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Related to that here is an interesting article that highlights that rebuttals might be effective in combating science deniers. https://www.nature.com/articles/d41586-021-02152-y Actual performance varies by audience, I am sure. Though we had good experience with folks who actually came individually to information sessions. Whereas if a bunch of connected folks appeared, they seemed to reinforce their beliefs. One thing that is also somewhat concerning is that quite a few folks were citing youtube videos as source. That makes it (by design, I would say) more difficult for folks to figure out where these folks get their "info" from.

Actually, the logic goes the other way around. If everyone is vaccinated, then it would effectively mean that the virus has already a reduced virulence and kills fewer people. As such there is less pressure to reduce virulence than in an entirely unvaccinated population where hosts are killed at a higher rate. However, one should take those arguments with some caution- these are only general trends. What actually happens in a population is obviously more complex and depending a combination of factors the there might be local optima for a certain combination of virulence and infectiousness. Or to put it differently, it is difficult to predict which trajectory a given virus is going to take at any given time. What we can say is that with a higher reservoir of folks carrying and producing the virus, we have a higher chance of continuously seeing new variants.

I would also like to posit that this may already be the case within the human population. Younger folks tend to have milder or no symptoms, while being able to transmit the disease (and young adults tend to be also on the more mobile side). One should therefore be careful to assume that lower virulence is inevitable or that it may happen on a quick timeline. There are also some other features (e.g. transmissibility prior to symptom development, as well as asymptomatic transmission) that could make it stay lethal for quite a while.

No, generally not. Competition against delta is a bit of a benchmark as it is currently the dominant variant in most areas. Something able to inch it out is a matter of concern. The only favourable outcome I can think of is if omicron turns out to be causing only mild symptoms. In that case you would want it to replace delta.

Going back to omicron, retrospective analyses indicate that omicron has been around in Europe as early as Nov 18 (i.e. before their identification): https://www.bbc.com/news/world-europe-59473131 While its potential to cause severe illness compared to delta is not known yet, the fact that it seems to be spreading (even in the background of delta) is of concern and worldwide efforts have increased to monitor their presence, both in retrospective (as the one linked above) or prospective surveillance. While the data could be biased due to ongoing efforts, preliminary data suggest that in SA omicron might be outcompeting delta. I have attached a figure showing the frequency of mutations in alpha, delta, and omicron in three of the genes (darker colour indicates higher frequency of a given mutation). Considering seemingly high transmissibility already indicates that the additional mutations in alpha do not hamper its effectiveness in infection. The important bit to figure out now are the health risks and then how well vaccinations are holding up.

That is very much expected. Preventing infection also prevents death from illness. Your original question was asking for evidence of efficacy of preventing infections, which you have received (repeatedly). And just to prevent a few rounds of arguing semantics I would like to point out some common usages in epi-data: "Infection" commonly refers to all positive tests, regarding of symptom status. Technically it refers specifically to the virus, but for communication with the broader population (e.g. via dashboards) it is sometimes conflated with COVID-19 infection (or similar). While this is technically inaccurate, it is simply a messaging strategy as the population was found to be more familiar with the name for the disease than for the virus. "Asymptomatic" is used if a positive test is found, but the patient does not present symptoms at time of testing. The issue is that folks are typically not tracked over time, so in some cases folks are actually pre-symptomatic (i.e. develop symptoms later in the infection process). Often the status of the patient at testing is not documented at all, so the frequency of asymptomatic cases is usually not well established. Moreover, in several areas testing strategies have switched to testing symptomatic cases only. As such in literature you will find a large range of estimates of symptomatic vs asymptomatic cases. Vaccine efficacy is the ability of the vaccine itself to improve disease outcome. This is generally done in controlled trials and historically this is based on disease presentation (i.e. showing symptoms of the disease). One of the reason is that in many diseases individuals do not spread the disease if they do not present symptoms (often indicating a low viral load). Due to the ability of pre-and asymptomatic spread of SARS-CoV-2 transmission is also monitored, but it is not as easy as tracking of symptoms. Vaccine effectiveness is basically a measure to look how efficacy translates into reality. This is done by capturing data during vaccine rollouts in an observational study. Here, it is important to segment the cohort according to the specific question. I.e. for example look at infected vs non-infected groups and check the vaccination status. Or conversely, segment for vaccination status and check for the variable of interest (e.g. infection rate or hospitalization).

@Sensei From this study: Levin et al. DOI: 10.1056/NEJMoa2114583 I have attached two graphs showing the 50% neutralization titer after Pfizer-BioNTech vaccination as well as an age-separated graph. It shows the decline within 6 months which can correlate to some degree with lower resistance to infections, especially with fast developing infections (such as delta), though as mentioned before, it is only one piece of the puzzle. The dots are the actually measured values, showing quite a range of individual responses.

