Bikers descend on Sturgis rally with few signs of pandemic

Sure, but beware of a trade publication and an article written by the person with the highest vested interest. *IF* this test proves to be accurate, then it's an advancement. Also consider this, from your own link:

"Recent studies have indicated that total antibodies, including neutralizing antibodies, do indeed reduce in both asymptomatic and symptomatic Covid survivors. A UK team suggested last week that this seemingly transient immune response, which included a reduction in neutralizing antibodies, might well be linked to the severity of the initial illness."

Sorry, no time to explore your other links. I have to go.

 

Here’s better information.
https://www.nature.com/articles/s41587-020-0631-z

https://www.mayoclinic.org/tests-procedures/covid-19-antibody-testing/about/pac-20489696

Yes antibody titers always decrease after viral infections. The do with SARS1 as well but are still detectible 17 years after infection with this test. If that’s the case, and a second wave of antibodies is appearing per the study I linked the other day, memory B cells are almost certainly in play.

 

They are not almost certainly in play, they are in play; that's what happens with all viral infections, B cells are the antibody factories and jump into production when the T cells encounter the virus again and pass on the information.

But my point is, even your source admits to neutralizing antibodies also decreasing, so, what I'm saying is, if you say that people are not getting diagnosed with antibodies because they have faded but more people have had the virus so HIT has been reached, do remember that if someone's antibodies do fade to untraceable degree, it may very well mean that the person no longer counts towards the HIT because the person will still be a carrier, shedding the virus, if the person gets reinfected, until the T and B cells can jump in and restart the chain that leads to new antibodies being manufactured by the B cells.

Like I said, cell immunity alone can't count for the HIT because it is delayed. The person will still be infectious for a few days until the cell memory triggers the new antibody production. The person is likely to have an asymptomatic or mild bout of the illness, given that before it gets serious, the new antibodies will take care of it. But before this happens, the person will still be contagious therefore is not an "immune" person for the sake of the HIT.

I'm just saying, your argument works both ways. You say that because serology surveys miss a lot of previously infected people due to fading antibodies, it means that HIT has been reached given a cohort of previously infected people that is larger than the serology surveys can detect. I'm saying, not necessarily because those faded cases may no longer contribute to herd immunity. They still have personal cell immunity but it doesn't help the herd.

That's why I'm saying that the herd immunity approach is variable, uncertain, depends on a huge number of intervening factors, so it's best to just avoid the infection as much as possible until hopefully a safe and efficacious vaccine comes along.

 

I wonder if that is the same reason plasma treatment doesn't work unless given at the very beginning of the infection.

 

It's the richness of antibodies in the plasma (obviously works better the richer it is - which varies according to the convalescent patients the plasma is harvested from so indirectly if they have faded in the donor, the plasma won't be as rich).

But beyond that, it's not that they fade once they are in; it's the fact that exogenous antibodies are not constantly being produced so they don't work as well as the patient's own antibodies would have worked if the patient had them (once they attach, they have been used up so if you don't renew them, you don't get all the billions of viral copies), and also, if you allow viral replication to balloon out of control there is little that can be done subsequently with antibodies, given that then the virus starts triggering other issues such as a hyper-immune response (thus why dexamethasone is more helpful in later stages).

The effect-size of early use of convalescent plasma, while statistically significant in the study with 35,000 people, is not huge.

When given within three days of diagnosis the mortality at day 7 was 8.7%. When given on or after day 4, the mortality went up to 11.9%, so, it may have saved 3.2% (or a bit more, as the 30-day mortality improved by 5.1%), a far cry from the fake 35% that the FDA commissioner wrongly mentioned in the infamous announcement by Trump. Do also notice that unfortunately that study was not randomized and had no control group (they compared timing of administration and compared high and low richness of antibodies in the plasma but did not compare to treatment as usual with a placebo in lieu of the active plasma), so even this small effect is questionable (we can't even be sure that the effect seen is actually attributable to the treatment, or to some unknown intervening factor), which is why the scientific community criticized Trump and the FDA for their over-enthusiastic announcement.

As the authors of the study correctly stated, only an RCT will bring answers. Actually the very Mayo Clinic lamented that they got 35,000 people on this, and failed to include a control group, so they missed the definitive answers.

What people who are not medical scientists repeatedly don't understand is that regardless of how impressive these observational studies are, ONLY RCTs provide definitive answers to the question of the efficacy of a proposed treatment. Anything short of this is hypothesis-generating but is not designed to answer the question.

