Study: Common Colds Train the Immune System to Fight Covid-19

Coronavirus disease cells, 3D rendering. new 2019 Novel Coronavirus (COVID-19) infection outbreak occurs from Wuhan, China

Guest essay by Eric Worrall

h/t Craig; A new study has been published which suggests some common cold strains have enough in common with Covid-19 that infection with those common cold strains can train your body to fight off Covid-19.

Exposure to common cold coronaviruses can teach the immune system to recognize SARS-CoV-2

Media Contact

Gina Kirchweger
gina@lji.org
858-752-6640

Researchers caution: It is too soon to say whether pre-existing immune cell memory affects COVID-19 clinical outcomes

LA JOLLA INSTITUTE FOR IMMUNOLOGY

LA JOLLA–Your immune system’s “memory” T cells keep track of the viruses they have seen before. This immune cell memory gives the cells a headstart in recognizing and fighting off repeat invaders.

Now, a new study led by scientists at La Jolla Institute for Immunology (LJI) shows that memory helper T cells that recognize common cold coronaviruses also recognize matching sites on SARS-CoV-2, the virus that causes COVID-19.

The research, published Aug. 4, 2020 in Science, may explain why some people have milder COVID-19 cases than others–though the researchers emphasize that this is speculation and much more data is needed.

“We have now proven that, in some people, pre-existing T cell memory against common cold coronaviruses can cross-recognize SARS-CoV-2, down to the exact molecular structures,” says LJI Research Assistant Professor Daniela Weiskopf, Ph.D., who co-led the new study with LJI Professor Alessandro Sette, Dr. Biol. Sci. “This could help explain why some people show milder symptoms of disease while others get severely sick.”

“Immune reactivity may translate to different degrees of protection,” adds Sette. “Having a strong T cell response, or a better T cell response may give you the opportunity to mount a much quicker and stronger response.”

The new work builds on a recent Cell paper from the Sette Lab and the lab of LJI Professor Shane Crotty, Ph.D., which showed that 40 to 60 percent of people never exposed to SARS-CoV-2 had T cells that reacted to the virus. Their immune systems recognized fragments of the virus it had never seen before. This finding turned out to be a global phenomenon and was reported in people from the Netherlands, Germany, the United Kingdom and Singapore. 

Scientists wondered if these T cells came from people who had previously been exposed to common cold coronaviruses–what Sette calls SARS-CoV-2’s “less dangerous cousins.” If so, was exposure to these cold viruses leading to immune memory against SARS-CoV-2?

For the new study, the researchers relied on a set of samples collected from study participants who had never been exposed to SARS-CoV-2. They defined the exact sites of the virus that are responsible for the cross-reactive T cell response. Their analysis showed that unexposed individuals can produce a range of memory T cells that are equally reactive against SARS-CoV-2 and four types of common cold coronaviruses. 

This discovery suggests that fighting off a common cold coronavirus can indeed teach the T cell compartment to recognize some parts of SARS-CoV-2 and provides evidence for the hypothesis that common cold viruses can, in fact, induce cross-reactive T cell memory against SARS-CoV-2.

“We knew there was pre-existing reactivity, and this study provides very strong direct molecular evidence that memory T cells can ‘see’ sequences that are very similar between common cold coronaviruses and SARS-CoV-2,” says Sette.

Looking closer, the researchers found that while some cross-reactive T cells targeted the SARS-CoV-2’s spike protein, the region of the virus that recognizes and binds to human cells, pre-existing immune memory was also directed to other SARS-CoV-2 proteins. This finding is relevant, Sette explains, since most vaccine candidates target mostly the spike protein. These findings suggest the hypothesis that inclusion of additional SARS-CoV-2 targets might enhance the potential to take advantage of this cross reactivity and could further enhance vaccine potency.

###

The study, “Selective and cross-reactive SARS-CoV-2 T cell epitopes in unexposed humans,” was supported by the National Institutes of Health’s National Institute for Allergy and Infectious Disease (AI42742, AI135078, UCSD T32s AI007036 and AI007384), National Institutes of Health contracts Nr. 75N9301900065 and U19 AI118626, and the John and Mary Tu Foundation.

Additional study authors include Alba Grifoni, Alison Tarke, John Sidney, Sydney I. Ramirez, Jennifer M. Dan, Zoe C. Burger, Stephen A. Rawlings, Davey M. Smith, Elizabeth Phillips, Simon Mallal, Marshall Lammers, Paul Rubiro, Lorenzo Quiambao, Aaron Sutherland, Esther Dawen Yu, Ricardo da Silva Antunes, Jason Greenbaum, April Frazier, Alena J. Markmann, Lakshmanane Premkumar, Aravinda de Silva, Bjoern Peters and Shane Crotty.

DOI: 10.1126/science.abd3871

About La Jolla Institute for Immunology

The La Jolla Institute for Immunology is dedicated to understanding the intricacies and power of the immune system so that we may apply that knowledge to promote human health and prevent a wide range of diseases. Since its founding in 1988 as an independent, nonprofit research organization, the Institute has made numerous advances leading toward its goal: life without disease.

Source: https://www.eurekalert.org/pub_releases/2020-08/ljif-etc080320.php

The abstract of the study;

Selective and cross-reactive SARS-CoV-2 T cell epitopes in unexposed humans

Jose Mateus, Alba Grifoni, Alison Tarke, John Sidney, Sydney I. Ramirez, Jennifer M. Dan, Zoe C. Burger, Stephen A. Rawlings, Davey M. Smith, Elizabeth Phillips, Simon Mallal, Marshall Lammers, Paul Rubiro, Lorenzo Quiambao, Aaron Sutherland, Esther Dawen Yu, Ricardo da Silva Antunes, Jason Greenbaum, April Frazier, Alena J. Markmann, Lakshmanane Premkumar, Aravinda de Silva, Bjoern Peters, Shane Crotty, Alessandro Sette, Daniela Weiskopf

Many unknowns exist about human immune responses to the SARS-CoV-2 virus. SARS-CoV-2 reactive CD4+ T cells have been reported in unexposed individuals, suggesting pre-existing cross-reactive T cell memory in 20-50% of people. However, the source of those T cells has been speculative. Using human blood samples derived before the SARS-CoV-2 virus was discovered in 2019, we mapped 142 T cell epitopes across the SARS-CoV-2 genome to facilitate precise interrogation of the SARS-CoV-2-specific CD4+ T cell repertoire. We demonstrate a range of pre-existing memory CD4+ T cells that are cross-reactive with comparable affinity to SARS-CoV-2 and the common cold coronaviruses HCoV-OC43, HCoV-229E, HCoV-NL63, or HCoV-HKU1. Thus, variegated T cell memory to coronaviruses that cause the common cold may underlie at least some of the extensive heterogeneity observed in COVID-19 disease.

