T cell cross-reactivity and the Herd immunity threshold

Reposted from Dr. Judith Curry’s Climate Etc.

Posted on October 14, 2020 by niclewis | 5 Comments

By Nic Lewis

An interesting new paper by Marc Lipsitch and co-authors, “Cross-reactive memory T cells and herd immunity to SARS-CoV-2”, has recently been published.[1] It discusses immunological and epidemiological aspects and implications of pre-existing cross-reactive adaptive immune system memory arising from previous exposure to circulating common cold coronaviruses. They argue that key potential impacts of cross- reactive T cell memory are already incorporated into epidemiological models based on data of transmission dynamics, particularly with regard to their implications for herd immunity. I believe that they are mistaken on the herd immunity point, as I will show in this article.

The first point to make is that cross-reactive T cells were never thought to be the main cause of the herd immunity threshold (HIT)[2] being lower for COVID-19 than the oft-quoted {1 – 1/R0} level, which generally applies for vaccination. Heterogeneity in social connectivity (contact rates) is typically estimated to lower the HIT much more than heterogeneity in biological susceptibility to the causative SARS-CoV-2 virus.[3]

Possible effects of cross-reactive T cells on infection progression

Lipsitch and co-authors note that recent reports have shown that SARS- CoV-2 cross-reactive memory T cells, very largely CD4+ T-cells arising from previous exposure to circulating common cold coronaviruses, are detectable in ~28–50% of individuals not exposed to SARS- CoV-2. They say that only tissue-resident memory T cells (TRM cells) can mount a fast response, with recirculating TCM and TEM T cells taking several days to start fighting an infection. They point out that CD4+ T-cells generally limit disease severity, reduce the viral burden and/or limit the duration of the disease rather than preventing an initial infection.

While I do not intend to challenge any of the foregoing points here, it should be noted that they treat an ‘infection’ as including a case where so few cells have been infected that any (RT-)PCR test for the virus would be negative.

The paper states that CD4+ T cell-mediated memory responses to a virus may involve some or all of CD4TFH cell types (required for B cell help and thus almost all neutralizing antibody responses), TH1 and CTL cell types (with direct antiviral activities in infected tissues), and that the CD4+ T cells involved may be TRM cells, or slower to respond recirculating TCM/TEM cells.

The authors go on to propose four immunological scenarios for the impact of cross-reactive CD4+ memory T cells on COVID-19 severity and viral transmission. The four model scenarios they put forward are:

  1. Reduction of lung burden: CD4T cells reduce COVID-19 symptoms and lung viral load but have minimal impact on upper respiratory tract (URT) viral load.
  2. TFH cell-accelerated antibodies: CD4TFH cells trigger a faster and better antibody response, resulting in accelerated control of virus in the URT and lungs.
  3. TRM cells in the URT: CD4+ TRM cells at the site of infection enable rapid control of virus in the URT and lungs.
  4. Transient infection: TRM cell immunity ‘blitzes’ viral replication in the URT leading to the elimination of all infected cells within a day of the initial infection, at the portal of entry.

The first three scenarios, along with the case where no cross-reactive T cells exist, are represented in Fig.1 of the paper, reproduced below.

Which models do the data fit?

The authors argue that biological evidence implies model scenario 4 is very unlikely where only CD4+ T cells are involved. They point out that if pre-existing CD4+ TRM cell immunity was so extreme as to preclude significant viral replication, seroconversion (that is, a de novo antibody response to SARS- CoV-2) would not occur. Such individuals would not be detectable by virological (e.g., PCR) or serological diagnostic tests and would not shed virus; effectively, these individuals would be immune to infection and not reported as cases. The authors say that evidence for other human coronaviruses makes this implausible, and that when epidemiological evidence of very high attack rates in some ship-based outbreaks is added scenario 4 is highly unlikely.

However, in the most studied ship-based outbreak the proportion infected was under 20%.[4] Moreover, the results of a study that Lipsitch et al. do not cite[5] show that, in households where one person was confirmed as having COVID-19, a substantial proportion of other household members had negative PCR test results, implying that they were not infective, despite most of them having typical COVID-19 symptoms. Moreover, these individuals did not develop detectable SARS-CoV-2 specific antibodies, but did develop SARS-CoV-2 specific (as opposed to cross reactive) T cell responses, implying that they had been infected to some degree by SARS-CoV-2 .

Notwithstanding that the sample size was small in that study, it appears to cast some doubt on Lipsitch et al.’s assertion that scenario 4 is highly implausible. It also casts doubt on their subsequent assertion that almost all people infected by SARS-CoV-2 seroconvert (develop antibodies against it), although the test used might have been insufficiently sensitive to detect low antibody levels. In that connection, Lipsitch et al. say that a recent study[6] observed [only] about 3 cases of non-PCR confirmed potentially asymptomatic COVID-19 cases with T cell responses in the absence of seroconversion, but their interpretation of that study’s results has been challenged.[7]

A substantial proportion of PCR-test positive individuals – in some localised outbreaks, the vast majority of them – have asymptomatic infections. In the most studied ship-based outbreak4 almost half of infected individuals remained asymptomatic throughout.[8] If that is due to T-cell cross reactivity, acting in combination with innate immune responses, then only model scenarios 3 or 4 would fit, since model scenarios 1 and 2 imply significant symptoms.

In the remainder of this article I will not pursue the possibility of model scenario 4 being relevant. Rather, I will focus on showing that the implications for herd immunity of model scenario 3 (possibly involving also model scenario 2), as varied to take account of variation in viral dose and innate immune system strength, are very likely not already taken into account in simple epidemiological models based on transmission dynamics data. In this connection, it should be noted that the extent and quality of the available data, both biological and epidemiological, does not provide high quality evidence, so drawing firm conclusions either way is difficult.

The low level of asymptomatic transmission

Importantly, there is quite strong evidence that infected individuals transmit SARS-CoV-2 much more weakly if they are asymptomatic (and not just presymptomatic). Biological evidence neither proves nor disproves that a positive PCR test for SARS-CoV-2 implies significant infectivity (although a negative PCR test can be taken as implying a lack of significant infectivity).[9] However, epidemiological evidence strongly suggests that transmission by asymptomatic individuals is far lower than that by symptomatic or presymptomatic individuals.

A number of studies have investigated transmission from index cases who remained asymptomatic throughout their infections. A review study[10] estimated that the mean household secondary attack rate from asymptomatic cases was only 3.5% of that from symptomatic cases. As that study noted, household secondary attack rate provides a useful estimate of both the susceptibility of contacts and infectiousness of index cases. However, both in that study, and in another review study[11] that estimated a much higher ratio than 3.5%, the statistical analysis appears to be seriously flawed.[12] It is therefore necessary to consider the actual results of the relevant original studies that they reviewed. Two of those studies[13] [14] found no instances of asymptomatic transmission, although the number of contacts concerned was very small in one case. Two other studies each found one case of asymptomatic transmission, out of respectively 305 and 119 contacts,[15] [16] with corresponding relative risks of 6% and 19%. Averaging the risk ratios of all four studies, in a way that gives appropriate weight to the evidence each provides, gives an overall transmission risk ratio estimate of 8% for asymptomatic cases, relative to symptomatic and presymptomatic cases.[17]

That is, an asymptomatic infected person, as in Lipsitch et al. model scenario 3, appears to be only one-tenth or less as likely to transmit the virus as does a symptomatic or presymptomatic person. This conclusion does not have to depend on asymptomatic infectees having a much lower viral load in their URT, which may not be the case. They could for instance transmit less because of an absence of coughing (particularly that involving expectoration15), less deep breathing or a similar factor; because more of their PCR-measured viral load does not represent viable viruses; and/or because their viral load remains at an infective level for a shorter period.

