Reposted from Dr. Judith Curry’s Climate Etc.
Posted on July 27, 2020 by niclewis
By Nic Lewis
I showed in my May 10th article Why herd immunity to COVID-19 is reached much earlier than thought that inhomogeneity within a population in the susceptibility and in the social-connectivity related infectivity of individuals would reduce, in my view probably very substantially, the herd immunity threshold (HIT), beyond which an epidemic goes into retreat. I opined, based on my modelling, that the HIT probably lay somewhere between 7% and 24%, and that evidence from Stockholm County suggested it was around 17% there, and had been reached. Mounting evidence supports my reasoning.[1]
I particularly want to highlight an important paper published on July 24th “Herd immunity thresholds estimated from unfolding epidemics” (Aguas et al.).[2] The author team is much the same as that of the earlier theoretical paper (Gomes et al.[3]) that prompted my May 10th article.
Aguas et al. used a SEIR compartmental epidemic model modified to allow for inhomogeneity, similar to the model I used although they also considered further variants. They fitted their models to scaled daily new cases data from four European countries for which disaggregated regional case data was also readily available. In all cases they found a better fit from their models incorporating heterogeneity to the standard homogeneous assumption SEIR model. They found that:
Homogeneous models systematically fail to fit the maintenance of low numbers of cases after the relaxation of social distancing measures in many countries and regions.
Aguas et al. estimate the HIT at between 6% and 21% for the countries in their analysis – very much in line with the range I suggested in May. They also found that their HIT estimates were robust to various changes in their model specification. By contrast, if the population were homogeneous or were vaccinated randomly, the estimated HIT would have been around 65% –80%, in line with the classical formula, {1 – 1/R0}, where R0 is the epidemic’s basic reproduction number.[4]
Aguas et al.’s Figure 3, reproduced below, shows how the HIT reduces with increasing variation either in susceptibility (given exposure) or in connectivity, which affects both an individual’s susceptibility (via altering exposure to infection) and infectivity. The coloured dots and vertical lines show the inferred position of each of the four countries they analysed in each of these (separately modelled) cases.
Aguas et al. Fig. 3 Herd immunity threshold with gamma-distributed susceptibility (top) or connectivity related exposure to infection (bottom). Curves generated with the SEIR model (Equation 1-4) assuming values of R0 estimated for the study countries assuming gamma-distributed: susceptibility [top]; connectivity (and hence exposure to infection) [bottom]. Herd immunity thresholds (solid curves) are calculated according to the formula 1 − (1/R0)1/(1 + CV^2) for heterogeneous susceptibility and 1 − (1/R0)1/(1 + 2 CV^2) for heterogeneous connectivity. Final sizes of the corresponding unmitigated epidemics are also shown (dashed).
As Aguas et al. say in their Abstract:
These findings have profound consequences for the governance of the current pandemic given that some populations may be close to achieving herd immunity despite being under more or less strict social distancing measures.
The underlying reason for the classical formula being inapplicable is, as they say:
More susceptible and more connected individuals have a higher propensity to be infected and thus are likely to become immune earlier. Due to this selective immunization by natural infection, heterogeneous populations require less infections to cross their herd immunity threshold than suggested by models that do not fully account for variation.
The Imperial College COVID-19 model (Ferguson et al.[5]) is a prime example of one that does not adequately account for variation in individual susceptibility and connectivity.
Aguas et al. point out that consideration of heterogeneity in the transmission of respiratory infections has traditionally focused on variation in exposure summarized into age-structured contact matrices. They showed that, besides this approach typically ignoring differences in susceptibility given virus exposure, the aggregation of individuals into age groups leads to much lower variability than that they found from fitting the data. The resulting models appeared to differ only moderately from homogeneous approximations.
A key reason for variability in susceptibility to COVID-19 given exposure to the SARS-CoV-2 virus causing is that the immune systems of a substantial proportion (35% to 80%) of unexposed individuals have T-cells, circulating antibodies or other components that are cross-reactive to SARS-CoV-2 and can be expected to provide substantial resistance to it.[6] [7] [8] [9] Such components likely arise from past exposure to common cold or other coronaviruses, or to influenza.[10] Not being specific to SARS-CoV-2, and typically not being antibodies, such immune system components are not normally detected in seroprevalence or other tests for immunity to SARS-CoV-2.
