This article focuses upon the vaccine trials which have not set out to prove efficacy in preventing mortality or viral transmission, and on the reactionary "science" that broke out as the pandemic unfolded and has not been updated as things became clearer.
Product Type: Vaccine
Item Code (Source): NDC: 59267-1000
Ingredients: RNA ingredient BNT-162B2 (UNII: 5085ZFP6S) (RNA ingredient BNT-162B2 - UNII:5085ZFP6S)
Basis of Strength: RNA ingredient BNT-162B2
Strength: 0.23 grams in 1.8 millilitres
lipid ALC-0159 (UNII: PJH39UMU6H)
lipid ALC-0315 (UNII: AVX8DX713V)
POTASSIUM CHLORIDE (UNII: 660YQ98I10)
MONOBASIC POTASSIUM PHOSPHATE (UNII: 4J9FJ0HL51)
SODIUM CHLORIDE (UNII: 451W47IQ8X)
SODIUM PHOSPHATE, DIBASIC, UNSPECIFIED FORM (UNII: GR686LBA74)
SUCROSE (UNII: C151H8M554)
The Covid-19 pandemic created an immediate discussion regarding the prospects for vaccination against the virus responsible for the cluster of symptoms classified as Covid-19, the now infamous SARS-CoV-2. Researchers around the globe working for various research institutions and pharmaceutical companies began work, much early research was based upon prior work regarding unsuccessful SARS vaccines. Throughout the Spring, Summer and beyond “experts” and government ministers promised, that if all goes well, an “effective” vaccine may be achieved by *insert various dates here.*
SARS-CoV-1 or severe acute respiratory syndrome referred to as SARS had approximately 100 cases in the United Kingdom, out of 8096-8422 total cases globally, and no deaths in the United Kingdom. The United Kingdom had 31 cases of MERS-CoV of a total of 2449 and two deaths in. the United Kingdom. Globally at least 774-916 deaths occurred (1), giving a case fatality rate of 11 per cent (2), which in theory suggest it to be highly lethal. Despite this, it seemingly mysteriously vanished. Coronaviruses, as previously discussed, are a large family of viruses, ranging from the common cold to more severe diseases, including the novel coronaviruses, including SARS and SARS-CoV-2.
SARS, the 21st Centuries first pandemic, was initially identified in China’s Guangdong province, in late 2002, by medical practitioners who became aware of “unusual” cases of pneumonia, but did not report it to the World Health Organization (WHO). In early 2003 an outbreak in Hanoi, Vietnam, involving a WHO officer that later died, was reported as a large outbreak on the March 10th.
A physician that travelled from the Guangdong province to Hong Kong while infected with SARS stayed at the Metropol Hotel, reportedly transmitting the virus around a dozen guests. Three returned to Singapore, two of whom then returned home to Canada, one to Vietnam, one to Ireland, and one to the United States. Thus SARS began its spread around much of the globe, but with most cases occurring in Asia.
SARS was described as both aggressive, and with high lethality, symptoms were typically reported within two to three days, and with limited reports of infections in the absence of symptoms. One must recall variances in test capacity in regards to total cases when comparing SARS and SARS-CoV-2. The recent pandemic has seen Covid-19 testing reach massive scales, with the United States alone, as of December 2nd, 2020, performing >196 million tests for Covid-19. (3)
In April 2003 the WHO suggested laboratory diagnostics tests, stating that;
“researchers in several countries are working towards developing fast and accurate laboratory diagnostic tests for the SARS coronavirus (SARS-CoV). However, until standardised reagents for virus and antibodies detection are available, and methods have been adequately field-tested, SARS diagnosis remains based on the clinical and epidemiological findings: acute febrile illness with respiratory symptoms not attributed to another cause and a history of exposure to a suspect or probable case of SARS or their respiratory secretions and other bodily fluids.” (4)
This means clinical symptoms such as respiratory distress were indicated as a need for further differential diagnosis. Thus samples from “suspected and probable SARS cases” were tested for SARS-CoV using the following methodology.
“Laboratory test result criteria for confirming or rejecting the diagnosis of SARS remain to be defined.
Molecular tests (PCR)
Polymerase chain reaction (PCR) can detect the genetic material of the SARS-CoV in various specimens (blood, stool, respiratory secretions or body tissues Sampling for Severe Acute Respiratory Syndrome (SARS) diagnostic tests). Primers, which are the key pieces for a PCR test, have been made publicly available by WHO network laboratories on the WHO web site. A ready-to-use PCR test kit containing primers and positive and negative control has been developed. Testing of the kit by network members is expected to quickly yield the data needed to assess the test’s performance, in comparison with primers developed by other WHO network laboratories and in correlation with clinical and epidemiological data.
Principally, existing PCR tests are very specific but lack sensitivity. This means that negative tests cannot rule out the presence of the SARS virus in patients. Furthermore, contamination of samples in laboratories in the absence of laboratory quality control can lead to false-positive results.
Positive PCR results, with the necessary quality control procedures in place. Recommendations for laboratories testing for SARS-coronavirus, are very specific and mean that there is genetic material (RNA) of the SARS-CoV in the sample. This does not mean that there is live virus present, or that it is present in quantity large enough to infect another person.