The likely importance of viral dose (inoculum) and innate immune responses

Two factors that Lipsitch et al. do not include in their model scenarios, but which seem likely to be very relevant, are the magnitude of the viral dose and the strength of a person’s fast responding innate immune system. Both the symptoms, as to their likelihood and severity, and the infectivity of an individual exposed to SARS-CoV-2 are expected to depend on the viral dose that their exposure involves[18] [19] and on the strength of their innate immune system, as well as on any cross-reactive T cell and/or antibody adaptive immune system memory. I will concentrate here on differences arising from the interaction between viral dose and cross-reactive T cells, but in reality differences in innate immune system strength, and in general health and other factors, will likewise affect how somebody reacts to viral doses of varying strength and to what extent they become ill and/or infective.

Box 1: Might low viral dose explain Tokyo’s COVID-19 epidemic?Evidence from a study[20] of 1877 asymptomatic (at time of testing) company employees from 11 disparate locations in Tokyo is consistent with the importance of viral dose. The study showed seroprevalence increasing from 6% to 47% between late May and late August. If the sample is representative of the Tokyo metropolitan area, which the authors suggest it may be, that implies seroconversion of about 5.7 million individuals during the study period.
Since the corresponding number of deaths attributed to COVID-19 appears to have been little more than 30, that implies an infection fatality rate in Tokyo that might be as low as 0.0006% – around a thousand times lower than generally estimated. In Japan, the very high rate of mask wearing (and generally high personal hygiene standards) may have reduced viral doses sufficiently for the vast majority of infections to be asymptomatic, and for almost all symptomatic cases to be mild, irrespective of the presence of cross-reactive T cells.[21] [22]

It seems entirely possible that where the viral dose is sufficiently low, a person with cross reactive CD4+ T cells might either be infected so little that – whether or not a PCR test would be positive, at a sufficiently large cycle threshold (high sensitivity) – they not only remain asymptomatic but also have negligible infectivity. In effect, given a sufficiently low viral dose, Lipsitch et al.’s model scenario 3 might produce rather similar effects to what their model scenario 4 would do for a high viral dose. It appears, for most purposes, to be inappropriate to regard such a non-infective, healthy person as a COVID-19 case or even as being infected at all.[23] Such persons are accordingly treated here as not having been infected. However, it appears possible that a low viral load might, without resulting in symptoms or non-negligible infectivity, nevertheless induce effective immunity through the development of SARS-CoV-2 specific antibodies and/or T cells.

By contrast, Lipsitch et al. appear to regard someone as having been infected even if only a single cell in their body has been invaded by a virus. While this definition may be logical from a technical biological angle, it does not seem appropriate from an epidemiological viewpoint. For epidemiological purposes, what is relevant is whether and to what extent a person is or will become ill, infective and/or immune.

Where the viral dose is fairly high, even if a person has cross reactive CD4+ T cells, they would almost certainly test PCR positive, and be more likely to develop symptoms. Model scenarios 2 and 3 in the paper may both be relevant in these cases. While in such a case the person concerned would be infective, albeit much less so if asymptomatic, if they had cross reactive CD4+ T cells they would probably be considerably less infective (and be much more likely to be asymptomatic or to have mild symptoms).

Insofar as infected individuals are asymptomatic and of low (but non-negligible) infectivity, it may be that in cases where they do transmit infection the viral dose is usually sufficiently low for the person thereby infected also to be asymptomatic and of low infectivity, in which case such asymptomatic transmission will contribute to the gradual spread of immunity while not leading to disease.[24]

Modelling the effects of varying susceptibility and infectivity arising from cross-reactive T cells

I have built a greatly simplified toy model that illustrates the possible implications for epidemic progression and herd immunity of cross-reactive T cells that have the effects discussed in this article. The model stratifies the population into two equal parts, one possessing cross-reactive T cells and the other not. It distinguishes symptomatic and asymptomatic infections, the latter having only one-ninth as high a probability of causing infection as the former.

The detailed assumptions made in the model are set out in an Appendix. While these assumptions are purely illustrative, they are intended to be broadly consistent with existing evidence and the foregoing discussion in this article. The key assumptions regarding the effects of cross-reactive T cells are that their presence halves the risk of infection from a potentially infective contact, quarters the probability of any infection being symptomatic, and may result in immunity developing in a substantial proportion of those cases where infection does not occur.

The modelled epidemic is seeded by the symptomatic infection of one naïve individual (a person without cross-reactive T cells). The number of close contacts per generation is then adjusted to produce, after the epidemic has adjusted from the initial seeding pattern to its natural pattern, a reproduction number early in the epidemic – which will therefore closely approximate R0 – of 2.4.

The toy model’s projections show that, after initial exponential growth, new infections start to decline, indicating that herd immunity has been achieved. At that point, 41% of the population has been infected, with approximately 43% of infections being asymptomatic. At 41%, the HIT is slightly over two-thirds of the classical HIT level for a homogeneous population, being 58%.[25]

A further 20% of the population will have become immune without, for all practical purposes, having had an infection. If on the other hand no exposed but uninfected (i.e., asymptomatic and non-infective) individuals develop immunity, then the HIT is closer to the classical level, but still lies more than 10% below it. If the probability of being infected is reduced by 85% in the presence of cross-reactive T cell memory, the HIT could be one-third below the classical HIT even if no exposed but uninfected person develops immunity. It is not suggested that such a large differential is  likely. However, it does prove that cross-reactive T cell memory, in combination with varying viral dose (and innate immune system strength) can result in a substantially lower herd immunity threshold than that estimated from data earlier in the epidemic using homogeneous population compartmental SIR/SEIR models, as is routinely done.

A more realistic model would incorporate continuous probability distributions for all the key parameters. But the basic point illustrated by the very simple model would remain valid. Homogeneous population based compartmental models imply that epidemic growth will slow pro rata to the shrinking pool of uninfected people. But where there is variation within the population as to how susceptible people are to infection, so that more susceptible individuals are on average infected earlier, the epidemic growth is bound to reduce more rapidly than that. As a result, the herd immunity threshold will be lower than if the population were homogeneous, with the reduction of the HIT being greater if less biologically susceptible individuals also have, if infected, lower biological infectivity.

Conclusion

I have demonstrated that the claim by Lipsitch et al. that the potential impacts on the herd immunity threshold of cross- reactive T cell memory are already incorporated into epidemiological models based on data of transmission dynamics is mistaken, even assuming that they are correct in arguing that their model scenario 4 is highly implausible.