The data provided by Swansont as well as the REACT-1 data from the UK both indicate lower infection rates in vaccinated folks. Indeed, but if you are wondering about the impact of vaccinations, you need to know the proportion of vaccinated folks in that graph. If for example the vaccine was 100% effective in preventing infections, the data could only contain unvaccinated folks and then the differential death rate would necessarily be caused by something else (e.g. age differences).

I don't think that this is even actually relevant. The original hypothesis was that vaccines are only (or mostly) effective protecting against developing symptoms. The poster did not spell it out and went on a tangent with an anecdote, but I took it as assuming that it is ineffective at preventing spread. That is also the only way the overinterpretation of the supplied graph in a later post makes sense. The focus is on transmission, so that is the element that needs to be traced in vaccinated and unvaccinated folks. The critical point that needs to be answered with regard to efficacy of the vaccine to curb spread is the difference in infection rate between these groups, which the poster continues to ignore (and which already has been posted). With regard to graphs I remember a few, but most are not neat comparative analyses, mostly individual patients with either condition (e.g. infection with SARS-CoV-2, one of the vaccinations etc.). I could pick out some if you'd like. However, it is important to note that antibodies are not telling the whole story when it comes to immunization. In all cases of infection and immunization the various antibody titres decline (but with vastly varying kinetics). However, an important of the adaptive immune system is the eventual formation of memory cells. Long-term protection is mediated by these T and B cells, as opposed to circulating antibodies. In the case of a new infection, these cells are necessary to produce new neutralizing antibodies to combat that disease. This is why even vaccinated folks with low circulating antibodies can mount effective responses, when exposed to the virus. Even in cases of successful infections (which practically means that the virus is able to replicate until they go over the sensitivity limit of established tests), the virus can be cleared out without resulting in associated damages and symptoms. Thus, declining antibody titres alone are insufficient to fully establish protective levels of a vaccine over time. That being said, a faster decline could indicate overall reduced responses, which see for example in the elderly. Recent infection data does indeed suggest that in these groups antibody titers decline faster and unfortunately also become more vulnerable to infections and sever outcomes (or to put it differently, the differential outcome between vaccinated and unvaccinated started to shrink in this group).

Please demonstrate how the infection rate among vaccinated is the same as among the unvaccinated based on the graph. What, in fact is the proportion of vaccinated folks in that graph. In case you forgot, you made two claims in the sentence. While mechanistically that is somewhat true (prevention of serious conditions is around 80%, depending on age and time of last jab, and reduction of infection of infection is about 50%), the provided data does not allow you to draw these conclusions. The minimum parameters that need to be established are how many among the infected are vaccinated or not (i.e. is there a bias between these groups). A second thing to establish is the age of infected in the last compared to the previous wave. Another, more technical issue is also how effective the testing program was in either time period (e.g. looking at test rate and test positivity). A simple alternative explanation (which is only partially true, but you would not know without looking at additional data) is that the third wave might have been driven by unvaccinated young folks, who have a reduced risk of dying.

Except of course that that data tells us nothing about the impact of vaccinations as the data is not separated between vaccinated and unvaccinated folks. The study above detailed that aspect by looking at differential infection rates and indicated the said difference (i.e. vaccinated folks have a third of the infection if using crude numbers, about 50% if adjusted for age and other factors). The sample size is meaningless if the necessary details are missing and therefore do not provide any information related to your claims.

IIRC, the cases in that report were based on cases before delta. The latter was found to have higher breakthrough rates. Not that it changes the argument, just nitpicking the actual numbers.

Read Elliot et al. Science 2021;eabl9551. It provides a comparison between vaccinated and unvaccinated populations.

Vaccinations reduce viral production and accelerate clearance and as such do mitigate infections to some degree. While breakthroughs still occur, risk of infection is about cut by half to a third, even with the delta variant. Risk of passing it on after transmission is also reduced a bit. But as delta seems to have a low infectious dose, the risk is still substantial. But especially in conjunction with masking and other public health measures we and others see less spread after a given outbreak after introduction of vaccines. That being said you are not wrong, with the disease getting endemic, new variants are bound to appear eventually.

Yeah, fair enough. My trust in the ability of humanity to pull together has been tested heavily. And I foresee a failing grade. Just like my class.

Or alternatively we forget all lessons learned within a few years and things will again go down the drain when feces hit the spinning thing again.

Also don't forget that while many richer countries have the capacities to vaccinate everyone as well as offering third shots, many parts of the world cannot afford even the first one. It is a general failing of all of us (as in humanity collectively).

As much of the world still remains unvaccinated, new strains continue to emerge. Recently a new variant of concern (B1.1.259, omicron). It carries 32 mutations compared to the original strain in the gene coding for the spike protein, raising worries that current vaccines might be less effective against this variant. https://www.who.int/news/item/26-11-2021-classification-of-omicron-(b.1.1.529)-sars-cov-2-variant-of-concern It is yet another reminder that the pandemic is far from being over.