Negative PCR results do not exclude SARS. SARS-CoV PCR can be negative for the following reasons: - The patient is not infected with the SARS coronavirus; the illness is due to another infectious agent (virus, bacterium, fungus) or a non-infectious cause. - The test results are incorrect (“false-negative”). Current tests need to be further developed to improve sensitivity. - Specimens were not collected at a time when the virus or its genetic material was present. The virus and its genetic material may be present for a brief period only, depending on the type of specimen tested.
2. Antibody tests
These tests detect antibodies produced in response to the SARS coronavirus infection. Different types of antibodies (IgM and IgG) appear and change in level during the course of infection. They can be undetectable at the early stage of infection. IgG usually remains detectable after the resolution of the illness.
The following test formats are being developed, but are not commercially available yet: - ELISA (Enzyme Linked ImmunoSorbant Assay): a test detecting a mixture of IgM and IgG antibodies in the serum of SARS patients yields positive results reliably at around day 21 after the onset of illness. – IFA (Immunofluorescence Assay): a test detecting IgM antibodies in serum of SARS patients yields positive results after about day 10 of illness. This test format is also used to test for IgG. This is a reliable test requiring the use of fixed SARS virus on an immunofluorescence microscope.
Positive antibody test results indicate a previous infection with SARS-CoV. Seroconversion from negative to positive or a four-fold rise in antibody titre from acute to convalescent serum indicates recent infection.
Negative antibody test results: No detection of antibody after 21 days from onset of illness seems to indicate that no infection with SARS-CoV took place.
3. Cell culture
Virus in specimens (such as respiratory secretions, blood or stool) from SARS patients can also be detected by inoculating cell cultures and growing the virus. Once isolated, the virus must be identified as the SARS virus with further tests. Cell culture is a very demanding test, but currently (with the exception of animal trials) only means to show the existence of a live virus.
Positive cell culture results indicate the presence of live SARS-CoV in the sample tested.
Negative cell culture results do not exclude SARS (see negative PCR test result).” (4)
Case detection in 2003 SARS pandemic took a different approach to SARS-CoV-2 in 2020, and the closest similarities may be seen potentially at the early onset of what became Covid-19 before the mass rollout of tests occurred outside of laboratory settings.
In 2003 severe respiratory illness needed to be within the context of “documented exposure risk” when diagnosing SARS-CoV disease. SARS-CoV disease was thus to be investigated in patients hospitalised for:
“Radiographically confirmed pneumonia or acute respiratory distress syndrome of unknown aetiology, AND
One of the following risk factors in the ten days before illness onset:
Travel to mainland China, Hong Kong, or Taiwan, or close contact with an ill person with a history of recent travel to one of these areas, OR
Employment in an occupation associated with a risk for SARS-CoV exposure (e.g., healthcare worker with direct patient contact; worker in a laboratory that contains live SARS-CoV), OR
Part of a cluster of cases of atypical pneumonia without an alternative diagnosis” (5)
Masks were used across parts of Asia, temperature scanners were introduced in major public gathering places, with quarantines implemented. A peak in viral infection seemed to occur around late May of 2003 before SARS-CoV seemingly disappeared the strict quarantine measures credited when the WHO declared the threat over.
Data on the number of tests carried out during the 2003 epidemic seems scant, no doubt diagnostic attempts were drastically ramped up for the 2019-2020 emergence of a “novel” coronavirus. I part that context needs including within the suggestion that 2003 SARS had a higher risk for mortality, but did not infect so many or last as long. One must consider that in 2020 after failure to implement testing, alongside track and trace (considering that the United Kingdom Government abandoned this strategy initially), testing was eventually conducted beyond the 2003 SARS criteria, including those that had little to no symptoms and or had been identified for testing by studies and contact tracers. As such, one may consider the sudden disappearance of SARS occurred due to searches being limited to those with more serious manifestations of SARS pathology. Hence the mortality rate was also substantially more severe in 2003-2004.
Concerning a SARS vaccine, the studies for SARS-CoV-1 were initiated and tested in began in animal models (this phase was bypassed in favour of human trials with the Covid-19 trials), with an inactivated whole virus being tested in mice, ferrets, and nonhuman primates. These studies suggested the vaccine provided protective immunity, but sadly in the animal studies it seemed to cause immune disease, specifically an immunopathologic-type lung disease, which given the nature of SARS was not a good outcome. (6)
Human studies were not conducted, and the vaccine studies petered out due to the apparent disappearance of the virus, which was attributed to a number of factors, including the weather in the summer (a fear during the Covid-19 trials was that participants would not be sufficient as the disease prevalence lowered in the summer months), the “strict quarantine initiated of not only those infected but those who had been in contact with individuals sufficiently identified as infected. In reality, nobody knows why the pandemic ended; viruses tend to be unpredictable. However, as written by the author in Pandemic Panic (7), viruses tend to mutate to less severe strains to survive. A virus that is either lethal to all hosts, or renders hosts unable to circulate in the community leads to less spread, and the virus cannot survive. Potentially in SARS, the increased mortality rate may have caused such a phenomenon. However, it seems more plausible, given that while mortality was suggested to be higher than SARS-CoV-2, it did not kill all those infected, that limitation of testing to those formally diagnosed as being infected led to the less severe strains running unchecked in so-called asymptomatic individuals. In SARS-CoV-2, mild and asymptomatic cases are being highlighted, giving the impression that this latest pandemic is less lethal but more virulent. Vaccine development for SARS-CoV-2 varies, with some using minute viral portions, or virus ribonucleic acid (RNA). (8)
This is suggested to circumvent the issues that occurred with the SARS-CoV-1 vaccine that relied upon greater amounts of the actual virus.