In this article I have only considered the possible effects of cross-reactive T cells. However, even when combined with other causes of interpersonal variation in biological susceptibility, including age, such heterogeneity is not thought to be the main reason why the herd immunity threshold will be lower than the classical level for a homogeneous population. In practice, interpersonal variation in contact rates (social connectivity) is usually thought to be a much more important reason. 3

Appendix – Assumptions made in the toy model of the effects of cross-reactive T cells

  1. The population is one million and is homogeneous except that only 50% of people have cross-reactive memory T-cells.
  2. The generation interval is fixed, infected individuals are only infectious in the generation interval after they become infected and are uninfectious and immune thereafter.
  3. Infections are by close contact only. The number of close contacts by an infected person is independent of their T cell status and whether or not their infection is asymptomatic (never symptomatic), and each person who becomes infected has only had one contact with an infectious person during the generation interval in which they become infected.
  4. A close contact between a symptomatic (including presymptomatic) infectee and a naïve individual (one without cross-reactive T cells) results in infection 90% of the time, with 80% of such infections being symptomatic, due to a high average viral dose being involved.
  5. A close contact between an asymptomatic infectee and a naïve individual results in infection 10% of the time, with 20% of such infections being symptomatic, the viral dose being lower.
  6. A close contact between a symptomatic infectee and a resistant individual (one with cross-reactive T cells) results in infection 45% of the time, with 20% of such infections being symptomatic.
  7. A close contact between an asymptomatic infectee and a resistant individual results in infection 5% of the time, with 5% of such infections being symptomatic.
  8. Where such a low viral dose is transmitted on a close contact that a resistant recipient not only has no symptoms but is completely non-infective, they are treated as not being infected but (except if stated otherwise) in 60% of such cases they nevertheless become immune.

Nicholas Lewis                          14 October 2020


[1]  Marc Lipsitch, Yonatan H. Grad, Alessandro Sette and Shane Crotty: Cross-reactive memory T cells and herd immunity to SARS-CoV-2. Nature Reviews Immunology 6 October 2020 https://doi.org/10.1038/s41577-020-00460-4

[2]  The herd immunity threshold is the proportion of the population that have become infected at the point where each new infection causes, on average, no more than one further infection. For an epidemic in a homogeneous population, it will be {1 – 1/R0}, where R0 is the basic (initial) reproduction number.

[3]  e.g., Tkachenko, A.V. et al.: Persistent heterogeneity not short-term overdispersion determines herd immunity to COVID-19. medRxiv 29 July 2020 https://doi.org/10.1101/2020.07.26.20162420

[4]  The Diamond Princess. 712 out of 3,711 on board tested PCR-positive, with at least 295 and probably closer to 334 cases (295 from Tokyo plus 40 returned on charter flights, one of whom died from COVID-19) remaining asymptomatic throughout their infection. https://www.mhlw.go.jp/stf/newpage_11441.html

[5]  Gallais, F., Velay, A., Wendling, M.J., Nazon, C., Partisani, M., Sibilia, J., Candon, S. and Fafi-Kremer, S., 2020. Intrafamilial exposure to SARS-CoV-2 induces cellular immune response without seroconversion. MedRxivhttps://www.medrxiv.org/content/medrxiv/early/2020/06/22/2020.06.21.20132449.full.pdf

[6]  Sekine, T. et al. Robust T cell immunity in convalescent individuals with asymptomatic or mild COVID-19. Cell https://doi.org/10.1016/j.cell.2020.08.017 (2020).

[7]  https://twitter.com/WesPegden/status/1313649435642077184

[8]  That is consistent with the findings of Sakurai et al., Natural History of Asymptomatic SARS-CoV-2 Infection. New England Journal of Medicine. 2020 Jun 12 https://www.nejm.org/doi/full/10.1056/NEJMc2013020

[9]  https://www.cebm.net/covid-19/infectious-positive-pcr-test-result-covid-19/

[10] Madewell, Z.J., Yang, Y., Longini Jr, I.M., Halloran, M.E. and Dean, N.E., 2020. Household transmission of SARS-CoV-2: a systematic review and meta-analysis of secondary attack rate. medRxiv. [1 August version]

[11] Buitrago-Garcia D, et al. (2020) Occurrence and transmission potential of asymptomatic and presymptomatic SARS-CoV-2 infections: A living systematic review and metaanalysis. PLoS Med 17(9): e1003346. https://doi.org/10.1371/journal.pmed.1003346

[12] Madewell et al. included a study where the secondary attack case rather than the index case was asymptomatic. Buitrago-Garcia D, et al., who estimated a relative risk of 0.35 for asymptomatic transmission,  included in that estimate a study of presymptomatic transmission (their reference 111) and an estimate based on combined asymptomatic and presymptomatic transmission (from their reference 65), and they wrongly estimated very high asymptomatic transmission risk from studies that found zero cases of it.

[13] Cheng HY, Jian SW, Liu DP, Ng TC, Huang WT, Lin HH, et al. Contact Tracing Assessment of Covid-19 Transmission Dynamics in Taiwan and Risk at Different Exposure Periods before and after Symptom Onset. JAMA Intern Med. 2020. Epub 2020/05/02. https://doi.org/10.1001/jamainternmed.2020.

[14] Park SY, Kim YM, Yi S, Lee S, Na BJ, Kim CB, et al. Coronavirus Disease Outbreak in Call Center,

South Korea. Emerg Infect Dis. 2020. https://doi.org/10.3201/eid2608.201274

[15] Luo L, Liu D, Liao X-l, Wu X-b, Jing Q-l, Zheng J-z, et al. Modes of Contact and Risk of Transmission in Covid-19 among Close Contacts. bioRxiv. 2020 [March 26 version] https://www.medrxiv.org/content/10.1101/2020.03.24.20042606v1

[16] Zhang W, Cheng W, Luo L, Ma Y, Xu C, Qin P, et al. Secondary Transmission of Coronavirus Disease from Presymptomatic Persons, China. Emerg Infect Dis. 2020. https://doi.org/10.3201/eid2608.201142

[17] Averaging over the four studies, weighting by the number of contacts by asymptomatic index cases, gives a pooled relative risk estimate of 8.2%. A more sophisticated meta-analysis using the R software Fixed effects (Mantel-Haenszel) function in the rmeta package estimates a pooled study relative risk of 7.9%, with a 75% probability that it does not exceed 13% and a 90% probability that it does not exceed 20% (assuming that the confidence intervals are symmetrical).

[18] Steinmeyer, Shelby H., Claus O. Wilke, and Kim M. Pepin. “Methods of modelling viral disease dynamics across the within-and between-host scales: the impact of virus dose on host population immunity.” Philosophical Transactions of the Royal Society B: Biological Sciences 365.1548 (2010): 1931-1941.

[19] Goyal, Ashish, et al. “Wrong person, place and time: viral load and contact network structure predict SARS-CoV-2 transmission and super-spreading events.” medRxiv (2020) [7 August version].

