Herd immunity is a theoretical construct. In practice herd immunity varies with viral load and a number of characteristics. There is no unique “number” for herd immunity. Also various definitions in the literature about what it means. The one I use is when the reproduction rate drops below 1 and the virus spread starts dropping off in a particular place. That’s the point I see as “herd immunity”. Herd immunity will be different in New York and in a remote rural setting.
My conclusion is that the pandemic is largely over in Sweden (has been over since mid-April) and any residual risk is comparable with that of common cold. Also USA is close to that stage – in a couple of weeks max.
It is true that if the Swedes (or Americans) who have not yet been infected rub shoulders in close proximity or talk loudly/ sing at each other for 1 hour, they will still get infected, but that’s not what most people do. Most of us remain at a good distance to each other and don’t loudly sing in each other’s face.
Except in prisons, choirs, meatworks and other high intensity environments, there is no evidence of this virus infecting more than 20% of the population simply because the viral load is insufficient or there is some innate/adaptive immunity – which is consistent with all previous pandemics. In none except Spanish flu actually infected more than 30% (which was around 35%). There are very few high intensity situations in real life.
After 8 months (this virus began in October 2019), all the necessary data are in. And all parts of the jigsaw puzzle fit. It is a very complex puzzle, though, and requires intensive study and an open mind – and a lot of questions. I studied a lot of advanced textbooks and published peer reviewed literature to form my view. Btw, Sunetra Gupta is no trivial scientist – being the Prof of theoretical epidemiology at Oxford – and she’s fully aboard this view (in fact she was one of the first to outline this view) – and I’m leaving out the super-brilliant Anders Tegnell here.
Basically, this is a far less dangerous virus than Asian flu, and has passed in many parts of the world. Its average death rate will end at around 500-600 per million across the world – which is peanuts in the big scheme of things. It will rank at the 5th or 6th position in the past century, starting with Spanish flu at the top. Never before did we lockdown, even during the Spanish flu.
This has been one of the most bizarre incidents in human history and a very bad portent for what governments will do when they get scared (irrationally) of “climate change”. The communists are in charge. Liberty and human dignity/choice is the last thing in their mind.
This is the post. And this is an email I sent out a moment ago to a number of people.
Things went pear shaped for all previous analyses and “models” when Stockholm’s data showed that it had crossed the herd immunity threshold in mid-April but serological studies showed far less than 20% people had antibodies at that stage. Everything had to fit this. So I became open to alternative explanations. I found some good leads in the work of Nicholas Lewis and Anne Marie Knott – despite potential questions about each approach.
I looked at the R0 concept closely and found it to be shockingly shoddy – with almost no possibility of getting a real handle on the actual number, which means herd immunity numbers floating around were simply speculative. Martin Kulldorff confirmed that: “No respectable epidemiologist would claim a certain percentage as needed for COVID-19 herd immunity. At this stage of the pandemic, we simply do not know what the number is”. I also studied some of epidemiological literature which is quite dismissive of the practical utility of this concept. I have come to the view that 90 per cent of epidemiologists in the public domain spout pure garbage – just like 90 per cent of economists and climate scientists. (Anders Tegnell and Johan Giesecke are among the few exceptions).
I then started looking into the actual spread of previous pandemics (flu) and found that most did not spread beyond 25%. Knowing fully well that this virus is a coronavirus, not flu, I still think these facts now all add up and suggest that this virus faces natural resistance. Immunological science explains why that might be so (innate immunity, cross-immunity etc.) – Btw, in this regard I’d like to share a recent study that SS Chakrabarti et. al of the Institute of Medical Sciences, Banaras Hindu University has sent to me (attached).
Good news: Sweden is now reopening high schools, colleges and universities for summer classes and the fall semester. Sweden has recognised that its pandemic is nearly over and life should be able to return to full normalcy within weeks.
And for India: Johan Giesecke was interviewed by Rahul Gandhi, a political leader from the ultra-corrupt Congress party. Leaving aside the question why Johan chose to speak with this super-corrupt man, his points are pretty much the same as our party has been advocating for three months: end India’s lockdown and focus on the elderly. I’ve extracted two minutes from the interview. (Johan, please do visit India but NOT on Rahul’s invitation. The man and his family have absolutely ruined India! – I’m fighting him and other corrupt socialist parties of India – politically – for the last 25 years. I’d be happy to connect you to really decent and respectable people from India).