BioNTech and Pfizer recently announced preliminary "evidence," and in the United Kingdom following hasty checks which some suggest to be a political move by a government reeling from the looming disasters of Brexit, and the poor handling of the pandemic. The United Kingdom became the first to approve the Pfizer/BioNTech vaccine, paving the way for so-called "mass" vaccination, after Britain's medicines regulator, the MHRA, suggested the product which allegedly offers "up to" 95 per cent "protection against Covid-19 illness," was safe enough to be rolled out. (9)
The news was greeted with much excitement, but one must consider that "up to" 95 per cent and "protection against Covid-19 illness" are not well defined.
The approval of an mRNA vaccine for use is a world first (10), and while the technology appeared in 1990 within the literature, it has been fraught with numerous issues that needed solving.
Vaccines in theory work via introducing material that is sufficient and specific enough to provoke an immune response. This is in theory achieved by an attenuated (weakened) virus, a virus that has killed, or a viral protein, such as occurs in an mRNA vaccine, in which a messenger RNA is introduced, this RNA is the genetic material utilised to translate the proteins used within our bodies.
The typical self/non-self model of immune function whilst still the predominant held view in immunology, and general practice has encountered problems since the 1980s. Dr Matzinger's Danger Theory (11), argues that tissues are a large factor in driving an immune response and that one occurs in response to a danger which may vary not only by the specific threat, but between individual response to a threat (e.g. older individuals may have a lower threshold). What may present danger to one, may not represent the same degree of risk to another. Certainly, this needs to be accounted for in vaccines that do not contain a live virus, and also in those with attenuated virus samples. Viruses that have been inactivated are less dangerous and produce a weaker immune response, necessitating immunologic adjuvants, and often multiple "booster" injections. (12)
Adjuvants in immunology refer to substances included to potentiate and improve the immune response. (13) Vaccine manufacture was assumed to cause significant variability in batch efficacy due to contamination within reaction vessels used within processing, however, when cleaning protocols were scrupulously increased, a reduction occurred in vaccine "effectiveness," and contaminants were noted to "enhance" the immune response. (14)
As can be seen at the beginning of the article, the vaccine includes the RNA ingredient BNT-162B2, and several other ingredients or adjuvants, namely;
lipid ALC-0159 (UNII: PJH39UMU6H)
lipid ALC-0315 (UNII: AVX8DX713V)
POTASSIUM CHLORIDE (UNII: 660YQ98I10)
MONOBASIC POTASSIUM PHOSPHATE (UNII: 4J9FJ0HL51)
SODIUM CHLORIDE (UNII: 451W47IQ8X)
SODIUM PHOSPHATE, DIBASIC, UNSPECIFIED FORM (UNII: GR686LBA74)
SUCROSE (UNII: C151H8M554)
Adaptive immune response theoretically occurs following an innate immune response (danger) that see cells such as the dendritic cells being engulfed by the pathogens, which migrate to lymph nodes and then causing reactivity in T cells that act as the adaptive immune cells. (15)
This activation causes mast cells to release both heparin and histamine that isolates the infection site to enable immune cells to clear out pathogens but also causes the release chemokines. Adjuvants are suggested to increase the local reactions and induce a larger release of danger signals, plus induce the release of inflammatory cytokines. The immune system is suggested to recognise these pathogenic molecules due in part to Toll-Like Receptors (TLRs).
Various medical complications are suggested to occur both in humans and animals due to adjuvants, with aluminium salts, utilised in numerous vaccines but regarded safe by the Food and Drugs Administration. (16) Yet, numerous studies indicate a role in the development of Alzheimer's disease (17), in which adjuvants may be too reactogenic, creating susceptibility to fever. Indeed fever post-vaccination is an expected outcome. The vaccination for "swine flu" H1N1 pandemic was associated with the incidence of the chronic sleep disorder, narcolepsy in both children and adolescents (18), which associated with an influenza vaccine called Pandemrix that has the AS03-adjuvant.
In animals, specifically mice, aluminium adjuvants which have been previously linked to Gulf War syndrome (GWS), following its use in anthrax vaccination, has been indicated to cause motor neuron death (19), increases in incidences of amyotrophic lateral sclerosis, as well as other related neurological disorders correlated with GWS. No doubt multiple environmental variables are noted, anthrax vaccination and the relevant adjuvants such as aluminium hydroxide and squalene have repeatedly and increasingly faced scrutiny. The use of squalene, a suspension of oil-water is also indicated as increasing the risk for auto-immune disease incidence in rodents. (20) Squalene itself is indicated in arthritis prone rodents as inducing rheumatoid arthritis. (21) A 2006 report by Richards et al. (22), found a relationship between vaccine-associated sarcoma (VAS), but conflicts exist on whether specific vaccines increase risk, manufacturing processes specifically, adjuvants, or other associated variables. (23).