[20] Hibino, Sawako, et al. “Dynamic Change of COVID-19 Seroprevalence among Asymptomatic Population in Tokyo during the Second Wave.” medRxiv (2020). [23 September version]

[21] Gandhi, Monica, Chris Beyrer, and Eric Goosby. “Masks do more than protect others during COVID-19: Reducing the inoculum of SARS-CoV-2 to protect the wearer.” Journal of general internal medicine (2020): 1-4.

[22] Gandhi, Monica, and George W. Rutherford. “Facial Masking for Covid-19—Potential for “Variolation” as We Await a Vaccine.” New England Journal of Medicine (2020).

[23] While such cases might give a positive result on a PCR test at some point, such a test result might represent  detection only of non-viable virus fragments, or a viable viral load that is too low to be infective.

[24] Unfortunately there are too few recorded cases of asymptomatic transmission to provide reliable evidence on this point, but what evidence does appear to exist is consistent with this argument. Zhang et al. identified one case of asymptomatic transmission, which resulted in an asymptomatic infection, while 73% of the eleven cases of symptomatic or presymptomatic transmission they identified resulted in a symptomatic infection. (Luo et al. unfortunately did not indicate the symptom status of the asymptomatic transmission case that they identified.)

[25] For an R0 of 2.4, the classical herd immunity threshold is {1 – 1/2.4} = 0.583

92 thoughts on “T cell cross-reactivity and the Herd immunity threshold

  1. This is over my head. I tried to understand, but failed, probably due to the fact that I have little knowledge of medicine.

    Despite that, I will dare to state that the general conclusion is suspect when comparing to mortality rate for various countries. I refrain from mentioning cases, as the numbers are said to be based on varying factors and protocols.

    Sweden may have a faster spread of SARS-CoV-2 and contracted COVID-19 faster than average countries. What we see now is that Sweden is down to about 1 daily mortality (0.1 per million) with trend going even lower. Whereas most other countries have seen a slight rise in mortality.

    Wasn’t there a paper or an announcement that it turned out (the non-existent) herd immunity finally turned out to be around 17.5%?

    Theory, as in the article is great, but what about judging real life data.

    Reference https://www.worldometers.info/coronavirus/country/sweden/

  2. So what…

    Surely a nutrient-free diet lacking in Vitamins B, C & D – also Zinc inside people is much more important than these dancing faeries?
    Zinc esp as its deficiency is caused by alcohol consumption.

    Maybe research The Cumming Effect here in the UK = one rule for them, another for everyone else.
    Sound familiar?

  3. How ‘bout some mo’ data, yum-yum, data.

    Global, WHO.
    The US, India and Brazil together have more cases than the ENTIRE rest of the world combined.
    The top ten countries have over 70% of the cases.
    The US, Brazil, India and Mexico together have more Covid-19 deaths than the ENTIRE rest of the world combined.
    The top ten countries have 72% of the deaths.
    Seems to me more of a problem with crappy health care systems in a few countries and not a global pandemic.

    US, CDC.
    NYC and six states have accumulated more Covid-19 deaths than the ENTIRE rest of the country.
    The top 15 states have accumulated over 75% of the US deaths.
    The 75+ demographic has more deaths than the ENTIRE rest of the country combined.
    The 65+ demographic represents almost 80% of the deaths.
    The 55+ demographic represents over 90% of the Covid-19 deaths.
    Japan has the highest percentage of 65+ in the world, 27%, yet a little over 1,500 deaths.
    What do they know/do that the lying, fact free, fake news MSM does not consider newsworthy?

    Denver, Arapahoe and Jefferson counties represent more Covid-19 deaths than the ENTIRE rest of Colorado.
    The top ten Colorado counties represent 90% of the state’s Covid-19 deaths.

    Why should the entire state/country/world suffer for these (BLUE) health care **** holes?

    The data absolutely BELLOWS SCAM!!!!!!!-demic!!!!!

    • I think it’s interesting that China’s two biggest adversaries have the most cases, especially the US. However, India and the US are the next two most populated countries.

      To control a viral outbreak you have to know where it’s at and you have to know when it started. Only one country on earth knows the exact answers to those questions.

      To see who it is, sort the data at
      https://www.worldometers.info/coronavirus/ by population. The answer is very, very obvious.

      How can anyone say that China doesn’t control this virus like a dog on a leash? They can sic that dog on anyone they please, whenever they want.

      • Except they can’t sick that dog on Taiwan. 7 deaths, yes SEVEN. An island of 24 million that is so densely populated you would have to put half a billion in Texas to get the same density.

          • Ummm …. There are millions of travelers between mainland China and Taiwan every year.
            A quick google flights search turns up non-stop flights to either Taipei or Kaohsiung from Beijing, Shanghai, Xiamen or Macao and one-stop flights from most major cities in China with the connection in either Shanghai or Xiamen.

            This video is from March 11 and explains the actual reason Taiwan has fared so well.

    • Could be the high fish diet in Japan. Fish has selenium especially tuna. Some studies suggest selenium May protect from virus.

      • Good point Stevec,
        I’ve been telling all who will listen to up their selenium levels with one or two Brazil nuts a day or supplements, one recent study found 30% of the population in Ebola districts had antibodies to Ebola, implying they had had asymptomatic Ebola, the only difference found in bloodwork was a selenium level above the general .

        Aids is very low in Senegal compared to the rest of Africa, selenium is high in soils in Senegal whereas demographics would point to higher rates, e.g. transport hubs and brothels.

        Hanta virus cases with ~40% death rate in China in the early 2000s was reduced to ~ a quarter of this with very high doses (up to 2 grams) of selenium.

        Selenium is used in around 20 different processes in the body, many to do with the immune system. Over the last 50 years the grain content of selenium has been dropping steadily in the UK, it used to come from the fallout from coal fired generation plants, Zinc used to come from galvanized pipes, and Vit D from sunshine before the sunscreen push came into being.

        As the Indonesian study showed the amazing difference between high Vit D status and low levels
        status in ICU( ~97% survival for high, v ~4% low,) with selenium and Zinc we should be bullet proof.

    • Schroder: What is this lousy-health-care-system effect? Do you dare to explain how this works?

      Wouldn’t there be some data to support your lousy-health-care theory? Such as portion with health insurance? Or available hospital beds?

    • Denver, Arapahoe and Jefferson counties are more than 1/3 of the population of Colorado, so their death rate isn’t that much higher.

      The top ten most populated counties are more than 80% of the population of Colorado, so their death rate isn’t much different from the rest of the state.

      I agree with your basic point that decisions should be based on local conditions, but you really need a better analysis.

  4. Yet another Nic Lewis wild guess speculation about a pandemic still in progress. I wrote a simple article on the experience in Sweden and what herd immunity really means on my politics blog simply because so many people jump to conclusions about both subjects based on their politics.

    There are no Covid experts before the pandemic ends, data are analyzed for accuracy, and then studied for possible conclusions. And if there is more than one strain of Covid, no conclusions may be possible.