Read more: https://science.sciencemag.org/content/early/2020/08/04/science.abd3871

Obviously if this cross-over memory effect is confirmed, it must be limited in some way, otherwise middle aged and old people who have the greatest exposure to different common cold strains would be more immune to Covid-19.

106 thoughts on “Study: Common Colds Train the Immune System to Fight Covid-19

  1. I think young children and their parents have the greatest exposure to the common cold (never sick until I had two little kids). Maybe why kids seem less affected by covid? Speculation but interesting nonetheless.


    • Health authorities in several federal states have urged parents to isolate their children from the rest of the family in case of suspected corona. If this is not done, the authorities even threaten to temporarily take their children away from the parents.

      An order sent out by several health authorities in July has been sharply criticised by parents’ associations and parents.

      As the “Neue Westfälische” reports, the public health offices of the Offenbach and Karlsruhe districts had ordered parents to isolate their children from the rest of the family if there was suspicion of a corona infection.
      “Your child must avoid contact with other household members in the household by ensuring that they are separated in time and space,” says a letter from the Offenbach district, a copy of which was published by the nationwide initiative “Families in Crisis”. “If possible, your child should stay alone in a room separated from other household members.”
      In addition, the authorities threatened to separate the children from their parents in the event of an offence and to place them in a designated facility for the duration of the quarantine. The recipients of the letters are the parents of children aged between three and eleven years.

      Child protection agency speaks of “psychological violence” against children
      As reported by the Protestant Press Service (epd), the city of Bruchsal had also sent a similar order. Among other things, parents were requested to have their child wear a mouth and nose protector at home if he or she has contact with other people.

      The co-founder of “Families in Crisis”, Diane Siegloch, explained to the epd that some parents therefore only let their children walk around wearing masks. For fear of being reported by neighbours to the relevant authorities for any violations, some families would also have shielded the windows with curtains.

      With reference to the order of the health authorities to isolate the children, Siegloch spoke of “mental cruelty” and acute “endangerment of the welfare of the child”. The German Child Protection Association also expressed criticism. “The situation of the quarantine is anyway very stressful for families, especially for children”, according to a press release of the organization. “To isolate children from their parents and siblings during this phase is a form of psychological violence.”

      The measures envisaged by the health authorities are “disproportionate and unacceptable”. In addition, families are made insecure by the “threat of the sharp sword of removal and placement in an isolation ward […]”.

      District defends itself against criticism

      The district of Offenbach reacts to the criticism with a statement and explains that the formulation of the order has led to misunderstandings.

      The means of coercion listed in the order “must first be threatened as a possible legal consequence in order to be able to be determined if necessary”. This is a legal necessity and also applies to all further measures.

      As the Circle further writes, the forced isolation of children only results from the general requirements for quarantine within the framework of the Infection Protection Act.

      The requirements of the law “must, however, be reconciled on the second level with the reality of the lives of those affected”. Various factors would play a role here.

      With regard to children, the measures must of course also be appropriate to their age and development. For this reason, employees of the public health department would also hold talks with affected families in order to clarify which of the quarantine regulations could actually be implemented in each case.

      “It is by no means a question of […] simply separating children from their parents and siblings completely, but rather – where possible and justifiable – to find alternatives in daily contact with each other,” the statement says.

      For example, a mother of two children, one of whom is in quarantine, could certainly continue to read to both of them. “However, at this point, one can consider whether both children really have to cuddle up in the same bed for an hour during this time.

      Translated with http://www.DeepL.com/Translator (free version)

      German source GMX

      So far about non infected children.

      • Really scary how the authoritarians come out of the woodwork at times like this. We must push back against these “moral busybodies” and not accept their fearful pronouncements.

      • The communists have long sought anyway they could to separate children from parents. All the better to indoctrinate the next generation.

        • Not just the communists – like in Animal Farm where the litter of puppies is raised by the pigs to be attack dogs. The muslims also raised captured children as warrior slaves – mamluk and janissaries. Steal the child from the family, and control them so they will fight for the ruling class. I wonder where the politicians got that idea?

    • Yes, this possibility has been around for months. The difference here is biochemical proof rather than simple speculation.

      Ever since european countries did NOT see the expected flair up as they unwound confinement regulations, it was obvious that the simplistic SIER type models were not correctly reflecting the reality of COVID-19 epidemic evolution.

      Once confinement ended ( or partially lifted ) there should have been an instant return to exponential growth patterns and this totally failed to materialise, despite continuing lower levels of infection throughout Europe.

      https://climategrog.files.wordpress.com/2020/08/2019-ncov-growth-italy.png

      Despite constant efforts in the press to create fear of a “second wave” or reanalyse the same low level case data as “clusters” to give the impression there is some new danger, it is clear that the classic simplistic models do not get us beyond the initial peak in infections.

      It’s great to see some proper scientific investigation of what is actually happening.

  2. This explains a lot of oddities.
    The very low first wave in Germany and Japan for example.
    Germany was overwhelmed by a cold wave in February.
    Everyone was ill.
    This helped to stop the first wave.
    Probably the same was in Japan.
    However, this immunity does not hold long.
    Look the second wave in Japan is already twice the first one.
    The same will be in Germany soon.