I will end with a follow up to my June 28th article focusing on Sweden. In it, I concluded that it was likely the HIT had been surpassed in the three largest Swedish regions, and in the country as a whole, by the end of April notwithstanding that COVID-19-specific antibodies had only been detected in 6.3% of the population.[11] I also projected, based on their declining trend, that total COVID-19 deaths would likely only be about 6,400. Subsequent developments support those conclusions. Swedish COVID-19 deaths have continued to decline, notwithstanding a return to more travel and less social distancing, and are now down to 10 to 15 a day. According to the latest Financial Times analysis,[12] excess mortality in Sweden over 2020 to date was 5,500, or 24%. That is only about half the excess mortality percentage for the UK (45%), Italy (44%) and Spain (56%), and is also lower than for France (31%), the Netherlands (27%) and Switzerland (26%), despite Sweden not having imposed a lockdown or shut primary schools. Moreover, total mortality in Sweden over the last 24 months is now lower than over the previous 24 months, despite an upward trend in the old age population.
Nicholas Lewis 27 July 2020
[1] One example, further supporting my superspreader-based evidence of variability in social connectivity, is Miller et al: Full genome viral sequences inform patterns of SARS-CoV-2 spread into and within Israel medRxiv 22 May 2020 https://doi.org/10.1101/2020.05.21.20104521 This paper shows that 1-10% of infected individuals caused 80% of infections. That points to variability in social connectivity related susceptibility and infectivity quite likely being higher than I modelled .
[2] Aguas, R. and co-authors: Herd immunity thresholds estimated from unfolding epidemics” medRxiv 24 July 2020 https://doi.org/10.1101/2020.07.23.20160762
[3] Gomes, M. G. M., et al.: Individual variation in susceptibility or exposure to SARS-CoV-2 lowers the herd immunity threshold. medRxiv 2 May 2020. https://www.medrxiv.org/content/10.1101/2020.04.27.20081893v1
[4] The basic reproduction number of an epidemic, R0, measures how many people, on average, each infected individual infects at the start of the epidemic. If R0 exceeds one, the epidemic will grow, exponentially at first. But, assuming recovered individuals are immune, the pool of susceptible individuals shrinks over time and the current reproduction number falls. The proportion of the population that have been infected at the point where the current reproduction number falls to one is the ‘herd immunity threshold’ (HIT). Beyond that point the epidemic is under control, and shrinks.
[5] Neil M Ferguson et al.: Impact of non-pharmaceutical interventions (NPIs) to reduce COVID-19 mortality and healthcare demand. Imperial College COVID-19 Response Team Report 9, 16 March 2020, https://spiral.imperial.ac.uk:8443/handle/10044/1/77482
[6] Grifoni, A.et al.: Targets of T cell responses to SARS-CoV-2 coronavirus in humans with COVID-19 disease and unexposed individuals. Cell 11420, 2020 https://doi.org/10.1016/j.cell.2020.05.015
[7] Braun, J., et al.: Presence of SARS-CoV-2 reactive T cells in COVID-19 patients and healthy donors. medRxiv 22 April 2020 https://www.medrxiv.org/content/10.1101/2020.04.17.20061440v1.
[8] Le Bert, N. et al.: Different pattern of pre-existing SARS-COV-2 specific T cell immunity in SARS-recovered and uninfected individuals. bioRxiv 27 May 2020. https://doi.org/10.1101/2020.05.26.115832
[9] Nelde, A. et al.: SARS-CoV-2 T-cell epitopes define heterologous and COVID-19-induced T-cell recognition. ResearchSquare 16 June 2020. https://www.researchsquare.com/article/rs-35331/v1
[10] Lee, C., Koohy, H., et al.: CD8+ T cell cross-reactivity against SARS-CoV-2 conferred by other coronavirus strains and influenza virus. bioRxiv 20 May 2020. https://doi.org/10.1101/2020.05.20.107292.
[11] Such seroprevalence is likely to significantly understate the proportion of the population who have had COVID-19, since asymptomatic or mild disease often results in undetectably low antibody levels (Long, Q. X. et al.: Clinical and immunological assessment of asymptomatic SARS-CoV-2 infections. Nat Med. 18 June 2020 https://doi.org/10.1038/s41591-020-0965-6 . Such patients will nevertheless be immune to reinfection (Sekine, K. et al.: Robust T cell immunity in convalescent individuals with asymptomatic or mild COVID-19. bioRxiv 29 June 2020 https://doi.org/10.1101/2020.06.29.174888).965-6
[12] https://www.ft.com/content/a26fbf7e-48f8-11ea-aeb3-955839e06441. Data updated to 13 July
Originally posted here, where a pdf copy is also available
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Could anyone please post a complete list of supplements that are suggested to help stay off Covid19?
