No, it does not.
The data from Israel only supports the claim that immunity from infection is longer lasting than from the vaccine, which should not have been a surprise to anyone.
It does not support any specific mechanistic explanation.
Note the "longer lasting and stronger".
> is longer lasting than from the vaccine
I really hope we don't end up with a Marek's disease, but in humans.
In the UK, 2% of people who tested positive have died. In the US, 1.7% of people who tested positive have died.
The mortality rate among hospitalized people even higher.
And there's reason to believe from HCoV-229E that immunity against coronaviruses is actually durable and that reinfection is due to mutation and immune escape.
https://journals.plos.org/plospathogens/article?id=10.1371/j...
This is news because the flu doesn’t do that every year or any year since 1919. It’s news because it’s the deadliest pandemic in over a century, and the death rate in some areas is at its peak and climbing, despite higher vaccination rates then a typical flu season.
I cannot understand why denial of this information is so important to you, but if you continue to spread doubt about taking more precautions than the flu, people may listen to you and those people may die.
625K war casualties[1] < 635K COVID-19 casualties[2]
[1]: https://en.wikipedia.org/wiki/United_States_military_casualt... [2]: https://www.nytimes.com/interactive/2021/us/covid-cases.html
I'm coming at this more from the perspective that the panic over delta being something straight out of a Big Bad TV Trope that breaks all the previous rules, is that it completely undermines the effectiveness of the vaccination campaign. The current best antivaxxer argument right now is just that all the headlines show that the vaccines don't work. I'm pushing back against that. It still looks to me like nobody has given me any indications the vaccines don't work. I think their VE against delta has been dramatically understated, the waning immunity has not been proven, and their efficacy against transmission is probably a lot higher than currently assumed.
At some point in the future I'll agree with the perspective that we need to start treating this more like the flu, but if the hospital systems are falling over we aren't there yet.
But that doesn't mean the mRNA vaccines would be failures.
Focusing on the spike was also done because mRNA vaccines against the nucleocapsid protein of SARS-CoV-1 showed evidence of ADE in animals models so nobody wanted to go down that road. That decision to run with the spike protein is very unlikely to be shown to ever be a mistake in hindsight and will have been the right choice (and certainly the right choice given the information at the right time and a decision which produced an entirely successful vaccine).
It is also a really pretty safe bet that this virus will evolve to achieve immune escape just like HCoV-229E does and will start reinfecting everyone again. That won't make this vaccine a failure. And that's a good thing since its more likely that forcing it to evolve to achieve immune escape will force it to made tradeoffs between immune escape and transmissibility/virulence/fitness.
You're right that the recent pre-print cited by GP - regarding the data out of Israel - does not prove or disprove any specific mechanistic explanation.
However, interpreting GPs comment charitably, that study does support the notion that immunity acquired through natural infection may be more robust to mutations and variants - the mechanisms of which have been articulated in a variety of other literature. See my sibling comment [1] for supporting citations and excerpts.
But is is acknowledged in the article linked here:
>> Specifically, antibodies elicited by the mRNA vaccine were more focused to the RBD compared to antibodies elicited by an infection, which more often targeted other portions of the spike protein. Importantly, the vaccine-elicited antibodies targeted a broader range of places on the RBD than those elicited by natural infection.
It does not follow that vaccination conveys better immunity than previous infection. Only better response to mutations in one area of the spike protein. Nothing else is being claimed in this paper.
Why is that? I have no background in immunology so it's mildly surprising to me.
But now we're back to speculation about mechanism, which GP was opposed to.
I find that surprising. Why did you expect that? Why should I have expected that?
Apparently it is a surprise for USA and Europe as the former only recognize infection based immunity for three months and the latter recognizes it for 6 months, while some EU member states recognize vaccine based immunity for 8 months.
please do not make stuff up to fit your narrative.
Now with death, one could argue that it does provide much longer lasting immunity....
Seriously though, for most people the severity of infection-derived immunity is preconditioned upon them surviving the disease so this looks like the classic "planes with bullet holes" image?
This is well-intentioned but false. The vaccines can send you to the hospital (side-effects). It's rare but happens. Similarly, you can be vaccinated, get infected with SARS-2, and end up in the hospital, so it's not even true that they avoid hospitalization from SARS-2 itself completely. (They help a lot with hosp/death from the virus, to be clear)
The vaccine can almost certainly send a few people to the hospital in the same manner that an airbag could almost certainly cause injuries during an accident.
It's very different from a natural infectionimo.
I know that it's a very unpopular opinion, but i'd say your statement is unfortunately still not 100% proven for every individual. A healthy 20 yo has "almost" 0 chance of having bad outcome from the covid. He also has "almost" zero chance of doing a hearth infection from RNA vaccines, and we have no idea about the long term consequences of both virus and vaccines, since both are only a few years old.
Making definitive statements in this context is hard.
But explaining to that same 20 year old that he might unintentionally bring COVID home from college and proceed to unintentionally infect high-risk parents or grandparents? That's where the real damage would comes from.
The peace of mind knowing I'm not going to unintentionally kill off members of my family is priceless.