    • It means for SEIR epidemiology models, there is not just social in-homogeneities (as suggested and modeled by Nic Lewis and others), but also individual immunological in-homogeneities in a large ppercentage (20%-40%, maybe 50%). Another way to say that, is not everyone is naive, immunologically speaking, to this SARS-2 virus. All of which lowers the Herd Immunity (HI) threshold and stopping the epidemic spread of the virus.

      • My modified SEIR models do allow for individual immunological inhomogeneities as well as social connectivity inhomogeneities. They do so by assigning a selected probability distribution to individual (biological) susceptibility to infection, with a substantial proportion of the population being assigned a very low susceptibility.

    • If, as the researches found and speculate that, 40% – 60% have T cells that can recognise Covid-19 that would seem to suggest that this immunity is reasonably long lasting rather than ‘does not hold long’, wouldn’t it?

      • That is what T-cells are good at –long-lived immunity. Long after the IgG antibodies have disappeared from the blood (a few years usually). We know this from Smallpox vaccination studies and Yellow Fever vaccinations. The antibodies disappear within a few years, but T cells to the virus can be identified 5 and 6 decades later. In other words, the person is reasonably well-protected from a severe re-infection of the virus or a closely related virus.

      • If it was long lasting and conferred substantial immunity older people would be less vulnerable. There must be some confounding factor.

        • T cell immunity wanes as we get older. Mostly related to “thymic involution.” Beyond 60 yrs old the T cell decline become markedly measurable in many people. This is also directly related to age associated cancer risk, tumor immunity is virtually completely mediated by T cells. (NK cells have some minor roles in early stage tumor surveillance)

          T cells unlike B cells have to go through a positive and negative selection process in the thymus before they mature to be released as circulating naive T cells in our bodies. The thymus cells that help T cells develop though begins to atrophy after puberty and by mid 50’s is mostly “involuted” and gone by 55-60 yrs of age. No more new T cell production in the aged. All that is left is the few waning memory cells for any one specific virus (except for persistent viruses like CMV).
          But there are a few who age with a healthy T cell immune repertoire of naive cells to recruit to fight new infections. Thus has been show to be related to maintaining telomere lengths in their T cells. Genetics , life style factors and infections like Cytomeglaovirus (CMV, which many of us have) all play a role.

          • Right to the point, Alex! There clearly is an important factor in actual deaths from Covid-19, and it is accumulated co-morbidities, which agrees with older persons experiencing more difficulty with the virus. Watch the reporting on who succumbed to the virus and you will see an accompanying list of co-morbidities.

          • Most of them trace back to the root cause: insulin resistance (metabolic disorder) caused by the accumulative effect of eating the Western Diet for decades. Lots of clinical trials, biochemistry science and thousands of clinical outcomes. See list to verify at the end of this.

            The Cliff Notes: The Western Diet creates chronic low grade inflammation and hyperinsulimia that wear down the bodies normal chemistry including dramatic decrease in the functioning of the immune system. This is the highest risk factor for nearly all the co-morbidities of poor outcomes from CV-19 – obesity, type 2 diabetes, heart disease, dementia, poor immune system response. Add in the overwhelming use of statins which dramatically decrease the primary immune systems building blocks (cholesterol) and it’s the root cause of elder deaths from CV-19.

            And it’s easily reversible. For the curious, browse videos and their links to Pubmed:
            https://www.youtube.com/virtahealth
            https://www.youtube.com/c/AdaptYourLife/videos
            https://www.youtube.com/user/KenDBerry
            https://www.youtube.com/user/annettebosworthmd
            https://www.youtube.com/watch?v=wG2GKEFywFs

            some starter books to browse (Amazon, other):
            Eat Rich, Live Long – Cummins, Dr. Gerber
            Anyway You Can – Dr. Bosworth
            Deep Nutrition – Dr. Shanahan
            The Big Fat Surprise – Teicholz
            The Obesity Code – Dr. Fung
            The Complete Guide to Fasting, Dr. Fung
            A Statin Nation – Dr. Kendrick
            Wheat Belly – Dr. Davis

            Certain foods are highly addicting (see above ref brain chemistry and involvement of the same areas as opioids). You can break the habit but it does take some work if one wants to avoid a premature death.

          • “cedarhill August 7, 2020 at 5:07 am” – I’d add Dr Barry Sears and his Zone Diet to your list.

        • As we age the thymus decreases in size along with t-cell production. Also, zinc is essential for t-cell production, and zinc absorption decreases with age. Another possibility for low zinc in the aged is chronic inflammation that causes serum zinc to be non-bioavailable because it remains bound to it storage/transport protein metallothionein due to insufficient selenium.

        • Plus another possible confounding factor: older people tend to catch fewer colds. It may be the case of course that the only colds they (we!) are vulnerable to are those caused by the four coronaviruses, 229E, NL63, OC43, and HKU1. Or maybe not. I don’t know if there’s any research out there to clarify this one way or the other.

        • Either that, or it just means that the immune system, along with pretty much everything else in the body, degrades as one gets older.

        • What Joel O’Bryan said, immune systems age too – even vitamin D synthesis declines with age, but also healthy diet, exercise and avoiding avoidable co-morbidities come into play.

          Quite possibly innate immunity responses to coronaviruses decline over time since last exposure, but I haven’t seen any data to support that hypothesis, just speculation. The sad truth seems to be that we have very little good data on immunity for most of the hundreds of viruses that plague us. No one really cared much before except for the real killers like Yellow Fever (and my impression is that the 10 year limit on that vaccine is just a conservative guess).

      • Not nearly as fast as the typical B-cell/plasma cell antibody production, but it stills fades with age.

        • So, is there anything we can do to maintain our T cell activity as we age? Supplements? Exercise? Social activity? Or is it just luck-of-the-draw?

          • you could vote agin Trump.

            this T cell thing is obviously his fault.

            i had blamed Bush in the past, but i’ve come around to recognize that it Trumps fault.