Here is what I know:
Vitamin C 1000mg or more per day
Vitamin D 125 mcg (5000 IU) per day
Zinc. 25mg per day (is 50 mg’s okay?)
Quercetin 1000 mg per day.
What else? Thank you in advance
If you have lung issues, take 1gram or research to find dos that works for you, of NAC.
It’s important to be balance, so I highly recommend veggies and fruits, so I take a juiced veggy and juiced fruit power too. As such my K levels are very high, based on recent blood test.
If you do not get sun without sunscreen and live in high lattitudes, I would up the D to 6000 which is what I have been taken for several years. I get sun and my level is 62ng per ml, but everyone is different and you can go online to get a blood work test for various elements.
If you are worried about flu and corona viruses (RNA) do not be deficient in Zn… the quercetin will help get it into your cells, esp lung. So will EGCG.
Selenium is apparently required to release zinc from its serum transport molecules.
Vitamin K is required when taking vitamin D to make sure calcium gets deposited in the right places.
NAC (N-acetylcysteine) mentioned above increases glutathione levels, which are the lungs’ primary antioxidant. Nebulized NAC is standard treatment for respiratory illnesses in ICUs.
Liposomal vitamin C is better absorbed and produces higher serum levels than ascorbic acid or ascorbate, but apparently taking both together increases it more than either one alone. Ascorbate is easier on the digestive tract making it easier to consume more.
50 mg zinc is probably OK. Upper daily limit is 45mg; most recommendations I’ve seen call for 35 mg.
EGCG is another zinc ionophore, like quercetin, and better absorbed. Most forms of quercetin sold are not very absorbable.
I’d recommend magnesium and vitamin E, but probably taking a multivitamin for these things is sufficient.
Thank you icicil & Mario…. a lot!
You’re welcome. William Astley seems to be well versed in this subject of nutrients.
I can tell you since NAC and upping Quercetin, my sinuses and lungs have never been better. I am for the first time in my adult life, I no longer need 12 hour nasal spray, taken 4 times a day.
Vitamin D helps to fix calcium in your body, which is great for your bones. However, you do not want calcification elsewhere such as your blood vessels. So, if you’re taking vitamin D supplement then vitamin K2 helps to prevent arterial calcification.
I was concerned about that so took a blood test for K and others. I was off the charts and take no “K” supplements. It did not break down K1 or 2. I think it’s from my diet… and at 2,500 pg/ml. D was 62 ng/ml.
I read a study that showed areas rich in selenium intake had less mortality
“ … circulating antibodies or other components that are cross-reactive to SARS-CoV-2 and can be expected to provide substantial resistance to it. Such components likely arise from past exposure to common cold or other coronaviruses, or to influenza.”
Do these antibodies arise from the “standard” anti-flu vaccine? In other words, to take the anti-flu shot this autumn will help?
A Dept of Defense study was done not long ago that found people who received the flu jab had a 36% increased chance of coronavirus infection due to something called viral interference. If you can’t find the study let me know.
Oral hygiene and COVID-19
This study explored the complications of COVID-19 seen among those with poor oral health and periodontal disease. The oral microbiome or the microbial flora of the mouth was explored and its connection with the COVID-19 outcome was analyzed. The authors wrote, “We explore the connection between high bacterial load in the mouth and post-viral complications, and how improving oral health may reduce the risk of complications from COVID-19.”
The authors of the study wrote that during lung infection, there is a risk of aspirating the oral secretions into the lungs, which could cause infection. Some of the bacteria present in the mouth that could cause such infections include “Porphyromonas gingivalis, Fusobacterium nucleatum, Prevotella intermedia,” they wrote. They explained that periodontitis or infection of the gums is one of the most prevalent causes of harmful bacteria in the mouth. These bacteria lead to the formation of cytokines such as Interleukin 1 (IL1) and Tumor necrosis factor (TNF), which can be detected in the saliva and can reach the lungs leading to infection within them. Thus, the researchers wrote, “inadequate oral hygiene can increase the risk of inter-bacterial exchanges between the lungs and the mouth, increasing the risk of respiratory infections and potentially post-viral bacterial complications.”
Results of the study
The team wrote, “Good oral hygiene has been recognized as a means to prevent airway infections in patients, especially in those over the age of 70”. Those with periodontal disease are at a 25 percent raised risk of heart disease, thrice the risk of getting diabetes, and 20 percent raised risk of getting high blood pressure, the researchers wrote. These are all risk factors of severe COVID-19 they wrote.
https://www.news-medical.net/news/20200630/Oral-hygiene-and-severity-of-COVID-19-e28093-the-connection.aspx
How to create a pandemic
Imagine that you want to start a pandemic, what would you need.