It's not that it's not evidence. It is. But it is evidence of a lesser quality than the one provided by an RCT.

Here is the study, if you are curious to explore more:

https://www.medrxiv.org/content/10.1101/2020.08.12.20169359v1.full.pdf

 

In initial viral infections there are only naive B cell that take several days to produce sufficient antibodies. Virus specific memory B cells do not require T cell activation when the virus is encountered the second time and can produce an antibody response in less than a day. If we knew previously memory B cells were in play there never would have been concern about immunity from infection in the first place. As I’ve said in the past, early on there was no evidence found of significant memory B cell formation. Now the evidence for it is emerging.

You are correct in that some memory B cells do require “help” from T cells, but only some do.

The new information is that even at very low levels, neutralizing antibodies can provide protection. If, and you say they definitely are, memory B cells are in play, new specific antibodies can be produced in a day even if titers of antibodies in the body are below detectable levels. These individuals would most certainly be counted in HIT calculations.

In the case of T cell memory only, you are correct. Memory B cells can mount a response in 24 hours or less to existence of antigen. T cell immunity takes 5-6 days to ramp up defenses.

Yes I agree with you if all we are dealing with is fade of non specific antibodies looked for by previous tests. But it appears we are not. We have neutralizing antibodies we couldn’t detect before. And we have evidence from SARS that even very low titers are protective. Also there is now evidence of second waves of antibodies after the undetectable period.

Also, I’m not versed enough yet in who spreads this thing and who doesn’t to say T cell immunity alone shouldn’t count towards herd immunity. If previous coronavirus infection cross reactivity immunity is responsible for less or virtually no contagiousness then we have a totally different scenario. Yes, you make a very good point and may be correct, but evidence continues to mount to the contrary.

Agreed. I will continue to reiterate my views and discussion of facts and hypothesis relating to herd immunity are not to be seen as advocation for natural herd immunity attempts.

 

If you use percent positive you use:
people with positive tests divided by tests. That leaves you with only percent positive so it is independent of the number of tests.

 

So, yes, that’s the primary study in circulation and the one used by many to “prove” there was no natural immunity to C19. Even though it’s one of the only studies until quite recently that accounts for neutralizing antibodies even after general titers are undetectable.

The other study you found in pre print but didn’t link to isn’t compelling but does show more fade of antibodies than the more legitimate one you linked. I’m not going to use the unlinked one as it looks hinky to me. Not very professional. I thought there were studies after this one that showed similar or worse fade but I can’t find anything at this point.

It’s clear I’ve made an error in using the 40% number on fade alone. Clearly it should be 20% total based on this study accounting for undetectable 13% symptomatics. I used a 40% asymptomatic rate in that calculation, is that acceptable to you?

40% without detectable antibodies times 40% symptomatic rate=0.12
13% without detectable antibodies times 60% symptomatic rate=0.078
0.12+0.078=0.198 times 100=19.8%

Then I’ll add in infected people missed by too early application of antibody tests before antibodies develop to keep my math in previous calculations honest as possible, allowing even with that addition, depending on actual rates of current infections when testing is done, my 40% may be a bit high. To account for that, I’ll add in previously not included (because I erroneously lumped everyone together) half life effect on the symptomatic cadre that leads to undetectable titers eventually, just longer than the 60 days for asymptomatics.

Thanks for checking my work. My goal is to be as accurate as possible.

 

Percent positives is dependent on tests. Your are using tests as the denominator of the fraction constituting percent positives. Take away tests and you have a mathematical operation that’s unsolvable because any number multiplied by zero is zero.

positive tests/total tests=% positive Solvable
positive tests/0=no solution

 

OK, I made a mistake here when I read your post too fast (I've been scrambling between breaks). You did say memory B cells in which case you are correct that they are not always involved. I meant that antibody production is always mediated by B cells. T cells don't make antibodies. Anyway, I'm guilty again of over-simplifying. So now let's look into the whole thing.

T cells come in various flavors. Helper T cells are the ones that pass information along and activate other immune defense cells. They secrete cytokines that help naive B cells differentiate into plasma cells (which are the ones that make antibodies). T Helper cells also activate Cytotoxic T cells, which kill infected human cells with the virus inside them. Then you will form Memory T Cells, which derive from activated Cytotoxic T cells and are longer lasting, leading to T cell memory. Incidentally, there are also Regulatory T cells which help modulate the immune system.