          • There’s some evidence that thermal hydrotherapy boosts the immune system. Since the Covid scare, I’ve been taking a 1- to 2-minute all-cold shower after every warm shower. Initially, it takes “nerves of steel” to begin doing this; but once it becomes a habit, I believe it can induce neuropeptides in a physiological cascade resulting, in a mind-over-body effect. — i.e. If I have the will and stamina to continue doing this ‘torture’ to my body, I should be able to successfully handle the onslaught of any cold or flu virus.

    • Agreed.
      Our R0 is over 1 now


      new inf. R0
      642 0,88 7/20/20
      403 0,81
      580 1,05
      672 1,44
      818 1,50
      372 1,58
      409 1,20
      638 0,97
      572 0,81
      860 1,02
      842 1,28
      1.012 1,47
      412 1,57
      385 1,07
      858 0,92
      760 0,73
      1.024 0,97
      1.106 1,41
      686 1,34 - today, still incomplete, may doubble 'til the night
      </codeY

  3. oh, oh, Twitter will ban this as soon as they see it. Too many facts and way too much logic! Endangers the keep schools closed and mail in ballots farce.

    • The Social mafia godfathers will have a heart attack (or as they call it – die of Covid)

  4. The bottom line is antibodies to SARS-CoV-2 Spike (S) protein are just correlates of immunity. If you have them, it correlates to your having (some) immunity to that speciufic pathogen. But their absence conversely says nothing about cross-reactive T-cell immunity from closely related viruses that may exist.

    If someone has IgG specific to the SARS-2 S-protein then that means CD4+ T-cells participated (“licensed” is the immunologists’ terminology) in the class switch (from IgM to to IgG) and affinity maturation/variable region hypermutation (affinity maturation selects for very high affinity antibodies that clamp like a vice onto the S protein parts to keep it from molecularly flexing and thus preventing the necessary conformational changes it needs to fuse for entry to the cell’s cytosol) that is necessary for B-cells to go on to produce plasma cells that crank out massive amounts of Spike protein-specific IgG antibodies to neutralize the free virus circulating in the blood and tissues. But free virus particles floating in blood, lymph, and tissues spaces is just part of the infection story. With viruses, the real infection is happening inside cells where antibodies can not reach. And you cannot understand what is happening inside the cells without a decent background in cellualr and molecular biology. And that is usually 3rd and 4th year college biology stuff or years at the graduate/post-graudate level to really begin to know where the science is on these issues.

    So antibodies are just half the battle. And in defeating viruses floating outside cells is just winning half the battle while getting killed inside cells and is like being half-dead. You’re still dead. You need T-cells to kill infected cells before and while they are making virus. Many viruses can and do directly infect adjacent cell-to-cell via membrane fusion and the inter-cellular pores that many tissues have to communicate between cells. Antibodies can’t touch that.

    With SARS-2, it appears CD4+ T cells have a predominate role in this cellular cytotoxicity (cellular killing of infected cells) with CD8+ T cells playing a minor role. I suspect CD8+ T cells are probably just as important in cytotoxicity as CD4+ T cells, it’s just that the lab assays being used right now are biased to finding CD4+ T-cells specific to the SARS-2 epitopes being “scanned” for T cells engagment and killing activity. (An epitope is a snippet of the virus’s own digested proteins from inside the cell usually) An epitope is a string of virus-derived amino acids (aa), usually 8-10 aa long for CD8+ T-cells, or 11-15 aa long for CD4+ T-cells) held in the clamps of a MHC molecule (major histocompatibility complex architectures is an entire 2 semester graduate level study on its own) on the surface of all nucleated cells for the T-cells to “taste” with a T-cell receptor (TCR). And like OJ and the glove, if it matches sufficiently, the -Tcell stays and engages and kills that cell with a whole host of tools that is anther entire semester of study. But if it (the TCR to peptide:MHC binding story, very complex subject) don’t fit, you must acquit. The T-cell, like the roving sentinel, goes on its way looking and scanning for new targets to taste.

    All virus molecular machinery have very specific amino acid (aa) patterns that T-cells can thus recognize in the context of a cell’s MHC surface presentation, sort of like showing your credentials to the cops to go on your way. If something is amiss, the cop stays and keep interrogating, same with T cells. The aa peptides strings come from the proteins of the virus molecular machines that are very difficult for the virus to mutate without severe fitness impacts to the virus ability to do what it has to to replicate, thus many aa epitopes tend to be highly conserved across the same family of viruses.

    But T cell immunity is very important to eliminating viruses, and cross reactive T cells have been shown in many other settings to help fight similar viruses (like in influenza A and B) and protect the host with an anamnestic response even though their immune system has never seen that specific virus.

    That is the rub. No one can predict a priori to any real accuracy, whether a T cell will find a closely related epitope “tasty” or not. The actual experiments with live cells and peptide (amino acid) epitopes has to be conducted. Very time consuming.

    This is why antibody testing for SARS-2 can find people who’ve been recently infected and cleared the virus, but there also likely many who were exposed to the virus and the T-cells fought it off before the B cell-antibody response came to play. But they may still be just as immune. Plenty of evidence of this kind of cross protection in other viruses and viral families.

    So just because someone doesn’t have antibodies doesn’t mean they aren’t protected from SARS-2. And this may be what is happening in children, why so many never have symptoms and their encounters with the virus is so mild is so many. Their T cells, as youngsters with long telomeres, may be much better at multiplying and differentiating to the various forms needed for an effective systemic response and fighting off the virus before they get overtly “sick” and make antibodies. A mild fever may be the worst symptom most children with SARS-2 get. The fever is good. Unless it is high, above 102F, probably best to let it run its course without aspirin or NSAIDS. Children with high fevers above 102F should immediately and always lead to rapid parental/guardian consultation with trained medical professionals.

    If the child makes antibodies, it means they were shedding virus at some point. This doesn’t appear to be the typical manifestation though with mild infections in children. Their really good T cell response protects them quicker than adults. as we know the at T cell immunity ages the fastest as we age. Much faster decline than B cells and the innate immune cells actually.