1. Find some vague criteria for what constitutes the symptoms you want people to look for. Anything subjective that a lot of people can identify with is ideal. Let us take memory problems and/or confusion + a few common ones from the Covid list. Tiredness, aches nd pains are common and subjective enough. (For covid 19 the symptoms are: fever
dry cough
tiredness
Less common symptoms:
aches and pains
sore throat
diarrhoea
conjunctivitis
headache
loss of taste or smell
a rash on skin, or discolouration of fingers or toes)
It wold be a good idea to take something that was very common in old people so that we can use death from old age as proof of the lethality of the new virus.
2. Then we would need something biological to test. Any RNA sequence would do as long as it is not present in the whole population. If it were, someone might claim herd immunity very quickly. Actually it could be a RNA sequence that does not really exist in humans but something that could exist as contamination in labs, e.g. in dust or water. That would be enough for a RT qPCR test to pick up as a false positive. Many RT PCRs have false positive rates of 3-5 % and that would be plenty to create a scare. (When it comes to Covid, the sales positive rate is impossible to know for sure, since we don’t have a gold standard to check against, but for many other similar tests, the average sales positive rate is over 3%. And different labs are testing for different sequences. We can count on over stressed labs to be more prone to contamination than labs taking past in research knowing they will be checked for accuracy, the ones that gave over 3% false positives. Maybe the error rate for the average stressed lab is as high as 8%. BMJ counts 5% as a reasonable estimate. With 8% we would have all positive tests in the US explained by false positives)
3. Then we are all set to go. We just have to claim that we have discovered a new cluster of symptoms and that is related to a new RNA sequence. It starts with memory loss, and confusion. In other words this is a neurotoxic virus, and it leads to death in all the ways old people can die, by strokes, heart attacks, pneumonia, kidney failure, sepsis, organ failure, dehydration. It sortant matter of the patient was close to deaths door anyway because of existing problems. We can always claim that without our new virus, they would not have died. Who cold counter that?( just like Covid; People die from all kinds of disorders act they already had before the god the cover test)
4. By some miracle we have already discovered exactly the virus that is responsible among the millions of different viruses that exist in any cubic centimeter of air. So we already have a RT PCR test read to go. This makes us look like very competent researchers. O course we have bought stock in the major testing labs ahead of time. We’ve bought stocks in the biggest vaccine manufacturers also of course. That will be the biggest money maler finally, hopefully for years since it will be difficult to get antibodies to something that doesn’t really exist. We can see to that the ting to test for will at least be present in dirty labs so that we can get enough false positives)
5. So now we just have to spread the news that a new deadly pandemic is spreading all over the world, and every country has to start testing. We can count on the 5% hypochondriacs in the general population to come forth to be tested first. It will always take some time for each country to get started and ramp up their testing, so the graphs are guaranteed to look exponential in the beginning.
6. All you need now is for people to bring their old and confused elderly in for testing, ansd with 5% false positives, we will soon have most hospital beds filled with olds sick confused patients. We can count on doctors to treat them aggressively. Most of these old people will be on a coctail of drugs already so adding a few more drugs as “heroic treatment” will be sure to push them over the edge. Many will have pneumonia from the seasonal flu, so we can just prolongue this by putting them in ventilators. Then they will die a month later and we can say it wasn’t the flu since the flu season should have stopped a month earlier.
7. The graphs of numbers tested positive will be exponential in the beginning, but flatten off as the testers reach their max level. After some time the lab technicians will be exhausted and tend to become sloppy, the pressure for testing will be relentless and the labs will get dirtier and dirtier, and we will get higher and higher false positive rates. Usually the media will be satisfied with reporting just the number of positive teste, but in case anybody should think of checking proportion of positive tests compare to total number of tests, they would get hisgher number each week because of overworked error prone labs. Eventually, society will run out of hypochondriacs who will come for tests voluntarily, and many will have understood that should they test positive, they will be put together with really sick people unprotected, since they all have the same virus…So the curves will flatten and start going down.
8. If you want to destroy the economy during the pandemic, you will get some programmer to make a prediction of millions of deaths ( actually 70 million die every year anyway, so that is not really difficult) if we don’t lock down society. We just have to scare them to lock downright before the curve flattens (when we are running out of the 5% hypochondriacs) and all the politicians will think they saved their country.