I have enough of you already. I have not downvoted you once, despite the fact that you keep calling me names and accusing me of some innuendo that appears to be entirely in your head. I have done my best to lay out my arguments, but you keep going down your ideological arguments. You are not even reading what I am saying. Nowhere I said that there was a third sex. In contrast, I laid out a couple of classifications that would create two categories. The big issue being that they do not cover all individuals and hence are incomplete definitions. Whether we need to define new ones or not is entirely contextual, but it just a fundamental truth in science, we only create representations of reality, not reality itself. Whatever else you think is going in is independent of my arguments I have it with your projection. It is ironic that I am the one being accused of PC that or postmodernism that or downvoting folks, whereas it is others that keep doing that. It is just clear to me that apparently many folks claiming to be science minded are only so as long as the science agrees with their worldview or is sufficiently intuitive for them to grasp. Confronted with even minor variations there is a lot happening that makes folks lose their ability to reason. It seems to me that many using science to argue against certain dogmatic aspects only do so not because they believe in scientific discourse, but rather because they are just against the dogma (or religion). You freaking did not, you just know to little on the subject to know that you missed by a mile. That is the abstract of the paper as googling seems to be beyond you. Have you googled sex pilus, for example? Read just a couple of papers on conjugation, or on the evolution of sex. What the heck do you think is sex in the first place but a means of genetic recombination? You can also find a summary from both authors summarizing their efforts in Science, 1953 118:3059 pp.169-175. Assuming you are able to find it, check out the title. Yes and that is why we obviously do have crated names for mixtures. After all we are (mostly) trichromatic so we therefore only have categories three colours. I think I am done here.

Oh science is now done in links? How brilliant. If I knew that I could have finished my PhD in a weekend. And of course it shows that you are missing the mark entirely as you only provide links to asexual reproduction. My question was aimed to help you understand what sexual processes are and where the overlap within the broader aspect of genetic recombination is. How about you read some Lederberg and Tatum who were among the first to characterize recombination in bacteria. (Nature volume 158, page558 (1946)). From then onward they described sexual processes in bacteria, specifically E. coli.

Then explain to me the fundamental difference and how we biologists got it so wrong for decades.

No, they are doing asexual reproduction. But they actually do have sex (in the biological sense i.e. sexual recombination, not the common use... though sex pili are involved, so perhaps not that far off).

What are you trying to say? Anything beyond a certain distribution is not part of the population anymore? I.e. NBA players are abnormal and therefore not human? Because if you argue that they are human, then obviously it means that whatever you define as "abnormal" is actually part of the population (just at the edge) and therefore are part of any categories you make. If you say all tigers have for legs, a two-legged animal born to a tiger would, according to this definition, not be a tiger. Since that does not make a lot of sense, it simply means that this definition on its own is not sufficient (e.g. to categorize that animal, one would need information like the identity of parents or genetic analyses). Likewise if a definition of a human would include being a maximum of 1.90 cm then clearly the definition is wrong. You cannot make the definition correct by declaring that anything not fitting into it is simply an outlier. Trying to bend existing reality according to ones definitions is a rather dogmatic approach, but we have been over that a couple of times by now. Objective reality is what exists, even in the absence of an observer. But only an observer defines what is consider normal and what is not. And any deeper dive into things we consider normal typically just reveals that it is either just something that we experience frequently or that we otherwise assume to be common. And as such, it is not a property of the object itself. There is no "normal" gene or normal height. Just a range of variation that exists in nature that we can segment in order to investigate or even talk about it. After all, you would not claim that a photon is actually a particle and if it behaves like a wave, well that is just an exception. What you seem to think is that just because nature does not have clear delineation, everything must be the same. That is of course not so. If there is a continuum, there are quantitative differences. A 2.14 person is not the same as 2.13 or a 2.12 person, despite the fact that most would call all of them tall. That just shows that a category such as "tall" can be helpful for rough distinctions but clearly it is not a fixed property. For example, depending on population a 1.80 m person might already be considered tall. But moving that person into a group of NBA player that description would seem out of place. Thus, the moniker of "tall" is variable and is only useful in a particular context. It is not the same as specific property that is largely invariable (e.g. having a certain DNA sequence or using height as continuous, rather than a categorical variable). I suspect that it won't help much to clarify as there is clearly some ideological overlay here, but what one could (mostly) accurately state is that in humans (and mammals) reproduction involves two sexes. However, this definition uses the reproductive angle, which means that individuals who are e.g. sterile from birth would not fall under either category.

I think OP could have saved themselves a lot of grief if they had framed the question more narrow. E.g. does human reproduction only involve two sexes? Once we include things like general physiology and the finer points of genetics biology gets really messy. I also think because we are all biological entities, we tend to overestimate our understanding of how we function. Many folks use simple concepts and then think that this all there is to it. Feynman was a good example who summarily dismissed biology as a student but came around when he actually did tried his hands on biological problems.