    Waiting and understanding is not a Nic Lewis methodology. Jumping to conclusions is his style.
    My blog article was last week at
    http://www.ElectionCircus.blogspot.com

    • You seem to have more faith in the quality of data than do I. I have made a post nearby somewhere, but the data I have looked at seems full of potential problems, but the serious are: 1) “cases” is a category not accounting at all for severity, 2) there is a real potential for double counting, 3) variations in reporting, building epicurves (often no epicurves at all, but just curves based on report date), 4) distortions caused by “smoothing” with a running mean, etc…

      • I comment on herd immunity in general without wild guessing for Covid as Nic Lewis does. I trust that Sweden has not lied about their Covid experience. Their results were nothing special compared with neighboring Norway and Denmark, not to mention most Asian nations, except China.

        National differences must be related to how many Chinese people flew in with the infections on early 2020, how well nursing homes were protectef, and random variations too.

        Sweden did have a partial lock down and voluntary social distancing … which hurt their economy in first half 2020 almost as much as the US economy was hurt by much stricter partial lock downs in most states.

    • Nic does not “jump to conclusions”, that seems to be your M.O. He presented his analysis, admitting what areas had weak underlying data, and pointed out the resulting limitations. His conclusions were modest, all things considered, but all the data and his methods are there for the reader to consider. If you have *specific* criticisms of his analysis, we’d all be happy to learn what they are. Otherwise, you’re just a troll pushing your own blog.

      • Penrosr
        I’m “smarter” than Nic Lewis simply by admitting I don’t know. That is also my conclusion about the climate in 100 years.

        I know Nic gets undeserved attention by speculating DURING a pandemic with questionable data on deaths. Flu deaths are always wild guessed because, at least as of 2019, flu was not one of the CDC’s 110 causes of death. Death is caused by major organ failures and whether to blame the flu is an estimate, formerly done by the CDC with computer models, NOT a list of actual names.

        There are no COVID experts during an ongoing pandemic. Perhaps next year Mr. Lewis will write an excellent article on COBID. Writing such an excelkent article now is premature and impossible to do. Mr. Lewis apparently does not realize that. Nor do you.

        My three blogs are free with no ads. I do them for free as a public service because the mainstream media are leftist-biased and that is not fair to the general public.

        It is a waste of time to comment on anyone’s specific speculations. It is not a waste of time to comment on Lewis’s premature “analysis” … and the two mindless character attacks on me on your comment. You made them without even reading my blog article. How fair of you!

        • The COVID death rate is down to about 1 of 1000 infections but roughly 600 of 1000 get normal or serious flu symptoms with far more hospitalizations and need for the ICU then a typical seasonal flu. I’d say the 600 suffering are more important than the one dying, compared with April when so many were dying, perhaps 1 of 100 who tested positive were dying at the peak in NYC — I know not many people were tested at first.

          I know three people infected who only lost their sense if smell and taste. Are they really “sick”? … Humans carry the herpes virus with no symptoms most of the time. Are they really “sick” when they do not have a cold sore?

          There are early reports of long term damage from COVID among the people who needed hospitalization and people who almost reached that point. And not just lung damage. That open question suggests getting to herd immunity could cause a lot of damage … and more additional deaths too.

          This is the first pandemic where healthy people were locked down and the partial lock downs caused more damage — economic damage, physical damage and mental damage –than the SARS2 virus itself. But SARS2 is NOT just another seasonal flu. And it’s too soon for anyone to be a COVID *expert*.

          • “long term damage from COVID”

            Anyone who was on a ventilator needs to be subtracted out of the long term damage from COVID category and added to long term damage from ventilator category.

            Patel believes there is wisdom in avoiding ventilating patients whenever possible. “If you check in with people six months after being on a ventilator, three-quarters of them will say they have some sort of disability,” she says. “A quarter of those will say it’s severe.”

            How One Covid-19 Doctor Became a Ventilator Whistleblower
            https://elemental.medium.com/how-one-covid-19-doctor-became-a-ventilator-whistleblower-a1c2dbdd1b06?gi=sd

            Additionally, per CDC data, covid is less dangerous than flu for those 50 y/o and younger.

          • Furthermore, covid mortality closely follows natural mortality, so in reality covid is just picking off low hanging fruit that gets picked off anyways.

      • “On a long enough timeline everyone’s survival rate drops to zero.” – Tyler Durden

        We are all leaving with a toe tag. When and by what manner is the great mystery.

  5. IF there is a herd immunity, how long will it last in an individual?
    Anti Cholera vaccination lasts only six months and then needs to be renewed.
    Yellow Fever 3 years.
    Diphtheria 10 years.
    Given that there are a few people who have caught WuFlu a second time, maybe the immunity, if there is any, won’t last very long.

    • We have vaccinations for Measles, Mumps, Chickenpox, Rubella, but none of these guarantee you won’t get the disease. Getting the disease doesn’t mean you won’t get it a 2nd time. The record I believe is a woman who has had Rubella 6 times. Herd immunity works because not enough of the population are vulnerable to a disease to allow it to thrive; it’s not about individuals.

    • Oldseadog,
      “Herd immunity” is just that – a population wide effect; there is no individual aspect to it. As far as re-infection is concerned: considering that millions of people have apparently been infected, and only a handful have apparently been re-infected (data is sketchy on that), I don’t think that’s anything to worry about. You have a greater chance of being killed by lightning.

    • “Given that there are a few people who have caught WuFlu a second time…”

      So they say. Doubtful. Virtually useless PCR tests coupled with lingering side effects of toxic medical treatments makes accurate determination of such impossible.

      • They say this guy caught it twice, but his second set of symptoms (100x worse) sounds suspiciously like the side effects of the methylprednisolone he took as part of the MATH+ protocol (I know because the doctor is a member of the consortium that promotes that treatment). One of the most serious side effects of that drug is osteonecrosis (death of bone tissue). Pay attention in the video that the patient says the best way he could describe the pain he felt was that it felt like it was running through his bones. Maybe his bones were trying to tell him something. Osteonecrosis was a common side effect of methylprednisolone treatment during SARS that appeared months after treatment.

        https://twitter.com/NewDay/status/1280851206190051330

    • At least it smells like TDS.
      The “authorities” prefer to mention “cases”/infections, trying to avoid any mention of mortality per million, and totally refrain from mentioning excess mortality.

  6. Where have the esteemed Lord Moncton of Brenchley’s posts of how awesome lock downs are gone?

    Now that Sweden is pretty much completely clear of the disease and Britain is under a morass of cases and supposedly high hospitalization rates I would like to know how many trillions of lives have been saved by locking people in their homes and behind masks. But he is no longer updating us on these things.
    Deaths per million…
    Sweden 584
    UK 635
    USA 670

    The lockdown capital of the world New York City 2974 deaths per million population.

    Does that look like masks and lockdowns worked or failed?

    Does the good Sir Lord Moncton of Brenchley still believe that all the numbers of dead were factually killed by the virus?

    Is it reasonable to run the tests through 37 to 40 cycles when evidence shows that only 40% of the time when they are run through 24 cycles that live virus can be detected and under no circumstances on 25 or greater cycles is it possible that live virus can be detected?