    So much still we do not know. But we do know that T cells are key to fighting this virus. And there has been too much focus on simply antibody production with SARS-2.

    • You know that childs fever is often higher than adults fever.
      What should not be done is to give meds to reduce fever, cold poultices on front or around feets is aleays the better way.

      I remember as as child, I got measles, the doc sais, don’t try to lower the fever, in contrast, make all to increase it, give a second blanked, encose the child (me) in, give a lot to drink, look at the thermometer, only in case of surpassing the 40.5°C make poultices and he will come to have a look.
      He was one of the few prescribing sunlamp therapy to children, that was in the early sixties last century.

      He had a nice picture in the waiting room:
      “Loved, lived, smoked, drunk, and then hope all from the doctor”
      “Geliebt, gelebt, geraucht, gesoffen,
      und dann alles vom Doktor hoffen”
      The picture remembered a Roman revelry, but was s.th. of the 20ies in Germay.

      • The Intro to their article (June Lancet article) suggests that Sars-2 is completely unique and that most humans need to get it to become immune. This was understood to be wrong even a few months ago when this came out. But, interesting to know that children have this strong immune response.

  5. mods, a longish comment of mine stuck “in moderation” because I can’t discuss T cell immunity without using the K word. That k-word moderation filter is really annoying.

    Any help is appreciated.

    Joel

    • Joel, when this happens you can still see what you posted. I suggest you copy-paste and repost having replaced the K-word with ki11 ( ki + eleven ) or similar.

      That will post in the normal way and when the mod gets to look at the held post, he will see you already reposted and bin it.

      That’s the way I usually catch it.

    • Joel,

      Thank you for taking the trouble to explain that.

      I’ll need to re-read it to grasp it properly – my biology A-level was a loong time ago…

      But thanks is the only assistance from me.

  6. now the count will be based on death certificates! and how reliable will they be?

    7 Aug: Metro UK: Nearly 4,200 deaths could be wiped from official statistics due to counting error
    by Edna Mohamed
    Around 10% of coronavirus deaths recorded in England – almost 4,200 – could be wiped from official records due to an error in counting, a review has found.
    Last month, Health Secretary Matt Hancock ordered a review into the way the daily death count was calculated in England citing a possible ‘statistical flaw’.

    Academics found that Public Health England’s statistics included everyone who had died after testing positive – even if the death occurred naturally or in a freak accident, and after the person had recovered from the virus…
    Numbers will now be reconfigured, counting deaths if a person died within 28 days of testing positive much like Scotland and Northern Ireland…

    Professor Heneghan, director of the Centre for Evidence-Based Medicine at Oxford University, who first noticed the error, told the Sun: ‘It is a sensible decision. There is no point attributing deaths to Covid-19 28 days after infection…
    https://metro.co.uk/2020/08/07/nearly-4200-deaths-wiped-official-statistics-due-counting-error-13094465/

  7. As it is impossible to avoid all viruses, it makes obvious sense that the immune system needs its regular exercise to cope with the regular viral mutations that float around. An artificially microbe-reduced or microbe-free environment allows the immune system to get lazy. When this artificial situation returns to normal, people will find themselves getting sick constantly.
    Why not make everything totally sterile all the time like the boy in the bubble the diaper-soiling brigade will bleat. Even that did not work, so it is impossible, to say nothing about being totally impractical.
    As it is, here in the antipodes, it is the middle of winter. Today is a cold wet miserable day after 2 days of blazing sunshine and warm weather in the coldest part of the winter. I should normally have a bit of a sniffle with this sort of weather, but the artificial environment is depriving my immune system of exercise.

    • high treason,
      That would also be the reason that mask mandates and lock downs don’t work! We need to be exposed to the Chi-Com 19 Virus, slowly if possible, to develope our own immunity; only those with high risk co-morbities and of advanced years should be concerned with PPE. Obviously, care givers and those who are spending long periods of time around sick or infected individual should as well. (I shouldn’t even have to write the previous sentence; but, in this time of hysteria, logic and facts seem to be lacking in many!)

      The best antidote for this scamdemic seems to be proper nutrition, healthy activity and the HCQ/AZ/zinc regimen or something similar as a prophylactic. Lockdowns and mask mandates do NOTHING for our immune system and they wreak havoc on our economic and political system.

      If Trump wins in November and there is a functioning government this politicization of a deadly virus will go down in history as the most harmful and egregious act of a US political party! The DemoKKKrats have willfully killed thousands of Americans to score political points and to try and drive Trump from office. And they never could have created this mess without the connivance of the LSM urinalists!

      • Abolition Man August 7, 2020 at 3:27 am
        high treason, That would also be the reason that mask mandates and lock downs don’t wor
        ——————-
        I assume you have been attending all the covid19 parties that you can? Why take hcq when you really need to catch this flu like covid 19 so you can get on with your life.

        just don’t come crying when you suffer lifetime heart/lung/muscle/smell/taste problems. Should you die then please let me know!!

    • Lucky so-and-so!

      Actually, for me my allergies have been going nuts! With all the rain we’ve had in my general area, mold spores and fungus spores are all about. We’ve seen more different types of mushrooms in my area than I’ve ever seen (no Morels tho).
      And while I’ve had a couple of flu-like days (in before the “official” SARS2 dateline), overall its been good for colds and such- mainly because the kids haven’t been in the schools picking up shared illnesses I imagine.

  8. “Obviously if this cross-over memory effect is confirmed, it must be limited in some way, otherwise middle aged and old people who have the greatest exposure to different common cold strains would be more immune to Covid-19.”

    Maybe older people get also more vaccinated and this prevents T cells from training to fight the common flu.

      • The Dark Lord
        August 7, 2020 at 1:03 am

        In contrary,
        Immune response upgrades and grows with age,
        else your “battery” will fade pretty quickly.