This chart below is the final nail on the covid panic (and yet, this is a serious disease – I don’t mean to downplay its seriousness – see my text below).
This chart was created by someone who used Neil Ferguson’s model, applied it to Sweden, and then plotted actual deaths (see tweet).
And btw, my research (a couple of hours of googling) confirms that for the world as a whole, there’s been virtually no virus that has ever infected more than 25% per cent of the population. Spanish flu infected only 25% or so (see my tweet thread) – that that was without any vaccination; H1N1 (2009) infected 24%, As a general rule, pandemic influenzas only infect a quarter of the people (see New York government’s website).
This confirms the validity of Anne Marie Knott’s analysis. Not more than 20-30% persons in the average country are likely to get this coronavirus, no matter how hard they try. This proportion is also called the attack rate by some epidemiologsts (e.g. Encyclopedia Britannica), but other epidemiologists use a different meaning for attack rate (the number of persons one infected person can infect), so let’s just call this the infection rate.
What explains this huge gap – why don’t the other 70-80% of the people get infected? The innate immunity issue is very significant here (and it varies for each virus), and the viral load factor. Viral loads are low in most adult interactions and probably highest in pre-school centres, but children seem to have innate immunity for this virus (something for future researchers to explain). In elders innate immunity decays rapidly – therefore two-thirds of Kirkland Life Care Center nursing home’s residents caught the infection. The 25% infection rate is only an average.
Now coming to Sunetra Gupta’s analysis that there will be no second wave in some places.
From the Spanish flu example (for which there was no vaccine), we see that herd immunity for such viruses is generally around 25%. The estimate of 60% bandied about by “experts” is absurd, to say the least. For COVID, HI levels should be in the same range, i.e. 20-30%.
Antibody figures in parts of UK and Sweden are close to 20% (or slightly more). And we know that the actual extent is likely to be higher since not everyone produces measurable antibodies. This confirms that the further spread of this virus in these countries is going to be extremely slow – close to non-existent. Therefore Sunetra Gupta is correct.
The basic point is that the initial modelling was absolutely off the charts. Neil Ferguson (copied into this email) might wish to publish a public statement withdrawing his extreme estimates.
I’ll do so some further work and write about it in next TOI blog post over the next few days. Happy to have any thoughts/ inputs to this analysis, so that I don’t make fundamental mistakes!
Following entry into the respiratory tract and infection of predominantly epithelial cells, viruses trigger the innate immune responses including the inflammatory response.
Neutrophils enter the lung parenchyma within hours of infection, followed by monocytes/ macrophages, natural killer (NK) cells and then T cells within a few days of infection. The T cell infiltration peaks at 7 days post-infection, correlating with viral clearance from the lung. Neutralizing anti-bodies are also present around 7 days post-infection, and are maintained in the host as a first line of defence against re-infection.
The innate immune cells elicit an early anti-viral response following recognition of the pathogen by pattern recognition receptors including Toll-like receptors (TLRs) and RIG-like receptors. The engagement of these receptors induces signalling cascades that generate type I interferon (IFN) and pro-inflammatory cytokines. These molecules control the infection by mechanisms of viral cleavage and inhibition of viral fusion, replication and translation, by activating cytolytic cells and stimulating humoral factors including acute phase proteins, defensins, collectins and complement proteins. However, as these responses can lead to immunopathology in the lung mediating the morbidity and mortality of respiratory viral infections, they require immune regulation. [source]
Innate immunity comprises a suite of individual defenses against pathogens that is genetically predetermined and that ensures immediate protection without requiring prior stimulation and subsequent reactive response (Rumyantsev, 1983; Soosaar, 2005). Innate immunity is a general biological principle that provides relevant antimicrobial defense to all types of living beings, including humans (Fig. 3). This type of resistance is of primary importance not only in its phylogenetic origins, but also for its contemporary significance (Rumyantsev, 1983, 1998; Kaufmann et al. 2002). Innate protection factors develop during ontogeny without interaction with any particular parasite or parasitic product. They are inherent and present in the body before attack by disease-causing agents. The manifestations of innate immunity can be observed in species, populations and individuals, as well as in cells and subcellular structures. [Source]
The nature of such innate insusceptibility remains undiscovered and the true number of susceptible individuals among humankind elusive. The mainstream of immunology has not been involved in this kind of immunity. Therefore, nobody can predict today which kind of influenza virus could induce the next pandemic among humans, or where and when such a pandemic might occur. [Source]
Species and individual diversity in genetic immunity to many infections is already a widely known fact. For a long time, however, this phenomenon was neglected by both immunologists and epidemiologists, although regarded as essential (Boyd, 1966; Kaufmann, 2002). Near the end of the last century, that situation began to change (Rumyantsev, 1983, 1998; Bieniasz, 2004; Kimman, 2001; O’Brien & Dean, 1997). It was discovered that this kind of immunity is determined by genetically programmed and very specific constitutional features of the individuals, populations and species. [Source]
Innate immunity is a pattern recognition mechanism – act on a wide range of viruses: a non-specific system.