Unfortunately, the recent news on that front don't bring much hope. Vaccinated people can be infected, and transmit the virus to elderly people (the rate at which they do being currently debated among specialist, some claiming it is much less, other claiming it is just as much as non-vaccinated asymptomatic people).
I do know I need to be able to live with myself, and if I accidentally hurt someone I loved due to being careless in the face of a real threat - it would tear me up. I'm sure others feel the same, and I hope people can keep it up through the fatigue. :)
> Specifically, antibodies elicited by the mRNA vaccine were more focused to the RBD compared to antibodies elicited by an infection, which more often targeted other portions of the spike protein. Importantly, the vaccine-elicited antibodies targeted a broader range of places on the RBD than those elicited by natural infection.
> These findings suggest that natural immunity and vaccine-generated immunity to SARS-CoV-2 will differ in how they recognize new viral variants. What’s more, antibodies acquired with the help of a vaccine may be more likely to target new SARS-CoV-2 variants potently, even when the variants carry new mutations in the RBD.
Anyone with more experience in immunology care to weigh in on why the second paragraph there follows from the first? Naively, one might expect targeting a wider variety of places on on the COVID spike protein to result in better immunity against variants, not worse. Why is the article saying the opposite?
immune systems dont look at everything at once, they find something that sticks and and over trials sharpen the response until highest efficacy of antibody epitope combination is found.
the vaccine is like a laser guided munition, natural immunity is like carpet cluster bombing; both highly effective but in different modalities.
The RBD is the part of the spike protein that latches onto the cell. Specifically it latches onto the ACE2 receptor. If the RBD changes too much then the virus can no longer infect its target cells (because it can't attach to ACE2 receptors). This means that there are probably strong limits on how much this section of the virus can change.
Because we expect the RBD to change less than other areas, and because the mRNA vaccines recognize more of these possible changes, then we have a reasonable expectation that mRNA based immunity should continue to be effective.
To make a crude analogy, ACE2 is a phillips head screw. The spike protein is a phillips screw driver. The tip of the screw driver is the RDB. Infection elicited antibodies recognize random spots all over the screw driver. mRNA vaccine elicited antibodies recognized spots all over the tip. Eventually you can turn the handle into a shape that won't be recognized, but there are strict limits on how much you can change the tip while still having it function as a philips screw driver. And of the ways that you can change the tip, the mRNA antibodies will match more of them than the naturally acquired ones. At least that's the expectation.
There are still possible ways that the virus might evade; perhaps by making shields for the tip that block portions of the antibody, but this seems like it might be harder than changing the handle's shape.
Infection's response to key antigens like RBD is inherently more limited because: 1) immunity creates antibodies and T cells that target a wider range of antigens, and 2) exposure to COVID antigens usually fades after 7-10 days, limiting the immune system's time to build further defenses.
The cited study in OP may have a slightly pro-vaccine bias, potentially because two authors have "the potential to receive a share of IP revenue" on a relevant patent, and because one author consults for Moderna. Regardless, the study presents scientifically accurate findings, but in a few places it tries to stretch those into questionable conclusions. For example, the authors write:
> At first glance, the RBD targeting of the vaccine sera neutralization might seem likely to increase susceptibility to viral mutations, but the rest of our results suggest that this MAY not be the case. [4]
So keep that tilt in mind when reading it.
> one might expect targeting a wider variety of places on on the COVID spike protein to result in better immunity against variants
Yes this is good intuition, here are excerpts from other literature illustrating why targeting a wide variety of SARS-COV-2 proteins can provide better immunity. In fact, this reasoning is why ongoing vaccine research is investigating formulations beyond the current solely spike protein focused vaccines. Notably, one shortcoming of the current mRNA vaccine formulations is that they do not induce nucleocapsid (N) protein antibodies - whereas natural infection does.
> The nucleocapsid protein of SARS-CoV-2 has been suggested to be an important target for T cell responses. [1]
> Firstly, this protein contains conserved cross-reactive T cell epitopes that are present among different coronaviruses, suggesting that it could be an ideal target for universal coronavirus vaccines. [1]
> Secondly, the nucleocapsid protein is among the most abundant structural proteins in the coronavirus lifecycle, which may facilitate early antigen presentation and recognition by T cells. [1]
> Previous knowledge on other related coronaviruses and the prompt sequencing of the SARS-CoV-2 genome early in the pandemic allowed to identify the spike (S) and the nucleocapsid (N) structural proteins as major targets of antibodies. [2]
> The surface glycoprotein S, which contains the receptor-binding domain (RBD), has a better known function in immunity and is the leading antigen candidate for vaccine development. N is smaller than S, lacks a glycosylation site, and is extensively used in leading serodiagnostics kits due to its abundant expression during infection and early antibody response but its immunological relevance is less established. [2]
> N forms ribonucleoprotein complexes during the virion assembly process by binding to the viral RNA genome and packing it into long helical structures. Its main function is to regulate viral RNA transcription during replication, promoting the synthesis of its own proteins while interfering with the metabolism, protein translation, and proliferation of the infected host cell. During the process of infection, N dissociates itself from the genome and is exposed to the host immune system, and its high immunogenicity has also prompted its exploration as vaccine target. [2]
> Interestingly, significant protein similarity between SARS-CoV-1, SARS-CoV-2, and other HCoV has been reported for N, including a highly conserved motif in the N-terminal (NT) half of the protein (FYYLGTGP) and relevant immunodominant epitope regions. [2]
> Evidence from multiple experimental studies showing that single RBD point mutations can lead to resistance to neutralizing convalescent plasma from multiple donors suggests that specific single mutants may be able to evade spike-targeting vaccinal immunity in many individuals and rapidly lead to spread of vaccine-resistant SARS-CoV-2. [3]
[1] Combining spike- and nucleocapsid-based vaccines improves distal control of SARS-CoV-2 https://www.cell.com/cell-reports/pdf/S2211-1247(21)01108-6....