What about B cells? They can also have memory. First, we have naive B cells when the person is first infected. They get activated by T Helper cells and make antibodies, in what is called primary immune response (each of these B cells only produces antibodies against one antigen, and one class (IgM, IgG, etc.), although they can do class switching). Then B cells will enter the spleen and the lymph nodes and will undergo further transformation. They proliferate, and they mutate (it's called affinity maturation). Their surface receptors will either increase or decrease their affinity for survival signals. Most B cells will become plasma cells. Some will undergo very specific mutations and will persist (by getting survival signals from T cells), and these are called B memory cells, and they are antigen-specific and long lasting. The ones that undergo mutations that drift them away from the survival signals will die out through apoptosis.

These B memory cells, because they survive in lymph nodes and the spleen, which filter the lymphatic fluid and the blood, respectively, will not need T cell helpers to get triggered by the virus, as the virus is likely to get to them in those locations just by circulating. When this happens, they will differentiate into plasma cells again (effector B cells) and indeed jump into fast and robust production of antibodies, called a secondary immune response.

How do B memory cells get formed? Unknown, to a degree. There are hypothesis of random creation, others say it's cytokine mediated, others say that paradoxically the B cells with the least affinity for the antigen will become B memory cells while the ones with the most affinity will become plasma cells.

The bottom line is, it's variable. A viral infection doesn't necessarily produce B memory cells. Or if it does, they may not survive. When they do survive and are distributed through lymph nodes that watch entry points, yes, they can react fast. But it's not a given that they are there, alive and ready.

If they are not there but memory T cells are, then it will take longer to mount a defense. A few days, like you said.

 

Excellent. Thanks for taking the time to write a very informative post.

On the subject of memory B cell creation I heard a really good podcast on them a while back, as well as the most current information on what we used to call clonal selection theory. I’ll try and find it again but it was a random thing I came across not something I subscribe to so no promises.

The immune system is amazing, isn’t it?

 

Tests are in the numerator and denominator.
So you divide by tests leaving 1 times positive tests divided by 1 times all tests. This leaves % positive.
But lets just leave it for now.

 

You're welcome.

Yes, clonal selection is the weirdest thing, resulting in B cells that have antigen-specific surface receptors BEFORE they ever encounter the antigen for the first time! It's Mother Nature's preparedness equivalent of that White House Biodefense team that Trump dismantled, LOL.

It sure is... when it doesn't turn against the person's own body... Then you get lupus, rheumatoid arthritis, multiple sclerosis, cytokine storms... Or else, when these cells don't proliferate into leukemia.

 

So let’s see... most medical experts put herd immunity to Covid at 60-70%.

Poster above puts it at 40% and then when it’s pointed out that neither we nor Sweden nor NY are anywhere near that... he finds a reason to claim it’s 30% and then ... 20%!

Sure. Why not just claim we’re already all immune! Oh wait. 50,000 infections and 1,000 deaths per day kinda makes that look ridiculous

 

Have you sued Pelosi for attempted homicide yet?

*Reminder you claimed i was trying to kill you by getting a hair cut*

 

More strawman argument. I’ve never claimed herd immunity is 40 then 30 then 20. Never. I’ve clearly stated I’m not qualified to state exactly what the HIT is.

You can’t tell the difference between cases missed by waning antibodies and herd immunity thresholds?

Try and be like @ronv and deal in facts. Then it’s interesting and informative for everyone.

 

I’d go back and quote it but it it would be a waste of time.

Go away

 

Life must go on, with or without the approval of COVID hysterics.

And as long as liberals can gather by the thousands to protest, riot, and loot across America, I see no reason why normal Americans cannot gather peacefully to enjoy the short amount of time they have on this earth.

If you're scared, then feel free to stay in your house forever. Or just accept that life comes with risks. But you don't get to make that choice for others. And that is something COVID alarmists will have to accept at some point.

 

Submitting to hysteria and pseudoscience is actually quite harmful.

 

Thanks for confirmation you don’t know what herd immunity is. You are responding to my posts of your own free will so if it’s a waste of time it was your choice.

Where would you like me to go? Since this is a forum and the mods haven’t any reason to make me go away I’ll likely stay and respond to your post to me and about me. The way to avoid me responding is to not quote me or talk smack about me without having the fortitude to quote me directly.

Or you can really show everyone how open minded and intellectual you are by putting me on ignore. I don’t use the ignore option because I learn from everyone and that’s why I’m here—to learn and expand my understanding of people who believe differently and have different life experiences than I. You continue to teach me much about the relationships between progressivism, authoritarianism, and tolerance/open mindedness. So no, I’m not going away. I like it here.