        And vaccines drill the immune system to a fairly basic minimal immune response for not known yet diseases, by the immune system,
        else interfere and jeopardize the immunity and immune response.

        cheers

  9. Eric, Respiratory Syncytial Virus, RSV, is a prime suspect.Most kids catch it by age three with almost zero symptoms and carry antibodies for five or six years then they catch it again because of the petrie dish conditions.Young adults continue this immunity because of partying until they grow up or pair off. Septuagenarians on the other hand end up in hospital as I did with severe heart rhythm problems.Many don’t survive it because of deficiencies of essential endogenous nutrients, so no immunity. So what now?

    • What now? In the UK deaths are below the long term average for the sixth week in a row. That’s what happens now – those who were going to die this month, died a few months early, so now we’re going to see a period with fewer deaths than would normally be expected.

  10. It’s cowpox/smallpox all over again?

    Anyway as has been noted, a virus that puts its hosts into isolation, intensive care, and kills them is not a very successful virus in Darwinian terms.

    Some readers of a certain age and of European origin, may recall the demise of the English Elm, struck down by that foul political invention (for all diseases are, by modern definition, political inventions, are they not?), Dutch Elm Disease, that left no Elm tree upstanding whatsoever apart from a few key specimens that were inoculated.

    Now on the hedgerows round my house, there were once many elms. And for the last 20 years any elm that seeded, or spring up from suckers, grew to at most 12 foot before the fungus killed it. There are examples all around.

    Until the last few years when sucker and self seeded elms have once again exceeded that figure, and there is no sign of disease. The fungus killed it’s own food source nearly completely , and died.

    Contrast that with the Birch Fungus, that whilst it does result in early demise of birch trees, does so only in later life.

    For whatever reason, COVID19 is selective in who gets sick and who dies. It is to be assumed that those susceptible will die, or go into quarantine and get better, and take the more deadly strains with them or develop immunity to them

    What will remain will be ‘just another cold’ , one suspects.

    • The pathogen that felled all the American hickory trees also claimed at least one human.

      H/t James Thurber.
      ========

  11. Sweden got herd immunity at a far lower rate on infection that the idiot BIG-BROTHER cult now controlling us ever imagined.

    The UK has had very much the same epedemic curve, as so is also very likely to have herd immunity.
    Some states in the US who had the peak some time ago are probably close to herd immunity.

    Given the huge loss of life and cost caused by the lockup, there should not be the slightest delay in returning to normal (albeit that the extremely vulnerable may THEMSELVES wish to isolate if THEY so wish)

  12. Sounds plausible, but what are the cross-reactive T cell levels in babies and children, who are not unusually susceptible to coronavirus?

  13. When I first started modelling the epidemic in January, I came across this figure which was that the virus could infect 80% of people. At the time I could find no scientific basis for this 80% figure and indeed I considered just setting it to 100% – meaning everyone was susceptible. But as it was part of the normal way of modelling, I eventually included it even though I couldn’t find any support for ti.

    What it meant was that “20% of people are immune to the virus”. But if 20% were immune, why not any other figure? So when the real figure from Sweden was looking less like 20% immune and more like only 20% were not immune, it didn’t seem a great change to me.

    But to the academics, who apparently picked this 80% figure out the air as the holy doctrine of epidemeology, it seemed to be an unquestionable part of their doomsday doctrine.

    • I wonder if it can be shown that Sweden has had more past Coronavirus infections than other countries?

      That data may already be available. Go for it.
      ===========

  14. Interesting. But, if the immune system is robust to begin with, then colds could be few and far between. Then too, it could be how much exposure you get. Perhaps it’s possible we can carry the cold virus without showing symptoms, in the same way that many carry the SARS-CoV-2 virus with no symptoms. So I think we first need a robust immune system, and memory T-cells work in conjunction with that. Then it comes back to having sufficient Vit. D, C, Zinc, etc., and as healthy a lifestyle as possible.

  15. First sentence is the most important:

    Researchers caution: It is too soon to say whether pre-existing immune cell memory affects COVID-19 clinical outcomes

    I would not bet on it that it protects from blood clotting and the immune system running wild as there are other pre-conditions and also genetic factors at play.

    Btw, COVID-19’s death toll in the US is hitting younger people on average than in Europe:

    https://www.economist.com/graphic-detail/2020/06/24/when-covid-19-deaths-are-analysed-by-age-america-is-an-outlier?fsrc=scn/fb/te/bl/ed/dailychartwhencovid19deathsareanalysedbyageamericaisanoutliergraphicdetail&fbclid=IwAR2J9ETA8oX39HVYHXUuxIa__7VqTzxfG3WDT589z04MPtbvMtLjBLv_7rg

    Median age is 48!

    So the plan “protecting the old, let the others go to work” will not work.

      • So at least 1/5 of the population in the US. Not great prerequisites for letting the virus run wild I would say. Overweight would be more than half the population.

    • People with a malfunctioning circulatory system, hypertension, heart disease, and increased cholesterol are at risk.

    • Clinical practice needs to be compared between countries. In other words, is there a correlation between intubations and deaths. I suspect the US intubates more because of its screwed up medical system and financial incentives to do so.

      btw, I looked at the VWF paper you linked to. I had already seen that because I wanted to find what you were talking about, and that was the only one I could find. But I concluded that couldn’t be the one because it doesn’t support what you say, i.e., that Von Willebrand Factor (VWF) is off-scale in non-ICU patients. Perhaps I’m not seeing what you’re referring to, but non-ICU patients’ VWF was 278% and ICU patients’ was double that at 565%. The non-ICU patients’ VWF level wasn’t that high (and certainly not off-scale) and is probably typical of other inflammatory conditions.

      So if anything, that paper supports my position that mechanical ventilation (MV) either causes hyper inflammation (which it can, even in healthy people) leading to systemic thrombosis, or it greatly exacerbates the inflammation of a typical respiratory infection (covid) thereby pushing the immune response into instability. Elevated VWF is not specific to covid; any inflammation can cause it to rise, including that caused by MV. In fact, MV upregulates IL-6, which can inhibit ADAMTS13 cleavage of VWF causing an increase in thrombotic activity.