    Lord Moncton of Brenchley was a useful idiot for those who wish western civilization harm. I would like to know if he is still under their full spell or whether he has finally wised up and if so, does he owe us any apology for having carried the water of those who wished us harm and in fact caused significant harm?

    Just so the good Lord Moncton of Brenchley does not think I am trying to attack him without his knowledge, I trust that plenty of people here will certainly let him know I am wondering about him.

    • Astonerii,
      Another country to include in your very short list would be NZ which had a complete lockdown
      eliminated the virus and deaths per million is about 6. You are currently 100 times more likely
      to die of COVID if you live in the US than if you live in NZ.

      • They destroyed their economy to pwn an illness that has a 99.5+% survival rate for those under 70 y/o (US data).

        Genius…

          • OK. So they destroyed 2% of their GDP to pwn an illness that has a 99.5+% survival rate for those under 70 y/o (US data).

            Genius…

          • For NL it may be a good choice. They are isolated and an island. Note though they must keep this going until there is a vaccine, until they are in line to get it and until enough people have taken it, or likely forced to get it. So all GDP damage up to that point must be added to the current numbers. Just as Sweden’s death per capita was higher in the beginning, but now has stalled and others are passing them.

            But I would not be surprised if for NZ it is worth it. Inside NZ life is normal, which it almost nowhere else is.

            Other Island nations like Hawaii and Australia have not succeeded yet in getting their internal life normal.

            So far Sweden and NZ seem to be the only two who did this, ironically with opposite strategies.

    • Melbourne, Victoria would surely give New York a run for the title of lockdown capital of the world. Less than 10 cases per day and were under effective house arrest with a “ring of steel” around the city.

      • Don’t worry a 10th court case has been launched against the lockdowns … this one is sure to win given the last 9 were rejected. What you really need is an anti-lock down group with an IQ that at least understands it’s a political issue not a legal one.

  7. Much of what Nic Lewis has to say seems pertinent to many observations I have made locally.

    The University of Wyoming had a reopening plan that had as its original goal preventing COVID-19 from getting on campus. The details are unimportant, but there was, and is, a heavy reliance on saliva PCR tests. I was surprised to find very little known about the false result rates of these tests at the time (mid August). More information is now available, but I couldn’t see at the time how they planned to make effective use of test results, and I didn’t see that this plan was robust in the presense of false test results.

    The plan broke down almost immediately. The county had a total of 134 infections from February through March. After reopening the campus and bringing limited numbers of students back, we had 441 new cases in September alone, and 339 so far in the first 13 days of October (USAFacts.org). There isn’t always solid data to sort out what has happened, but this same scenario has played out on smaller scale at the community colleges around the state. The interesting result is that the progress of the epidemic in the entire state has now changed.

    First, the Wyoming Department of Health (WDH) has maintained a real epidemiological curve, with an attempt to place new cases at the time of onset of symptoms. This curve had no tendency to display a weekly periodicity until September, but now has an obvious, and large spike in cases each Monday. These are cases with no symptoms, and no way to place them at onset of symptoms. They have to be left at report date. While I am now retired and rarely around campus, I do keep in touch with lots of students, I overhear student conversations around town, and there has been some limited data on “dashboards” occasionally to suggest that about one-half these new cases show no symptoms. Actually, students who have tested positive and have shown symptoms have indicated their symptoms consisted of a runny nose, maybe a loss of some sense of taste or smell, perhaps a headache. The worst I have heard about is ordinary cold-like. Perhaps the “asymptomatic” cases actually do have symptoms, but so mild that students don’t even recognize they are sick. At any rate, after being told to not return home, a large number did on weekends, and have stirred the virus around. Of course this stirred virus eventually reaches some people who are very susceptible.

    The epidemiological curve at WDH is very noisy. A curve smoothed with a Kalman filter shows an initial run up that flattened out by March 20 even before the state orders closing down bars and restaurants. Then with the protests in late May there was another run up in cases starting May 31 which continued until July 20, then another run up beginning September 1 with the opening of college.

    Each new stirring of the population, making the population appear more homogeneous in a number of ways, causes a new rise in cases. What is more, students are required to get two tests per week. Positives are expected to self-quarantine and other people exposed to them expected to isolate for two weeks. Everyone apparently has to start testing again before returning to campus, which presents the possibility of PCR tests picking up non-infectious fragments in recovered cases. Students who I know have tested positive are not advised at all, let alone advised not to return to testing immediately. I have no idea how many of our new cases are duplicates.

    However, per Nic Lewis’s thesis, there is plenty of evidence of a huge range in susceptibility to infection, resistance to progress of the disease, and of displayed symptoms. The rises in cases always seems related to a stirring of the population. Heterogeneity is an important issue.

    • I find it curious that Democrats and Fauci et al are continuing to push for more federal money for more expanded PCR testing and paying for more public testing sites to open. I live about 3 miles from one of Pima County’s and Tucson’s major drive-thru testing sites. It is open to the public for free screening testing (nasal swab PCR).
      The folks working there are bored most the day. Very few people are using these free testing sites for the past two months. They are getting only a few dozen a day (at most), versus the many hundreds to thousands they want or expected.

      Basically if you feel sick stay home until you are well and then wait an additional 3 days of symptom free health before going back out. Continually getting tested when you feel fine is simply tempting the False Positive fate of around 2%.

      • I agree entirely, but the endless emphasis on testing is just the tip of the hysteria around here. There are rules at the U for travel by foot on campus, travel paths through doors, how to place persons in a U vehicle, tattle tale site, daily covid pass soon to be tied to evidence of a test, an assumed ability to withhold pay to get compliance, and on it goes. I am unsure where it will all stop, but nothing would surprise me.

        I would guess that by mid August mask usage was 85% or more compliant, yet the epidemic took off.

        • My guess is that the push for the expanded testing sites is the precursor move to switching them over to vaccination sites. So increasing the number of testing sites and getting people to line up in them like sheep is the first step.
          The worst thing that could happen is a Dementia Joe or Komrade Kamala issue a Presidential diktat making the COVID vaccination mandatory for interstate travel and the like.

          That would be severe 1st Amendment violation of course. Hence they’d need a packed supreme court (with liberals of course to rubber stamp the Democrat Bolsheviks).

    • Similar story at the University of Colorado in Boulder. Students say that almost everyone that tests positive, and is given timeout, has no symptoms. A two and a half week all online break from in person instruction just ended. It’s back to a hybrid in person/online system of teaching.

      A professor told me that in a general chemistry class of about 150 students, only 2 students showed up in person and only 34 showed up online. The actual learning that is happening this semester will not be good.

  8. Folks should note the conflict of interest statements by the Nature Communications authors.
    ”Competing interests
    A.S. is a consultant for Gritstone, Flow Pharma, Merck and Avalia. S.C. is a consultant for Avalia and JPMorgan. M.L. discloses honoraria/consulting from Merck, Affinivax, Sanofi-Pasteur and Antigen Discovery; research funding (institutional) from Pfizer; and unpaid scientific advice to Janssen, AstraZeneca, 1DaySooner and Covaxx (United Biomedical). Y.H.G. discloses consulting from Merck and Quidel; and research funding (institutional) from Pfizer.”