On the 8th December 2020, the United Kingdom began rolling out the Pfizer vaccine candidate, an mRNA (messenger RNA) type of vaccine as previously discussed, that enables synthetic genetic material which is enveloped in lipids to transfect (infect) the cell, which occurs due polyethylene glycol (PEG). In what is often referred to as conspiracy theory circles, public awareness usually focuses upon PEGs use in anti-freeze type products that may be utilised in motor vehicle radiators amongst other uses. PEG aids in the Nucleoside modified mRNA encoding for SARS-CoV-2 full-length spike protein antigen and is combined with a lipid nanoparticle (LNP) formulation. (24)
Polyethylene glycol forms part of the formulation of lipid nanoparticle that envelops the specific mRNA genetic material, which was previously noted as ALC-0159, which is the name for 2[(polyethylene glycol)-2000]-N,N-ditetradecylacetamide. (25)
Knop et al. (26), reviewed the use of polyethylene glycol in delivery of pharmaceutical drugs, indicating that as early as the 1950s they were linked to a propensity to cause cellular clumping and blood clotting, which increases the risk for embolisms, including pulmonary embolisms, as well as inducing an inflammatory cytokine storm. Polyethylene glycol is suggested to be linked to high incidences of drug-related adverse reactions, including but not limited to anaphylaxis. (27; 28; 29; 30; 31; 32; 33; 34; 35)
Indeed, as indicated by Pottel et al. (36), medications tend to constitute relatively minute amounts of the active pharmaceutical ingredient, with the majority of tablets, capsules, liquids, and injectables such as vaccines including numerous components such as dyes to help distinguish drugs, preservatives to ensure stability and shelf life. Alongside antimicrobials and excipients compounds that may be either act as fillers or as is suggested in vaccines, it must be essential to ensure the active ingredient is delivered "safely" and effectively (i.e. create immune response).
It is generally accepted that ingredients listed as excipients are biologically approved due to an absence of acute toxicity in studies using animals. Pottel et al. (36), searched for subtle long-term effects, and interaction with other medicines, stating that many excipient effects may have been previously unappreciated and may play an important role in health outcomes and disease.
The use of lipid nanoparticles in the Pfizer vaccine, like one from Moderna, is suggested to be approximately 100 nanometers in diameter, similar to the actual coronavirus. Pfizer suggests it uses four different lipids in a "defined ratio", with lipid ALC-0315 being a primary ingredient within the formulation that is ionisable and can be positively charged. At the same time, the RNA has a negative charge causing the two to attract each, but that it is a component known to able to cause side-effects. (37)
Errors made by the Scientific Advisory Group for Emergencies (SAGE), ones that have continued throughout the pandemic, were discussed in other works by the author (7), made the assessment of the unfolding SAR-CoV-2 pandemic predictions grossly inaccurate, which was seen to have both disastrous effects upon the nation's response to Covid-19, and also necessitated frequent and drastic re-evaluated estimates. SAGE's initial estimates followed a narrative that SARS-CoV-2 was a novel coronavirus and that the cases found in late 2019 were the initiation of its spread. Thus the pandemic was in early stages, and that the majority of the United Kingdom population (as high as >93 per cent) had not been exposed to the virus and were at risk of infection. A failure to act would lead to 500,000 deaths if no action were taken. (38)
This modelling assumed the total population to be susceptible to SARS-CoV-2, with no pre-existing degree of immunity present within communities. Yet as described by Doshi (39), who highlights six specific studies that report SARS-CoV-2 T cell reactivity in between 20 to 50 per cent of individuals with no documented viral exposure.
Ng et al. (40), studying samples of blood collected in the United States between 2015 and 2018, found 50 per cent had some form of SARS-CoV-2 T cell reactivity. Weiskopf et al., utilising specimens collected in the Netherlands found T cell reactivity in two out of 10 individuals that had not been virally exposed. (41)
Further reactivity was identified in individuals in the United Kingdom, Germany, Sweden, and Singapore. (42; 43; 44; 45)
Whilst small in scale and unable to provide accurate estimates of whom might have prior immunological SARS-CoV-2 responses, that findings indicated across continents, and various laboratories suggest that further research is warranted.
Chavarria-Miró et al. (46), indicate the detection of SARS-CoV-2 in sewage retrospectively tested in Barcelona, long before their first case of Covid-19 presented. This suggests that SARS-CoV-2 was present within the population prior to reports of a global pandemic.
Indeed, Basavaraju et al. (47), indicated SARS-CoV-2 infections within the United States in mid-December 2019, further evidence that supports the notion that this strain of coronavirus was spreading throughout many nations before the reports of initial cases in Wuhan, China. Sadly, entering further into such narrative potentially labels one as a "conspiracy theorist", a term some suggest is linked to the United States Central Intelligence Agency (C.I.A). (48) That said, failure to consider all theories and possibilities risks one being a "complicity theorist."
Anyone reading The Devil's Chessboard by Talbot (49), will have little doubt of the levels the United States have previously, and presumably will still go to maintain and further their cause. The book details the morally corrupt and somewhat cynical rise of the United States intelligence apparatus that documents from official records and their capability to intervene clandestinely in internal affairs of both competing nations and on a domestic front.
From the fanaticism brought on by the Cold War against Soviet Russia, and the "necessity" for unaccountable secret institutions to distort home politics and undermine the "democratic" elsewhere. One must draw parallels with the ideology to secretly fight communism, even to the degree that Dulles engaged in secret activities following World War Two, working to establish "ratlines" that aided Nazis considered useful to the United States in the new Cold War against the Soviet Union could both travel to the U.S, and avoid prosecution, and the secret testing on many U.S citizen via the MKULTRA project. (50) Dulles led the CIA-engineered coup in Iran in 1953 that toppled the democratically elected government of Mohammad Mossadegh and installed Shah Reza Pahlavi (who ruled until 1979) an apparent bold and daring triumph for the United States in the cold war against the Soviets.