      • You seem to have difficulties looking precisely at figures and reading texts carefully.

        I said some non-ICU patients had VFW activity that hits the upper limit of the scale and that is what the figure shows.

        The non-ICU patients’ VWF level wasn’t that high (and certainly not off-scale)

        Way higher than the ULN. Way, way higher.

        and is probably typical of other inflammatory conditions.

        That is only speculation and need to be determined.

        Anyway your statement that the coagulation is mainly induced by the use of ventilators is disproven by the data of the paper. It’s there already if you are ill enough to go the hospital.

        • You’re acting like you think only covid can cause elevated levels of VWF. Stress, exercise and any inflammatory condition can raise VWF. I’m not doubting that covid does raise VFW, because it is an inflammatory condition. But as far as I can tell there is no evidence that covid by itself raises VWF to the levels seen in intubated ICU patients. We need some data on what VWF typically is in other illnesses.

          • You’re acting like you think only covid can cause elevated levels of VWF.

            Bogus, I never said that anything like that. COVID-19 is just quite unique in its ability to push this mechanism in susceptible individuals until it crashes.

            I’m not doubting that covid does raise VFW, because it is an inflammatory condition. But as far as I can tell there is no evidence that covid by itself raises VWF to the levels seen in intubated ICU patients.

            That just shows your lack of understanding at which stage people are admitted to the ICU and ventilated. Low PaO2/FiO2 (usually <150) is the criteria here and before that happens something has to go on first. That just not happens out of thin air.

            People are collecting the data right now to show that worsening of the coagulation factors over time leads to admission to the ICU and is therefore predictive for clinical outcome.
            But there is data already that showed it was worse at the time of admission therefore before invasive ventilation compared to patients that did not have to be admitted to the ICU.

            https://link.springer.com/article/10.1007/s00134-020-06062-x?code=afba2dc4-923d-4edc-86eb-db01ae50ff50

            Many patients had also already acute renal failure at time of admission which is linked in other studies to thrombosis in the kidneys.

            https://www.kidney-international.org/article/S0085-2538(20)30369-0/fulltext?rss=yes

          • It’s like your basing your understanding of why patients are intubated on that Seheult video (or whatever his name is). That might be what’s done in his hospital, but in some hospitals a blood sat below a certain arbitrary level that can’t be maintained at 6 l/min O2 or less is reason to intubate. I’ve already provided evidence of that.

            Yeah I get that patients are dying of multi-organ failure from thrombotic microangiopathy, but that 2nd study doesn’t mention anything about those patients being intubated or not. So what was the point?

          • The PaO2/FiO2 as criteria for intubation or not is in the fricking NIH guidelines, Not only for COVID-19 but for ARDS as well. Do you think each hospital is making up their own standards out of doctor’s guesses?

            I’ve already provided evidence of that.

            No, you didn’t. Neither evidence nor “some” hospitals. Just hearsay and gossip.

            but that 2nd study doesn’t mention anything about those patients being intubated or not.

            If a condition is already there AT admission to the ICU it is NOT and CANNOT be caused by treatment in the ICU including invasive mechanical ventilation because the patient didn’t get any further treatment yet!

            What is so damn hard about understanding this?

          • The 2nd study mentions nothing about the patients’ conditions. You’re trying to assume from the 1st study that the patients in the 2nd study had the same numbers as in the first study. No evidence for that. That’s very sloppy thinking.

          • “COVID-19 is just quite unique in its ability to push this mechanism in susceptible individuals until it crashes.”

            I agree except for “until it crashes” because there’s no evidence for it. Those people are put on mechanical ventilation which greatly exacerbates the inflammatory pathways until they crash. Crashes from VILI (ventilator induced lung injury) are well known. They very well might not crash if kept off ventilators, which is what a lot of doctors are seeing.

            I keep hearing that we are intubating for sat. in 80’s-70’s immediately, instead of a trial of non invasive like high flow oxygen for fear of patients crashing… in 4 months, i am yet to see that crash.

            https://twitter.com/DFarcy/status/1282051526912024576

          • No, that’s how science works. There is never a study that proves it all in one, it’s pieces of evidence put together to build a picture of reality.

            All patients in the 2nd study with acute renal failure died from respiratory failure.

            So you suggest to be convinced clinicians should not put patients on ventilators when their PaO2/FiO2 ratio indicates that to try to safe their lives and let them die, then making autopsies to prove there is the same pattern without ventilators?
            That is what you implicate with your way of arguing.

            Well, then I hope you’ll never be convinced as that would mean clinicians wouldn’t try everything up their sleeve to safe a patient.

          • I agree except for “until it crashes” because there’s no evidence for it.

            Of course there is, I showed you studies where people died without ever being in touch with a ventilator. How did they die? Suicide by voluntarily stop breathing?

            You should pay more attention to the literature how ventilators can safe lives than what could be possible complications. There is ample of it.

          • Doctors are doing that very thing and keeping patients alive because of it. The doc in the link above had a patient show up with a sat of 64 (that’s a very low PaO2/FiO2), treated him with high flow oxygen and proning (no intubation), and the patient was discharged from the hospital after 8 days.

            So this claim that all patients will die if they aren’t intubated is just bullshit. Some patients do need intubation, but most don’t.

          • “No, that’s how science works. There is never a study that proves it all in one, it’s pieces of evidence put together to build a picture of reality.”

            That’s exactly how science works. But it’s not the way sloppy scientists work.

          • The doc in the link above had a patient show up with a sat of 64 (that’s a very low PaO2/FiO2), treated him with high flow oxygen and proning (no intubation), and the patient was discharged from the hospital after 8 days.

            There are also people who take globules and are cured from cancer but most just die, so what?
            Anecdotal evidence is not how science works. How many patients needed intubation later?

            Some patients do need intubation, but most don’t.

            Yeah? Is there any proof beside you claiming it like a clinical trial I wonder?

          • Here w/o messed up formatting:

            The doc in the link above had a patient show up with a sat of 64 (that’s a very low PaO2/FiO2), treated him with high flow oxygen and proning (no intubation), and the patient was discharged from the hospital after 8 days.