[2] Immunogenicity and crossreactivity of antibodies to the nucleocapsid protein of SARS-CoV-2: utility and limitations in seroprevalence and immunity studies https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7879156/
[3] Risk of rapid evolutionary escape from biomedical interventions targeting SARS-CoV-2 spike protein https://pubmed.ncbi.nlm.nih.gov/33909660/
[4] Antibodies elicited by mRNA-1273 vaccination bind more broadly to the receptor binding domain than do those from SARS-CoV-2 infection https://pubmed.ncbi.nlm.nih.gov/34103407/
Such analytics are now beginning for software supply chains, thanks to a Presidential Executive Order. As warfare spreads from kinetic to cyber to psychological, we will need more tooling to keep pace with the analytical descendants of Cambridge Analytica. Social discourse can be mined in real time to identify high-leverage, transient gaps in narratives, to influence far-reaching real world policy.
Individual humans, parsing text for meaning, have an uphill journey.
TODO: create Streisand bot to extract downvoted comments from HN, differentiate between legitimate vs targeted downvotes, then republish to an audience for critical response on any valid points, i.e. use the infrastructure and human resources of would-be censors, to generate new signals.
Natural immunity knows only of COVID-19 Alpha. But it knows it well. All those nooks and crannies the other variants may not have, the natural antibodies can latch on to.
In addition, the naturally-infected and vaccine populations are not the same. For example, having a bad experience with a natural infection of Covid may cause people to not participate as much in virus-risky behavior. On the other hand, people who seek out vaccinations may have done so for business or personal reasons that make them more prone to expose themselves to the virus. It is also possible that (re)infection for the two groups are not monitored at the same rate. Without controlling for these factors (which your first link does not) you cannot make any judgement about which immunity is stronger from your cited data.
Lastly, your second link and your last link directly contradict each other — the second link claims "Recovered COVID patients don't benefit from vaccine" but your last link says "Individuals who were both previously infected with SARS-CoV-2 and given a single dose of the vaccine gained additional protection...." If you're going to cite sources, they should probably have a consistent message :).
While the author’s opinions on the necessity of vaccines do differ, they do agree on my main point: that empirically, natural immunity is indeed robust and tentatively even better than vaccine acquired immunity.
It looks like getting a vaccine helps boost immunity in all cases, whether you had a previous infection or if you had 2 doses and I would bet even after the booster, each additional shot will continue to provide some marginal benefit. So keep getting jabs, I guess, or you’re killing grandma.
I think at this point throwing in “you should vaccinate (regardless of your individual circumstance)” into your conclusion, even if it’s a complete non-sequitor, is a hedge against losing your job/funding/respect of your equally frightened peers. The COVID research equivalent of the “making the world a better place” SV trope.
In oder to acquire that immunity you have a 1% chance of dying, 2% chance of ending up in the hospital on a ventilator for a month, and a 20% chance of long haul covid.
To acquire immunity from a vaccine you have a 0.001% chance of an allergic reaction.
Which risk do you choose?
Which risk do you choose?
Either way, at a <= 1% risk of re-infection, I’m no longer a real liability to society so please just leave it for me to decide and don’t force me undergo any unnecessary medical procedures.
Does this mean inacticated vaccines work better against variants?
It it mutates to a different spike shape, it's very unlikely that it will keep that breakin power.
Or at least that is the assumption :)
We need a vaccine for delta. Unfortunately from MBA perspective it is much more profitable to push the current vaccines down the throat of the populace through forced mandates and hysteric propaganda instead of investing additional billions in the vaccine for the mutated virus.
2 shots don't work, thus the 3rd, "booster", then what? the 4th? It is pretty typical for the medical industrial complex to push to sell more and more product in response to low effect, like that opioid dosage increase.
That is simply not a statement you can make without supporting evidence.
Your immune systems binds to irrelevant targets all the time. People normally got measles once, but lots of people got it multiple times.
It is entirely possible that your immune system will bind to something that mutates rapidly and have worse response than the vaccine.
As someone who got the Covid19 in Original Flavor(tm), I still went and got the vaccine. I don't want to be one of the unlucky ones whose immune system didn't flag the spike protein for destruction.
Is there a good reference for the percentage of people who did?
https://www.israelnationalnews.com/News/News.aspx/309762
https://www.israelnationalnews.com/News/News.aspx/310963
https://www.medrxiv.org/content/10.1101/2021.08.24.21262415v...