically said that the USA is really bad at following rules, which we are, and that with the recent holidays (Halloween, Thanksgiving) and because of the cold weather (people stay indoors more, share the same air, air being recycled and heated in HVAC systems to reduce energy consumption), that numbers would rise. And so they are. I think these human explanations are the main source of the rise in numbers.
Another interesting one was in a WHO release a few weeks ago, that people seem to be experiencing "mask fatigue", or what is more generally known as "caution fatigue", where people, after having to be cautious for a long time, and not experiencing the source of that caution personally, just lose their ability to pay attention to the problem. It's the same reason the TSA inserts fake firearm pictures into the x-rays of luggage, and the same reason the military regularly inspects guard posts in key locations.
It got cold outside. The curves match other respiratory viruses - or put another way, it's flu season.
This was one of the running theories back in the spring, but it was hard to tell for sure until seeing it spike back up this fall exactly as one would expect if this were the case.
> - Masks aren’t as effective as we think
Also this, I think - masks are good at catching droplets from talking or coughing, but sometime between summer and now it's suddenly become commonly known that this virus can hang in the air for an extended period indoors when there isn't good ventilation - being truly airborne like that means it can just slip around the edges of the mask as you breathe. Even disregarding that it was known back in March that fabric masks only reduced the amount of virus that could get through the mask, it didn't actually completely stop the virus as people nowadays seem to want to believe.
It's hard. Few of the later measures taken against coronavirus are grounded in very strong scientific evidence. It isn't easy conducting randomized trails in an ongoing pandemic.
What you see practiced in hospital and intensive care units is what works.
The rest have spotty evidence at best. Hopefully something good will come out of this and we will see more research on public health. Look at the recent Danish on general public face mask use as a good example.
Towards the end of the article is a particularly good nugget of information.
> Since then, there have been documented reports of individuals being reinfected with different versions of the virus.
Yes, reinfections have been extremely rare so far. But if the immunity really is strain-specific, the warnings about Covid becoming endemic in the global population should now carry a lot more weight. The virus will mutate. In a likely scenario, previous immunisations are likely to be less useful, and we all need annual shots against the newly emerging strains.
On the upside, if Covid strains become just another aspect of the flu jab, then we at least already have an existing infrastructure to manage it in the future. Production capacity of vaccines will take some time to ramp up, though. Maybe now would be a good time to invest in drug manufacturing and logistics?
Planet Money did an episode on Covid vaccine logistics and one data point stuck with me. The global production of vaccines is between 3.5B and 5B doses a year. That's for ALL vaccines, across the entire spectrum of diseases and treatments. Adding another 12B to 16B doses on top of that is going to require a lot of new infrastructure, from production facilities to all the materials needed in the logistics chain.
> > Since then, there have been documented reports of individuals being reinfected with different versions of the virus.
> [...] But if the immunity really is strain-specific
Reinfections have been recorded from different strains because it's much easier to demonstrate that someone has been reinfected with a new strain. If someone has been reinfected with the same strain then it is hard to distinguish that from an infection that wasn't fully cleared originally. It doesn't necessarily mean that immunity is strain-specific.
(I don't know why you were downvoted; your comment seems reasonable to me!)
People are really enjoying WFH and don't want it to end. It's important to keep the fear strong.
Meanwhile, I am baffled we didn't prioritize n95(or kn95) masks. Well... It's government, I'm not that baffled
A significantly more rational policy would have been to prioritize masks with filters and for the less than 1/12 of elderly people who live with younger generations, move them into a hotel room and pay for food delivery and care services.
All of this is cheaper and healthier than what was done.
1. Risk groups are not just old people, but also include a lot of people (e.g. asthmatics) that are a central part of the work force. Not all of these can WFH, they might be working in supermarkets, etc.
2. Some people don't even know they are at risk especially when they are young.
3. You can't fully isolate old people anyway. That's why we continue to see infections in hospitals, nursing homes, etc.
4. Even if you managed to isolate all risk groups, the spread of covid19 without any restrictive measures would be extremely rapid. While only a small fraction of the rest of the population would become severely ill, a tiny fraction of a large population can still be huge and might be enough to overwhelm hospitals.
If it were as easy as you suggested, surely it would have been tried - at least somewhere on the planet.
> Meanwhile, I am baffled we didn't prioritize n95(or kn95) masks. Well... It's government, I'm not that baffled
They did. Production is up 5x. But factories take time to build.
Entire new types of filters have actually been invented this year, going forward humanity is going to have a lot more choices when it comes to high quality filtering masks.
That "spike" in the graph comes from sequences in the nucleotides coding the spike on the virus, which is somewhat expected given it's repeated on the surface of the virus membrane.
Apparently most of the spike encoding is from a South Asian fish. Reference in the repo.
It’s not like the flu. The strains aren’t functionally different, with the possible exception to the one that spilled back over from infected mink which was slightly less responsive to human antibodies in lab experiments. Unless there’s more significant change the vaccine should work for all the different variants.
EDIT- Be careful reading too far into statements like “XYZ mutation makes it easier to bond to ACE2 therefore it’s more contagious” Infection is more than just binding to a receptor, even if lower quality preprints jump the gun in their conclusions
The very first strain isolated in Wuhan, but the most prevalent S protein mutations in subsequent strains are fairly buried. None have yet been shown to affect immune recognition, as far as I know.
There was a suggestion that one of the variants seen in Denmark's mink infection, might make at least some of the vaccines slightly less effective. But even in that case the effect was not large, and in any event the variant in question hasn't been seen since September.