In an era in which Wall Street is untouchable, China may be the United States current fear. Whilst stories should be considered and rationalised, it is not farfetched to suspect that we will read about these aspects at some point via declassified intelligence documents long in the future. The 6th August 2019 saw the United States main laboratory facility for biological warfare being issued a "cease and desist" order due to safety standards, protocol, and leaks violations. (51) Whether this was a convenient back story to cover for any clandestine activity remains unknown, but it all adds to the plausible deniability, a central tenet of CIA activity.
What do we know about the facility? Numerous experiments were engaged in by the United States. From the case in 1954, when seven inmates, notably all were black males, were isolated and fed mass doses of Lysergic acid diethylamide (LSD) for 77 days by Isbell. (52) "Work/research" that formed part of a highly secretive C.I.A program attempting to develop methods for mind control that was based at an inauspicious Army base, Fort Detrick.
Fort Detrick in Frederick, Maryland, just 50 miles from Washington was initially selected as a site for the development of secret plans for germ warfare. Until recently it thrived as the Army's principal biological research base with approximately 600 buildings spread across 13,000 acres. Through declassified documents that were not destroyed, we can establish that secret programs occurred to develop biological weapons, such as the Whitecoats. (53; 54; 55)
Little has been said regarding Covid-19 by Fort Detrick, and that little mention is made of Covid-19 seems curious given the study available freely on available (56), by Hensley et al.
Lisa E. Hensley is described as the Associate Director of Science at the Office of the Chief Scientist, National Institute of Allergy and Infectious Disease Integrated Research Facility in Frederick, Maryland. Before that acting as a civilian microbiologist in the virology division of the United States Army Medical Research Institute of Infectious Diseases (USAMRIID) also located on Fort Detrick, Maryland. Acting as a subordinate lab to the U.S. Army Medical Research and Development Command (USAMRDC), which is also headquartered on the same installation. (57) Hensley is one of the premier researchers of some of the world's most dangerous infections, including Ebola hemorrhagic fever, and Severe acute respiratory syndrome (SARS). Holding various patents for vaccines and treatments, Hensley seems to be erroneously forgotten in the current climate. (58; 59; 60)
Is it likely that the intelligence services wished to impact China or its own citizens with a viral infection? Hopefully not, but given past actions, and the serious breaches in safety, one would expect a better account to explain such instances. The United States seems to be positioned as ever to maintain plausible deniability. Is it possible that SAR-CoV-2 was already present in the United States and other nations, and Wuhan, China was simply the site at which it was formally identified?
In the United Kingdom, and indeed many other nations, one must first consider that the scientific advisory group for emergencies (SAGE), consisted of no clinical immunologists, nobody with a degree in biology, or post-doctoral specialisations specifically in immunology. Some were medics, but sociologists, psychologists, economists, political theorists, and a profuse amount of mathematicians formed the modelling group responsible for much of the pandemic response. (61)
Modelling does require specific expertise to achieve their desired outcomes. Such outcomes may not specifically be based on the full available evidence, but in an ideological stance that misses context and skews the outcome predictions. When modelling is structured by those with little expertise in the specific subject-matter, it risks foundational errors that are missed by the modellers, and often by those tasked with implementing policy and operational changes due to a false belief in the disproportionate power of models. However credulous the modelling group within SAGE may appear, the claims made about the processes and pathways of pathological diseases such as Covid-19 fails to account for specific biological variables and makes assumptions of crucial factors such as the starting point for SARS-CoV-2 spread.
The models utilised on the suggestion of Imperial College were inherently flawed for several reasons. However, primarily as discussed above, that SARS-CoV-2 was a novel virus, and thus conferred no prior immunity within the community. As has been discussed earlier, the evidence currently suggests SAR-CoV-2 emerged before the date in contemporary literature and the media, and that T-cell reactivity is evident to some degree of the population, which would be expected given that SARS-CoV-2 is a mutation of the coronavirus and not a totally new emerging virus. (62)
This assumption that 100 per cent of the population were susceptible to SARS-CoV-2 infection led to a further false belief that studies of antibodies within the blood allowed a model to be constructed that determined the percentage within the population that had been infected.
SAGE suggested as of September 2020 that >90 per cent of the United Kingdom population remained at risk. (63) Which when combined with the “data” from the REal Time Assessment of Community Transmission (REACT) study suggests “that slightly under 6 per cent of the population may have antibodies for the virus by the end of June…” indicating that such individuals were “likely” to have been exposed to SARS-CoV-2, or suffered with Covid-19 “disease”. (64)
One could therefore assume that the United Kingdom government-backed stance on SARS-CoV-2/Covid-19 risk suggest that circa 94 per cent of the population have not been infected. A figure which seems disconcertingly high when one considers the narrative that while SARS-CoV-2 carries less mortality risk than SARS, it is suggested to be more prevalent and spread more easily, even within individuals classified as asymptomatic, i.e. people who are not displaying symptoms of the disease.
The official data suggests a fatality rate circa 3.5 per cent (65), with 1,766,819 positive tests, and 62,566 deaths recorded “with” Covid-19 identified. With a U.K. Population of 68,045,779, a six per cent infection rate should mean that over four million eighty-two thousand seven hundred forty-six people have been, or are infected, which gives a fatality rate of approximately 1.5 per cent.