There are three types of cells in the innate immune system. 1. Sentinel cells in tissues: dendritic cells, macrophages and mast cells 2. Circulating phagocytles and granulocytes: neutrophils, monocytes and eosinophils 3. Lymhpocytes – mainly the NK or natural killer cells.
A word about the lymphocytes: There are two other types – the T lymphocytes and B lymphocytes, which are part mainly of the adaptive immune system.
Mammalian cells have evolved conserved pattern recognition receptors (PRRs) that sense pathogen associated molecular patterns (PAMPs) derived from viruses, bacteria and parasites (31–33). Following virus infection, infected cells initiate signaling events that induce the expression of antiviral and pro-inflammatory cytokines (33–35). Antiviral cytokines, such as interferons (IFNs), activate the expression of IFN-stimulated genes (ISGs) that inhibit virus replication through different mechanisms [Source]
Emerging bat-borne viruses, such as coronaviruses that cause SARS and MERS inhibit innate antiviral responses in the infected host while inducing a strong pro-inflammatory cytokine response that is associated with immunopathology and significant morbidity and mortality [Source]
SIGNALLING NK CELLS
Interferons (Type I, being alpha and beta) are a cytokyne produced when a virus infects a cell. They percolate outside the infected cell and latch on to neighbouring cells, leading them into an anti-viral state. These interferons also signal NK cells to kill the infected cells.
NATURAL KILLER CELLS PLAY A KEY ROLE IN FIGHTING SARS-COV-2
INNATE IMMUNITY IS NOT JUST REACTIVE, IT IS ADAPTIVE AS WELL
It is crucial to note that “there is a growing appreciation that the adaptive and innate immune systems may have many similar characteristics.” [Clinical Immunology Principles and Practice, 4e by Robert R. Rich et al]
This suggests that those with prior exposure to coronaviruses (in common cold) are likely to have had stronger innate immunity. This is also the reason why “trained immunity” occurs, and virtually any live vaccine can trigger a wider innate immune response.
CORONAVIRUSES ARE GOOD AT EVADING INNATE IMMUNITY
The current coronavirus is pretty good at evading the innate immune system, unfortunately, [Source]
INNATE IMMUNITY AND CORONAVIRUSES
For many coronaviruses, there is no known mechanism of how they evade the host innate immune system. It is hypothesized that it is by either (1) actively producing IFN antagonist proteins, (2) using their own replicase proteins to modify host proteins or by (3) the formation of double membrane vesicles and compartmentalizing replication and perhaps other coronavirus RNAs. The use of double membrane vesicles could hide the RNAs produced by protecting them from the RNA sensing machinery. There may also be a role for N in shielding the viral RNAs from the dsRNA and ssRNA sensing pathways. Many of these possibilities are being actively investigated. [Source]
coronaviruses are RNA viruses that replicate in the host cytoplasm and evade innate immune sensing in most cell types, either passively by hiding their viral signatures and limiting exposure to sensors or actively, by encoding viral antagonists to counteract the effects of interferons. [SOURCE]
Innate immunity is considered as the first line of defense against invading pathogens. The cells engaged in the innate response include phagocytic cells (monocytes, macrophages, and neutrophils), natural killer (NK) cells, and other cells releasing inflammatory mediators (basophils, eosinophils, or mast cells). During the development of an innate immune response, neutrophils and macrophages play an essential role in the elimination of microbes using various mechanisms, including the production of reactive oxygen species (ROS). In addition, this frontline protection is supported by NK cells guarding against infections and tumors (Delves and Roitt 2000). [Source: Immunomodulatory Role of Vitamin D: A Review – Agnieszka Skrobot et. al]