“If the virus changes substantially, particularly the spike proteins, then it might escape a vaccine. We want to slow transmission globally to slow the clock,”
Is this why some are saying we might need a booster shot in a few years?
There is little selection pressure on the virus for the spike proteins to evolve and change. SARS-CoV-2 infects human cells just fine using its current spike protein. [1]
Yay, then lets see how the spike protein evolves after mass vaccination. In my understanding the vaccination targets exactly that protein so there should be plenty of selective pressure in case mass vaccination takes place
That seems to be an incorrect understanding. Selective pressure is only one of the factors influencing how frequently the virus has mutations. Self correction mechanics in the RNAs replication seem to have a much more stronger effect, since they “correct” the mutations. The article specifically mentions that the timeline for significant mutations is likely in the order of a few years.
A slow mutation rate reduces the rate of change if all other variables are equal but increasing the selection pressure can drive that rate of change higher by clearing the field of competitors and providing only one clear path to success.
Thanks for that Nature news feature, it summarized the research on SARS-CoV-2 mutations quite well.
We’ll have to watch for signs of selection pressure as more and more of us get vaccinated to recognize the spike protein. Hopefully SARS-CoV2 mutates too slowly to escape the vaccines, or can only escape with sharply reduced infectivity and virulence.
> Studies of common-cold coronaviruses, sampled across multiple seasons, have identified some signs of evolution in response to immunity. But the pace of change is slow, says Volker Thiel, an RNA virologist at the Institute of Virology and Immunology in Bern. “These strains remain constant, more or less.”
So there seems to be a pretty good chance that this won’t really be an issue.
No, different reason, booster shots, are needed to "remind" your immune system that the virus is still out there, and keep it on fighting shape, and as far as I am aware, the early discussions for booster shots, were about 6, to 9 months. But all of that is up in the air, there's no data for how the vaccine will develop that much into the future yet
Anyhow, if the spike proteins vary too much, then we'll need a new vaccine all together, not just a booster for the current one
I don't think so. I believe that is related to the immune system's ability to "forget". I believe a new strain which evades the current vaccine schemes would need an entirely new or significantly altered vaccine.
As noted in sibling, the booster shots are to "remind" your immune system that an infectious bug is out there.
If COVID begins to mutate in ways that make the vaccine (and anti-bodies it causes) less effective, we would be in a situation like the flu - annual vaccines based on that year's strain (which takes some guesswork). The disease is then called endemic.
But, there is currently no indication COVID will become endemic. It might. It might not. We don't know, but current knowledge tends to indicate it won't.
In case there's further whining about this comment being downvoted: I didn't downvote due to hivemind mentality or agreement/disagreement about the original, I downvoted because whining about downvotes makes boring reading.
Additionally, it takes a single, random HN user with 500 karma to put a comment into "downvoted" state. It takes three or four to be "heavily downvoted" (which doesn’t apply to your original comment). Just not a very meaningful thing to draw conclusions from.
A comment that just says "thank you this was a good post" is basically an up-vote in the form of a comment; it doesn't add any substance to the conversation. That would be a polite response in another context, but on HN the goal of the guidelines as I understand them is to keep the signal to noise ratio high - basically to increase the density of useful information and insightful argument in comments. In order to do that, comments that don't add substance to the discussion are discouraged here.
Thank you for the note, I suspected as much but I do appreciate your elaboration on the topic.
I don’t agree with the approach (I would say for submissions that don’t have as many upvotes that somebody who took the time to write a thank you note reflects they actually read the article and it was worth the effort to write a note (which takes more effort than an upvote). This can be a important signal for others. It also I think is a nice feedback to the author, I always want to try and encourage people — when I receive positive feedback, it makes my day).
In some ways it’s a reflection of how the community (at large, not any individual in particular) views itself — to be such stringent guardians of information density, when in fact a large portion of the comments are relatively useless and misinformed (usually the most knowledgeable people speak less as they are busy actually working in their field, although they pop up from time to time).
What I try to do in those cases is find something to say about the content itself. Could even include the 'thanks' that way if you wanted. Like, "Thanks, I didn't realize that <interesting thing learned from the post>." That way you're at least contributing by drawing people's attention to an interesting part of the original article.
This is why I get so frustrated with people justifying continued shutdowns "until it's cured by the vaccine". Almost every highly contagious virus mutates quickly. Same with bacteria. The cat is already out of the bag, even if we do manage to completely eradicate it it'll take years. (To be clear I'm not against virus control measures, I'm just frustrated with the flawed reasoning that all this will just go away when the vaccine is within reach. It couldn't be easier to get a flu shot and yet we'll probably be dealing with the flu long into the future. If we know this will stretch into say 2022 I have to imagine that will change a lot of peoples attitudes as to how society should react)
We don't know that for sure, and it has 7 different (known) strains already. Why would this be any different than the flu in that regard?
Besides, we already know there are a lot of ridiculous anti-vaxxers out there who will refuse the vaccine regardless. And a lot of those people are elderly or at risk!
The longer this situation goes on, the less palatable shutting down huge chunks of society seems to me to be. If this is going to be endemic, which a lot of signs and common sense reasoning points to, then the management of the disease needs to change.
I think it is interesting to note that the immune system itself is largely responsible for spreading most RNA viruses: inflammation, coughing, sneezing etc. Is this us evolving population-level (probably more like Dunbar number than 8B) defense in response to the general threat of viruses, or is it a weakness that each individual virus evolves to exploit. It seems to me that this involuntary spreading behavior is much more pronounced in humans than other mammals.
https://scopeblog.stanford.edu/2020/04/03/how-coronaviruses-...
https://mbio.asm.org/content/2/5/e00150-11