    Most of the vaccine companies are named above. Missing is Johnson&Johnson and Moderna, the two working towards an mRNA based COVID vaccine.

    Big Pharma and governments have many billions of dollars and euros on the line in getting people to line up for their vaccines. Pushing naturally acquired herd immunity ideas, as Sweden has adopted, lowers people’s urgency to get a needle containing one of those vaccines (once they become available) stuck in their arm, versus taking their chances with what for most adults is a mild cold.
    We already have surveys indicating that over half the population in many countries are extremely hesitant to take a SARS-CoV-2 vaccine. Mistrust in a vaccine is thus already running high.

    As a note,
    1. I have no pharma affiliations, or financial conflicts of interest in owning these any stocks of those companies. I divested from most of my stock positions in January this year.
    2. I generally strongly support vaccines that have decades of research and clinical support behind them. These include the MMR vaccine, the Yellow Fever Vaccine, the ZosterVax (shingles and chickenpox vaccines), the Small Pox vaccine (based on a vaccinia virus near cousin of the Variola Major virus which causes small pox), the HepB vaccine, the the HepA vaccine, and several others. All of these vaccine modalities are live, attenuated viruses. Initial viral replication life cycles inside the susceptible cells in vital to getting the immune response properly programmed. Trying to trick the immune system to merely getting an antibody titer is a fool’s game IMO.
    3. The mRNA and DNA modality vaccines should be approached very cautiously. These non-replicating immunity-induction modalities may induce antibody production, but may skew the immune response away from a protective Th1 response to a pathogenic Th2-type response in some people who acquire the live infection after the vaccination. An eosinophilia, airway hyper-reactivity may result then in a few of these cases, leading to greatly enhanced morbidity and possibly mortality if not quickly treated.
    4. I agree with Nic’s conclusion on lack of incorporation of T cell cross reactivity and the original epidemiology models and their projections. I find it quite unlikely the SEIR models from this past spring incorporated the fact of T-cell cross reactivity in their assumptions of susceptibility. No one in the epidemiology literature was discussing this possibility when those models and their projections of millions of deaths were being put forth. The immunologists were of course discussing this, but largely ignored by the hyperventilating epidemiologists eager to get their scaremongering projections published and discussed.

    I find it noteworthy now that Dr Fauci is poo-pooing the idea of naturally acquired herd immunity as an approach to eventually letting the virus epidemic wane on its own timeline. I can understand why he is saying this. The idea of a Sweden style approach greatly diminishes the eventual public acceptance of a SARS vaccine.

  9. This is old news. Numerous studies around the globe have been investigating this topic. Why has Asia had such incredibly lower fatality rates? They were better at mask wearing? They were better at contact tracing or isolation? Or, maybe, this corona virus, is not so unlike past viruses and so most people in Asia had an immune response that suppressed the virus enough to make it not lethal. If that is true then we are much closer to herd immunity than we thought. https://www.bmj.com/content/370/bmj.m3563

    • It seems to explain the observations, and there certainly is a lot of opposition to this line of thinking from those with financial and political interests in vaccines.

    • Rates of T2D (type 2 diabetes) are also much lower in Asia. Same with overall population levels of obesity and the co-morbidities that brings (even before SARS-2 arrived as a new morbidity/mortality factor).
      Asians are also predominately Blood Type B. Blood type has found to be a factor in mortality rates.
      Disentangling all the confounding factors will takes years of retrospective study.

  10. To save many ‘very susceptibles’ outside campus the best would have been to let it spread as fast as possible on campus where we have the biggest strong immune system group especially after summer. Now we drag it around all autumn winter and spring what makes it much more likely it will reach the very susceptible on the worst moment.

  11. When they say the science is settled more CO2 more warming than more masks more Covid cases means wearing masks is bad?

    • Latitude
      October 15, 2020 at 10:00 am

      Masks are very very much prone to high contamination, from bacteria and microbes.
      Mass application of masks in populations increases considerably the contamination and spreading factor of multiple bacteria and microbes in the population… especially when considering the very “poor” and careless methods and “protocols” of utilization an masse.
      Added on top of the quasi already handicapped health care systems and there it is a highly and
      very dangerous herd health issue in making… one that does not discriminates.

      Too bad.

      cheers

  12. Until doctors focus on the role of the ACE2 enzyme in the blood vessels (canceling it causes an increase in angitensin II, which leads to blood clots), Cov-19 disease will take its toll.

    • That’s very odd. I’d rather have a select bottle of Jack Daniels.

      I wish we really knew all of the financial incentives that are in place right now.

  13. Masks might be a tool to use for achieving herd immunity with very low death rates. Wear (good) masks, but make normal contacts.

    The virus spreads widely (Tokyo @ nearly 50% infection rate by August) but mildly (extremely low 0.0006% death rate) with infections caused by low viral loads which is provided by wraring masks.

    Masks don’t seem to prevent viral infection spread well at all as seen by the very high infection rate in Tokyo, but the resulting infections are mild.

      • For absolute safety maybe we should all resort to wearing CO2 rebreathers which are used for diving. Always wanted to buy one for gold mining under water, if I had the money to be able to afford one. It would be truly neat to be able to walk into a river and spend hours underwater without being tied to a hookah setup, or having to wear scuba gear.

    • Save the Turtles

      When Californians learn that disposable masks kill more turtles than plastic straws, they will surely ban the dreaded disposable face mask!

  14. There is a need for yet another model, one which includes a seasonal effect.
    So far, SIR and SEIR models assume that you are either susceptible or immune.
    It is looking like there is more to immunity than antibodies. The body has multiple layers of defense.
    The innate immune system’s protective capability may vary, for example with seasons. Because of Vitamin D and other things.
    The models need a factor or parameter to account for these changes is susceptibility.

    If this virus is like some others, it will become endemic. It will be seasonal, fading in the summer, but at a level high enough that it is still around when its victims become more vulnerable in winter.

  15. This will all be very interesting when the “virus” is actually isolated. Until the “virus” has been isolated and proven to exist, then all of this information is worthwhile. The discussion should be “WHERE IS THE VIRUS?”

    FROM THE CDC/FDA OWN PAPERS (dated July 13, 2020):

    https://www.fda.gov/media/134922/download

    SEE document page 38 (Acrobat, page 39):

    “Detection of viral RNA may not indicate the presence of infectious virus or that 2019-nCoV is the causative agent for clinical symptoms. ” (this is at the first bullet point on the page)

    THE REAL “KICKER” page 39 (Acrobat, page 40):

    SINCE NO QUANTIFIED VIRUS ISOLATES of the 2019-nCoV ARE CURRENTLY AVAILABLE ……. (emphasis, mine) (FIND THIS under “Performance Characteristics” second paragraph, beginning near the end of the second line)

    Find the virus, then we can talk. Sure, people are dying, for many reasons: they always have and always will. Sure, some may seem to be dying for the same reasons — always have, always will. But to label everyone who “tests positive” (when the test is known to produce be 89%-94% false positive), or has had close contact with someone who “tests positive,” and dies with some of the vast multitude of symptoms be given to “covid,” does not prove the person who died had “covid.” The CDC would agree with this last statement.