However, as discussed, it seems curious that SARS-CoV-2 would infect such a low population percentage, even if one considers that it only began its global spread in December 2019. Indeed, Ioannidis (66) studied globally collated data suggest an infection fatality rate circa 0.2 per cent as the best estimate.
This error or flaw in the policies and models comes from the initial assumptions that SARS-CoV-2 was a novel virus. While the event that led to finding SARS-CoV-2 made it seem novel, we neither know how long it existed undetected nor know the immunity granted from prior coronaviruses infections. In short, viruses have genetic ancestors, and the previous “novel” coronaviruses already discussed, 2003 SARS and 2012’s MERS in 2012 (67), have similar DNA sequences and structures to the current virus, with SARS being indicated to be as much as >85 per cent identical.
In prior work (7), I spoke about endemic coronavirus that remain linked to the common cold, which continues to circulate freely within both within the United Kingdom and globally. Modernity, specifically a tendency to remove sick pay in less affluent social communities, seems to cause a faster and easier transmission of such viruses. Human coronaviruses (hCov), such as hCoV-HKU1, hCoV-OC43, hCoV-NL63 and hCoV-229E are discussed in detail by Zhu et al. (67) While discovered in the 1920s in animals (68; 69), it wasn’t until the 1960s that human coronaviruses were identified. (70; 71; 72; 73; 74) As before, discovery does not mean they were non-existent and newly emerged, just that research has “isolated” and identified something which was considered new. That hCoV-HKU1, hCoV-OC43, hCoV-NL63 and hCoV-229E tend to either led to asymptomatic or mild type respiratory and/or gastrointestinal infections, does not discount from their circulation within humans since their first identification, and no doubt before their documented existence. While accounting for between five to 30 per cent of all common colds, hCoVs are rarely considered serious until the occurrence of global pandemics such as in SARS-CoV, MERS-CoV and SARS-CoV-2.
Initial opinions of coronavirus appear to have considered them to be relatively harmless pathogens, yet they have become globally associated with potential severe clinical complications in recent months. Coronavirus, an enveloped type virus identified by a positive-strand ribonucleic acid (RNA) genome, primarily targets mucosal surfaces within both respiratory and the intestinal tracts in various mammals and birds. (75; 76)
Human coronavirus isolates known as hCoV-229E and hCoV-OC43 were correlated with the “common cold”, and symptoms in the upper respiratory tract that are both mild and self-limiting. (77; 78) When the so-called new variant SARS-CoV was discovered, which initiated an outbreak globally of acute instances of often severe cases of atypical pneumonia, circa 2003, led to an interest in human coronaviruses and the identification of two further novel variants, HCoV-NL63 and HCoV-HKU1. (79; 80) These showed an ability to cause serious complications in the respiratory tract, particularly in patients with existing comorbidities.
The initial discovery of human coronaviruses in the 1960s (70; 81), involved two different isolation methods. One, by Kendall, Byone and Tyrell (82), at the British Medical Research Councils Common Cold Unit, in which B814 a common cold novel virus that was unable to be cultivated using standard techniques previously used to successfully cultivate adenoviruses, rhinoviruses, and others associated with the common cold. (83) Tyrell and Byone instead used a method in 1965, that involved serial passage through a human embryonic trachea organ culture. A 1966 paper by Hamre and Procknow (84), from the University of Chicago, describes the isolation of another novel cold virus, hCoV-229E, which was sourced from medical students, and grown in a culture of kidney tissue.
Human coronaviruses are indicated to act with renin-angiotensin proteases (enzymes that breakdown proteins and peptides). To both establish and maintain a cycle of infection, coronaviruses require that they deliver genetic material inside the intracellular space, mediated by glycosylated spike proteins, which are discussed in other works. (7)
Angiotensin Converting Enzyme 2 (ACE2) is suggested to act as a functional receptor for human coronaviruses (9), with antibodies that direct against ACE2 theorised to prevent SARS-CoV infection. (85)
The renin-angiotensin system (RAS), is a well-described endocrine system, vital in the maintenance of cardiac function, arterial pressure, homeostasis of fluid, and salt balance, along with regulation of tissue remodelling, particularly in the proliferation of cells, angiogenesis and apoptosis. (86)
Aside to the physiologically normal processes, RAS is correlated with a variety of pathophysiological actions. (87) Abnormal RAS activation is established as a variable in the development of numerous cardiovascular diseases, including hypertension, diabetes and renal disease. (88; 89)
Within RAS, synthesis of a variety of angiotensin peptides occurs, which are degraded by the precursor angiotensinogen via a series of complex enzymatic reactions. Specific components of RAS generate within specific body regions. For example, renin is generated within the kidneys, while ACE is derived from the lungs, with the liver responsible for angiotensinogen. Angiotensin synthesis is suggested to be evident to some degree in all organs, RAS activity initiates via the kidney, following juxtaglomerular cells releasing renin (90; 91), which acting as an aspartic protease works to cleaves its substrate angiotensinogen, that is then produced in the liver and forms the inactive angiotensin peptide, Ang I or Ang 1–10. Ang I converts to either And II, a RAS effector peptide, or Ang 1–8 via the protease ACE which is dependent on zinc. (92)