            There are also people who take globules and are cured from cancer but most just die, so what?
            Anecdotal evidence is not how science works. How many patients needed intubation later?

            Some patients do need intubation, but most don’t.

            Yeah? Is there any proof beside you claiming it like a clinical trial I wonder?

    • The US has a much lower extended family level than Europe, it is likely that in the US it has been much easier to isolate the elderly so they don’t get it in the first place. So its not a higher level of young dying from Covid but a lower level of elderly dying.

  16. herd immunity is when 50 to 83% of population become immune (assuming immunity is retained – not yet proven)

    Sweden with population of 10million would require 5million with acquired immunity c19 has Infection Fatality Rate (0.5% to 1%) so take ~0.6% . Deaths would be 30,000 actual 6,000 so no herd immunity

    USA pop 330million need 165million with immunity. This would get 1million deaths actual 160,000 so no herd immunity.

    • No kidding people are dying left and right from Covid now. On my walk into work I had to jump over all the piled up corpse.

    • Herd immunity occurs at whatever level of immunity in the population that kills of the virus. If it were a very similar virus to previous ones, it could be a few percent. If it were an entirely new virus with a very high level of transmission (i.e. a very long period when someone is infectious), it could be close to 100%.

      The virus has all but naturally died out in Sweden so it has herd immunity.

  17. Edward Jenner made the observations about conferred immunity against Smallpox by Coxpox the first effective vaccine. This does not surprise me at all. It’s possible why countries like Japan, South Korea and other Asian nations have not been so hard hit because they were more exposed to the SARS virus years ago.

  18. “These finding of cross-reactive HCoV T cell specificities are stark contrast to HCoV neutralizing antibodies, which are HCoV species-specific and did not show cross-reactivity against SARS-CoV-2 RBD (33–35). Based on these data, it is plausible to hypothesize that pre-existing cross-reactive HCoV CD4+ T cell memory in some donors could be a contributing factor to variations in COVID-19 patient disease outcomes, but this is at present highly speculative (36).”

    cross reactivity can in fact lead to worse disease outcomes.

    you.
    simply
    dont
    know.

    https://science.sciencemag.org/content/early/2020/07/15/science.abc8511

    • We do – Sweden shows us that herd immunity is achieved with a very low level of infection. That means most people were immune to it before this daft covidaphobia started.

    • Steven Mosher
      August 7, 2020 at 5:22 am

      you.
      simply
      dont
      know.
      ————–

      Fair enough Steven;
      which does leads to:

      they too
      simply
      don’t
      know

      Interesting point but wholly bollocks… in the part of “they”.

      cheers

  19. suddenly im pleased Ive caught nearly every cold going for decades;-)
    might be older ,but Ive had plenty of memory kicks for the system;-)

  20. Yup, this speculation that other coronaviruses may give partial immunity is one that I have had since March, or maybe since February.

    I’m glad it’s being studied and surprised it hasn’t been speculated more widely because it is eminently reasonable and furthermore engenders hope.

    Maybe I’ve just answered the question of my surprise.
    =========

  21. places where schools are closed and where some isolation is occurring will see less colds and flu since cross contamination from the infected is less. Children are particularly bad since classes require close proximity of others and class rooms are good incubation boxes. Since sending our children into the world we rarely get colds (and no longer get flu! ) Just like is and will happen with covid 19 wrt lockdowns and schools.

  22. That’s good, if true, but I’m skeptical. I’m 73 y/o and in fairly good health, but one of my weaknesses is susceptibility to the common cold. This past winter is one of the first winters that I didn’t catch a cold. If catching colds builds up immunity to covid-19, why doesn’t it build immunity to other coronaviruses?

    • Scepticism is good, but with Sweden, which didn’t lockup, peaking way below the level predicted (like an order of magnitude) and now having more of less finished, it is very clear that herd immunity comes at a much lower level than we were told. Indeed, so low that in most countries a vaccine isn’t needed , which is why there are big companies so anxious to avoid the public knowing that we don’t need a vaccine.

      As for coronavirus, the reason we keep getting it, is because it keeps changing, and the reason we don’t die, is because our immune systems are incredibly good at fighting off these viruses (much to the dislike of those trying to flog us a vaccine).

  23. Were they able to identify which strains of the cold virus was able to trigger this response?
    Aren’t there several million cold virus strains?

  24. The us military death rate is extremely low, 42,000 cases, 70 deaths. less then 2/10th of a percent, common flu levels or below.

  25. Dear Mr. O’Bryan,

    If exposure to “common cold” corona viruses confers long term immunity (via T-cell memory) to SARS-CoV-2, a novel and different strain, then why does exposure to older strains of influenza not also confer immunity to new strains of flu?

    Is it not well-established that vaccines for and/or exposure to last year’s flu do not immunize against this year’s new strain? Both SARS-CoV-2 and influenza are single-strand RNA viruses with aa epitope strings that ostensibly are difficult for the virus to mutate without impairing replication. Why the difference in acquiring long term immunity across strains of these two viruses?

      • They don’t? I heard (rumor) that there are 2 to 8 new strains of WuFlu already. Can you cite your source on slow mutation rates for corona viruses? This might be an important issue vis alleged vaccines.

        • Most probably what considered as mutations are detection of different values of quality of the same virus.

          Simply due to extra value added in the quality due to (re)production.
          Simply the save virus but better made through reproduction, stronger and more enduring.

          cheers

  26. This is the basis of the now-launched Russian vaccine.
    They have modified a cold adenovirus to look even more like covid19 than it already did.
    A smart approach to safety and efficacy – let’s see how it works (e.g. on Putin’s daughter).

  27. I have never had the “flu” that I know of and have never had a flu shot. I have not had a cold in over 9 years. I do have seasonal allergies. I did get a Pneumonia shot last March to help defend against common Pneumonia. I looked at is as an “arrow” in my immune system quiver. I am 74 and male

Comments are closed.