9. Just for fun, to see how strangely we could make gullible people act, we could invent different strategies for protection. Social distancing can look really funny in a supermarket, and all the original ways of saluting is interesting , leg touching elbow touching (even if we cough in our elbows now). We could make a lot of money on masks, gloves and sanitisers too.
10. In order to make money on vaccines, we will start testing antibodies. Here the false positive error rate is even greater, so we may easily get 10% with antibodies just from false positives. But on retest, we will statistically get only one percent testing positive if we test the same people. That means that we will need may boosters of the vaccine. In order to maximise the profit, we may put something in the vaccine that make people sick and then we can cure them with a very expensive drug produced by a company we have already invested in. But to be sure maximum number of countries will pay almost any price for the vaccine, we have to wait until they re really desperate.
11. We can always count on several waves of the virus since the common flu and colds will come every year and kill hundreds of thousands like , and 3-10% of them will test false positive for our virus every time. So we have a fantastic money maker for years: Expensive tests, expensive drugs, and expensive vaccines for 7 billion people every year.
12. We can count on doctors being sure that they are right in all they do. They will counter each other in every turn, and since there is no real new disease to cure, the research will run into endless blind alleys. This will prime all doctors for accepting a vaccine. We just have to make sure there is no cheap effective drug for common ailments that can kill people. We can always pay some doctors to make up some numbers and pay journals to publish (like the fake negative HydroxyChloroquin research).
How does the PCR find something if there is nothing?
Your odds of dying from Covid19:
https://www.bitchute.com/video/f9IyNp8OAqKU/
And that’s just based on a pre-existing immunity from the “novel” coronavirus. Boost the immune system with D,K,C, and zinc, and that makes the odds of dying even less. Exercise, eat as healthy as possible, keep your weight down, and you reduce it to about the chance of being struck by lightning.
“Herd immunity” is important only to the extent that the underlying pathogen mutates very slowly, or not at all.
Just ask yourself why, after more than 100 years of the seasonal flu (at one time called the “Spanish flu”) circulating around the world in epidemic-pandemic fashion, humans have not yet developed her immunity to this terrible virus.
I would not at all be surprised if COVID-19 does not have similar capability to mutate faster than herd immunity can be established around the world.
As one example: in an article titled “Mutated COVID-19 Viral Strain in U.S. and Europe 10 Times More Contagious than Original Strain” reference is made to the original COVID-19 strain from China, dubbed D614, while the more deadly one found in the UK, Italy and North America in May is dubbed G614.
source — https://www.biospace.com/article/mutated-covid-19-viral-strain-in-us-and-europe-much-more-contagious/
As recent as May 7, 2020, medical science was proclaiming that there was only one strain of SARS-CoV-2, which causes COVID-19 (see https://www.virology.ws/2020/05/07/there-is-one-and-only-one-strain-of-sars-cov-2/ ), but this has since changed. What do they know to any degree of accuracy?
Serious questions.
Immunity, or not, that is the question.
What sort of HIT do we get when no-one develops effective immunity and can be re-infected every few months or so?
If each time you are infected you get some permanent tissue damage (lungs, blood vessels, neuro cells, etc) how does no or limited immunity impact these models?
Finally, Sweden seems like some sort of example, however don’t forget that while lock down was not imposed, some significant portion of the population voluntarily locked down and that may be what you are seeing, plus of course the normal flow of people in and out of the country stopped as well.
Sweden seems to be well on the way to recovery:
https://www.bloomberg.com/news/articles/2020-07-28/sweden-unveils-promising-covid-19-data-as-new-cases-plunge
“With numbers diminishing very quickly in Sweden, we see no point in wearing a face mask in Sweden, not even on public transport,” he said.
He is for some unknown reason fanatically opposed to face masks.
And new cases aren’t “plunging”, they are decreasing slowly (250 new cases today). As would be expected since an exponential decrease goes slower and slower as time passes.
Nic,
I am definitively unsure of what is meant by HIT, or perhaps more precisely by what your computations are measuring.
I mean, that you compute what may be the % of people having been infected by the virus at the time the pandemic becomes very mild.
But why conclude that it may be due to a herd immunity effect ? It may be for any other reason.
Of course, in Europe, for climate/seasonal or any other reasons, the pandemic is slowing much (even if with higher testing, much more social contacts in the cities following lockdown end, and much more transportations, there are still relatively high numbers of new infected people registered) , but in other countries like the US, we see very different patterns between northern and southern states. And we see the development in Latin America.
Would be interesting to see whether your HIT computations would accommodate Southern US states and Latin American countries.
Daniel