 

I’ll stick with the Mayo Clinic which puts herd immunity at between 60 and 70%.
But that’s me

 

Then stop with the pseudoscience

 

Well, you are wrong. And the Mayo Clinic was just employing a simplification for the consumption of lay people. Herd Immunity Threshold is variable. There is no such thing as "The SARS-CoV-2 has a HIT of 60 to 70%." It's not written in stone. It depends on a number of factors for different populations and different subsets of a population.

This is not pseudoscience. This is... science. The HIT for a population that is equally susceptible to the virus, is calculated as 1 minus 1/R0 multiplied by 100. So for an R0 of 2.0, 1 minus one half is one half, multiplied by 100, we get 50% of people needing to be infected for the HIT. For an R0 of 4, it's 1 minus 0.25 = 0.75 times 100, 75% of the people need to be infected for the HIT.

But R naught, the virus reproduction number (how many people get infected by one carrier), is variable according to the environment, the population density, population behavior, how many people are susceptible versus how many are naturally resistant to the virus, etc. So, the HIT is also variable.

Here, read this (this is science; published in the journal Immunity and reproduced by this agregator provided by the NIH (National Institutes of Health), and authored by scholars from the University of Chicago:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7236739/

"Assuming an R0 estimate of 3 for SARS-CoV-2, the herd immunity threshold is approximately 67%. This means that the incidence of infection will start to decline once the proportion of individuals with acquired immunity to SARS-CoV-2 in the population exceeds 0.67. As discussed above, this model relies on simplifying assumptions, such as homogeneous population mixing and uniform sterilizing immunity in recovered individuals across demographic groups, which are unlikely to hold true."

In employing the simplified model for the sake of the argument (they are talking here about the price to pay for the herd immunity approach (I agree with them), the authors add the following:

"We do not consider numerous complexities of viral spread and infectivity, including variation in R0 across time and populations, heterogeneity in the attack and contact rates across demographic groups, and inter-individual variation in communicability and disease severity, although these aspects are essential to understand the full picture of SARS-CoV-2 community spread. While these epidemiological factors have important implications in the context of herd immunity, currently, they are difficult to estimate given the limited data available.

Differences in population density, cultural behaviors, population age structure, underlying comorbidity rates, and contact rates across groups influence transmission dynamics within communities, so the assumption of a uniform R0 across populations is not realistic."

In summary, given that a population is heterogeneous, and not everybody is susceptible, the true HIT is often smaller than it would otherwise be if the population were homogeneous and everybody was equally susceptible.

Does the Mayo Clinic know that? Of course it does! When they publish a scientific paper, they take it into account. But when they place an informational page on their website for the consumption of the lay people, they will not get to this kind of detail, and will employ the simplified model. Do you think that the lay public consulting their pages for general medical advice, will be sophisticated enough for a full blown discussion of Herd Immunity Threshold? No.

This paper above is an interesting and accessible read, that explains the issues in clear terms.

Now, look at this for a more in-depth treatment:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7331793/

This is a model that DOES take into account the heterogeneity of the population. See what they conclude, which is VERY MUCH aligned with what 557 was saying:

"We estimate that if R 0 = 2.5 in an age-structured community with mixing rates fitted to social activity, then the disease-induced herd immunity level can be ~43%, which is substantially less than the classical herd immunity level of 60% obtained through homogeneous immunization of the population. Our estimates should be interpreted as an illustration of how population heterogeneity affects herd immunity rather than as an exact value or even a best estimate."

Again, the above is not pseudoscience. It is... science. Published in the prestigious and aptly named journal... Science. The authors are scholars from Stockholm University and Nottingham University.

OK, so, come again? Is this pseudoscience???

-----------

In this, @577 is correct and you are not.

Your accusations of "pseudoscience" and your attitude of saying "who the f.... are you?" and "go away" are frankly, uncalled for. I'm no moderator so it's not up to me to tell you how to behave, according to the rules of this forum, but as a member here who values civility and a good discussion, I would like to ask you (nicely) to moderate your tone and to consider what 557 is saying with more civility. It's always for the best when we can exchange ideas in a civil way, without personal attacks. Cheers.

 

Ok fine. So what is the "correct" number for herd immunity?

It "sorta" said 43% above but then it hemmed and hawed.

Give us a number

And oh by the way...neither Sweden nor Stockholm nor NY nor the US is anywhere NEAR 43%

 

I'm not sure anyone is arguing that mitigation cannot change R0. I mean that's the only way we have right now of stopping it.
I think the argument comes when someone says the basic number is different than the open loop number.
I love this demo.