Higher ACE expression occurs on vascular endothelial cell surfaces, in particular within lung tissue. (93) Ang II generation from Ang I can occur via enzymes that are not ACE related, such as chymase, a serine protease. Whilst ACE is considered to be the primary enzyme responsible for Ang II-conversion, research indicates that Ang II conversion occurs via chymase enzyme in certain pathological vascular conditions. Indeed, it must be noted that chymase activity is evident in pulmonary membranes, aiding Ang I conversion into Ang II within lung tissues. (94)
RAS is typically considered a system of endocrine and circulation predominantly. Yet, it is now well established that alongside RAS peripherals, RAS is both tissue-specific and abundant in independent localised systems. Indeed, within various organ systems, such as the lungs, kidneys, liver, heart, brain, vasculature, pancreas, and within the reproductive, nervous, and the digestive system. (92)
In-spite speculation regarding the existence of RAG local airway capacity intrapulmonary generation of Ang II was a recent confirmation. (95)
Alveolar mast cells within both the lower and upper respiratory tract are evidenced to express renin levels, which triggers the formation of pulmonary Ang II. (96;97)
RAS components are also abundant in airway tissue in humans, including ACE and angiotensinogen, with pulmonary epithelium evidenced as the primary circulatory source for ACE. (98)
Receptors for Ang II are evidenced to be expressed within lungs, in the form of the subtype AT1 which is found in the smooth muscle bronchial cells, and bronchial receptors AT2 receptors within the epithelial brush borders. (99)
The expression of ACE2 in both alveolar, bronchiolar epithelial cells, and pulmonary endothelial cells is well documented. (100)
Lung masts cells are evidenced to have chymase, potentially being the major enzyme responsible for Ang II-generation within the lung. Local RAS activity within pulmonary tissue has been indicated as contributory in tissue remodellings, such as alveolar epithelial cell apoptosis regulation, fibroblast proliferation, and collagen production within the lung. (101; 102)
Thus, it is suggested that activation that is inappropriate with regard to specific local components of the airway RAS, specifically ACE2, may initiate factors that exacerbate the pathophysiological development of symptoms associated with SAR-CoV-2, and the severity of disease outcome in covid-19.
ACE2 and SARS-CoV-2
Angiotensin-converting enzyme 2 (ACE2), plays a major role in RAS homeostasis, converting Ang II to Ang (1–7), and the activation of the RAS putative pathway. ACE2 is thought to be responsible for regulating net Ang II tissue levels, as an antagoniser of fibrotic and hypertrophic effects due to the AT1 receptor being the binding site of Ang II. (103; 104)
ACE2 may exhibit a role of counter-regulation that seems critical for RAS homeostasis within the lung. (104; 105) Thus, improper regulation leads to increases in both ACE and Ang II levels which are associated with the pathogenesis of numerous variations of lung disease, such as sarcoidosis, pulmonary hypertension, pulmonary fibrosis, and more importantly in the context of COVID-19, acute respiratory stress syndrome (ARDS). (106; 107; 108)
Studies conducted in-vivo confirm an association between the severity of ARDS, and the outcome, with pulmonary RAS. (109) ARDS, a severe acute lung injury, is characterised by an accumulation of inflammatory cells, pulmonary oedema, and severe hypoxia (110), as prevalent in documented cases of covid-19. ARDS may be triggered by various pathogenic states, such as sepsis, pancreatitis and severe trauma/shock. (111)
Previous studies indicate pulmonary RAS in ARDS pathogenesis, and that ACE antagonists such as AT1 receptor blockers delay the onset of ARDS in rodents exhibiting acute lung injury. (112)
Negative contributions of ACE to the pathogenesis of ARDS occurs via a variety of mechanisms, such as increases in vascular permeability. (113)
Imai et al. (109), identified a protective role of ACE2 during acute lung injury such as ARDS, in counterbalancing the induced pathophysiological effects of angiotensin II. Mice bred with an abrogated expression of ACE2 expression exhibited more severe disease patterns than control mice, with an enhanced degree of vascular permeability, lung oedema, and decreased lung function.
SARS-CoV & HCoV-NL63 in relation to RAS activity
The 2003 epidemic of SARS-CoV, was a disease that remained relatively rare, with an incidence 8,422 cases, and a total fatality rate of circa 11 per cent (114), which is primarily suggested to be attributable to ARDS induced respiratory failure. Indeed, the fatality rate is variable, mostly dependent on factors such as age, and treatment methodology, to be between 0 and 50 per cent (115), with SARS patients < 24 years evidenced to be less likely (< one per cent) to die from SARS, that those > 65 who had a 55 per cent mortality rate. (116)
SARS-COV infects host cells via ACE2, the component of RAS, which is evidenced to protect against ARDS induced acute lung failure. (117; 118)
As aforementioned, the spike protein engages with ACE2, and a reduction occurs in the cell surface. Thus ACE2 functional capacity is down-regulated (117; 119), a phenomenon that is evidenced to provoke increased severity and risk of lung failure in rodents infected it SARS-CoV. (120)
It is also worthy of note that the within the SARS-CoV-2 spike protein, a pocket of the free fatty acid, linoleic acid has been indicated to increase SARS-CoV-2 binding (121),
Interestingly, despite this research, the team consider linoleic acid to be a viable potential therapy due to the fatty acids so-called "essential" nature.