    “Anti-bodies” being “proven” by tests manipulated to try and locate fragmented RNA that have never been proven to be a symptom of the cause of death of anyone does not prove anything. Just “smoke and mirrors.”

    Enough is enough. Let’s get back to real science — isolate the virus in a proper way where only the virus exists (floating in a medium of glucose at the appropriate density, centrifuged so the material has been separated from everything else, then proceed as you have been with cultures, electron microscopy ….). After isolating, get a huge group of people together who test “positive,” and isolate viruses from them and then see how many of them are actually sick. Do this with several different groups. IF THIS IS SO IMPORTANT, do the work and stop destroying lives and economies until you know for certain there is a common disease that is transmissible.

    Regards

    AK in VT

  16. There is no “herd immunity” to Meteors, Comets, Solar Novae, Moon impacts, Nuclear Weapons, High Explosives, Landmines, Bullets, Swords, Drowning or Coronaviruses.

    Coronaviruses are tiny little complex molecular landmines that go BOOM and inject RNA into your cells when they touch the right point. You are NOT immune, you may have a phage response of less than a few hours to infection blocking all spreading and retransmission of developed nodal bodies but if you were sprayed with enough weaponized coronaviruses they would kill you even without reproducing in your cells long before the density of the spray became noticeable to your senses.

    In order to be immune to SarsCov-2’2019 part of your metabolism must either be shut-down or mutated to a new structure throughout your body.

    What we are talking about with the term “herd immunity” is our bodies becoming readily able to interrupt the carrier state and block progression to the spreading state.

    As we have seen with “common cold” that isn’t going to ever [snip]ing happen.

  17. I don’t think it is a good idea to allow the Wuhan virus infection to run its course in the human body.

    The death rate from the Wuhan virus is very low, but the health complications it can cause are something to take very seriously as large percentages of people who have recovered from the Wuhan virus are showing a lot of inflammation in many parts of the body.

    The Wuhan virus has been found in the brain and in the eyes. It can probably be found anywhere a blood vessel might go.

    To allow the Wuhan virus to run its course in the body is to take the chance that you might be a victim of long-term, detrimental health effects from the virus infection.

    The sooner one can eliminate the Wuhan virus from the body, the better.

    Fortunately, we have medications such as the HCQ treatment or the Regeneron cocktail, and other drugs that can shorten the stay of the virus in the body, which presumably would prevent some of the damage done to the body.

    Unfortunately, the government does not have a policy of beginning treatment for the Wuhan virus as soon as a person tests positive, which is the best time to start treatment.

    I think people gamble with their long-term health if they don’t take steps to minimize the damage from the Wuhan virus. And even people with mild cases of the virus infection are still having detrimental effects from it long after they recovered from the disease.

    I heard a story this morning about a guy who had the Wuhan virus and was very sick. He said he was running a very high temperature for over a week and then was given the HCQ treatment, and he said within 24 hours his temperature broke and he was feeling much better.

    We need to have a policy of treating the Wuhan virus immediately upon a person testing positive.

    This may save us a lot of trouble in the future.

    The Wuhan virus is not your normal flu virus.

        • Your graph is meaningless as it purports to show infection fatality rates when we have no idea how many are infected.

      • “For those under 50 y/o that’s correct; it’s less deadly than flu.”

        Less deadly, but it has many more adverse side effects than other flu we deal with. You survive the Wuhan virus, but you are debilitated for possibly the rest of your life from the after effects. I repeat, the Wuhan virus is not your normal flu virus. And its debilitating after effects are showing up in people who had mild or no flue/respiratory symtoms. Large percentages of those who have recovered are having these problems.

        I see where Taiwan is starting a drug trial using hydroxychloriqune and administering the drug as a nasal spray for both preventing getting infected with the Wuhan virus and treating it after infection..

        I see where a study has declared that Remdesivir is not effective against the Wuhan virus.

        If that’s the case, then I suppose the Regeneron cocktail Trump got is responsible for his rapid turnaround.

        Previous studies claimed Remdesivir reduced the stay of the Wuhan virus in the body by about five days, which would be a considerable reduction in the time the virus can do damage to the body. I don’t know if this new study refutes that claim or not.

    • And the (Hydroxy)chloroquine acts as a zinc ionophore so that the zinc in the plasma can become intracelular. Quercetin appears to be a viable alternative where the quinine based drugs are being witheld.
      ACE-2 inhibitors appear to reduce zinc levels. https://heartmdinstitute.com/health-and-wellness/ace-inhibitors/
      Also, it has been suggested that the zinc deficiency caused by ACE- inhibitors results in a loss of taste. Is it just a coincidence that this is also a symptom of COVID-19?
      The treatment protocol HCQ/Zinc/Antibiotic that many Doctors have had succeess with in treating COVID patients should have been selected for the medical trials rather than a TOXIC dose of HCQ. If paracetamol was proposed as a cure, but the dose proposed by an Oxford professor was 20 tablets each day, it would have been dismissed before any lives were lost. Why did they poison people with toxic doses in the RECOVERY trial?

  18. How is the cross-reactive T-Cell defined and measured?

    Is it simply the bulk proliferative response of memory CD4+ T-Cells, or the response of a defined sub-population responding to a known specific MHC Class II-bound peptide epitope? And if the latter, do they measure specific cytokine responses as well as cell proliferation? These could have profoundly different effects on the immune response and eventual disease outcome.

    I am also much enjoying articles like this.

  19. Once again Biden makes the false statement that mask wearing can save 100,00 lives by the end of the year. This is about the 4th time that he has made this claim. According to current numbers and even going back retroactively to the beginning of September only around 84,000 people will die from the virus in these last 4 months of the year. So, obviously masks can not save 100,000 lives because only about 84,000 deaths will occur. between September and the end of the year. This shows just how bad Biden is with numbers, and also shows how badly he is being advised on this subject.

      • The daily death rate has been steadily declining since the second week of August. Over the last 3 weeks it has been around 700/day. Extending that out to the end of this year that means that there should be a max of around 50,000 deaths between today and January 1st. So for Biden’s claims to become factual the daily death rate would have to soar to around 2,500/day starting today and continuing through to January 1st. The total daily global, 7 day average death rate has been slightly over 5,000/day despite the record high new case numbers which was set yesterday at 418,000+. Daily new cases have now almost quadrupled since April. While at the same time the global daily death rate has remained in a range between 4,500 to 5,500 per day.

        Note that I did not claim that it was impossible. I am only stating that it is highly improbable. Therefore I consider it fear mongering on Biden’s part to continue to make such claims. If Biden had half a brain, then he should readily comprehend that the numbers given to him to repeat to the nation are greatly flawed.

Leave a Reply

Your email address will not be published. Required fields are marked *