Ling et al. (122), studied rodent fatty acid profiles alongside inflammatory markers utilising animals fed a diet considered essential fatty acid-deficient (EFAD) constituting 2 per cent hydrogenated coconut oil (HCO) for two weeks. Alongside groups supplemented with 1.3mg of arachidonic acid and 3.3 mg of docosahexaenoic acid (AA + DHA) which created a 2 per cent fat diet. Upon exposure to lipopolysaccharide, the rodents on the EFAD diet had significantly lower levels of various inflammation markers, such as tumour necrosis factor (TNF) and interleukin-6.
Increases in serum levels of C18 unsaturated free fatty acids are discussed by Bursten et al. (123), as being a significant predictor in acute respiratory distress syndrome (ARDS) development, which was examined within both Controlling Intuitive Appetite (124), and Pandemic Panic (7), which suggests that increases in ratios of unsaturated serum acyl chain occur between those codified as healthy and those patients which suffered severe outcomes, were both sufficient to identify those likely to suffer ARDS and provide insights regarding the essentiality of unsaturated fatty acids.
Hanna and Hafez (125), discuss arachidonic acid being an unsaturated fatty acid that is sourced either via direct dietary means or indirectly via the metabolism of linoleic acid. Its release occurs via the breakdown of phospholipids under the action phospholipase A2. Various factors, including mechanical through to chemical stimuli, may induce a cascade of arachidonic acid.
Malcolm et al. (126), compared the composition of fatty acid in adipose tissue samples taken from 143 adults autopsied humans aged 24 to 61 years, one from a deep-seated site (perirenal) two from subcutaneous sites, the buttock and abdominal areas. Proportional saturated fatty acid levels were highest in samples of adipose tissue found in the perirenal, whilst the adipose tissue buttock was lowest in saturated fatty acids. Proportionally level of both linoleic and linolenic acids was similar across all sample sites, leading them to conclude adipose tissue found in the buttock has a greater degree of unsaturation than abdominal adipose tissue.
Mamalakis et al. (127), in a study of 475 adolescents aged 11 to 18 years (138 aged 11 to 16 years completed all variables), assessed levels of physical activity, serum lipids, and both buttock and abdominal composition of adipose fatty acids, finding that like adults, the composition of fatty acid in the abdominal adipose tissue of children is supposedly less favourable that the buttock. With abdominal adiposity once again exhibiting the much-maligned elevated proportions of saturated fatty acids, with decreased proportions of both monounsaturated and polyunsaturated fatty acids when compared to buttock adiposity. Such findings are corroborated in adults by Pittet et al. (128), and Phinney et al. (129)
That unsaturated fatty acids are suggested as being important in the binding of the SARS-CoV-2 spike protein, and are indicated to be higher with age seems to correlate well with the susceptibility of aged subjects to SARS-CoV-2 infection and increased mortality.
The team (123) states that activity in the linoleic acid metabolic pathway can trigger both systemic inflammation, acute respiratory distress syndrome, and cause pneumonia, all pathologies observed in severe Covid-19, ARDS, Sepsis patients. (7)
El-Kurdi et al. (130), concurs that mortality increases in relation to unsaturated fatty acid, both with exogenous consumption and administration and also due to adipose lipolysis. Indeed, as Covid-19 pathology worsens, dietary intake may reduce due to loss of appetite, which increases fatty acid oxidation, potentially of unsaturated fatty acid. Unsaturated fatty acids seem critical in the SARS-CoV-2 spike proteins' ability to attach and enter the human body, specifically via the ACE2 receptor.
Validation by research from Bristol University (121), which seeks a possible basis for a pharmaceutical intervention that may prevent the Sars-CoV-2 virus from entering the human body, consists of a research team, led by both Christiane Schaffitzel and Imre Berger. They that found unexpectedly that linoleic acid was exhibited within a pocket of the protein. Linoleic acid, a constituent of widely available linseed oil, is also a component of many industrial processes such as the manufacture of linoleum, a floor covering consisting of canvas with a preparation of linseed oil as a backing. Linoleic acid (18:2ω6; cis, cis-9,12-octadecadienoic acid) is the most highly consumed n-6 polyunsaturated fatty acid (PUFA) in the human diet (131) and can be obtained from vegetable oils such as sunflower, safflower, soybean, corn, and canola oils as well as nuts and seeds.
The maintenance of n-6 polyunsaturated fatty acids as a so-called "essential fatty acid" as they cannot be manufactured endogenously (132), which is suggested to be required, among other things, to maintain cell membranes in the lungs, which continues to be the consensus belief (133), despite issues with membrane theory as described by Ling (134), in which he discusses a;
"concept that the basic unit of all life, the cell, is a membrane-enclosed soup of (free) water, (free) K+ (and native) proteins is called the membrane theory. A careful examination of records shows that this theory has no author in the true sense of the word. Rather, it grew mostly out of some mistaken ideas made by Theodor Schwann in his Cell Theory. (This is not to deny that there is a membrane theory with an authentic author, but this authored membrane theory came later and is much more narrowly focussed and accordingly, can at best be regarded as an offshoot of the broader and older membrane theory without an author.) However, there is no ambiguity on the demise of the membrane theory, which occurred more than 60 years ago, when a flood of converging evidence showed that the asymmetrical distribution of potassium (K+) and sodium (Na+), observed in virtually all living cells is not the result of the presence of a membrane barrier that permits some solutes like water and K+ to move in and out of the cell while barring--absolutely and permanently -- the passage of other solutes like Na+. To keep the membrane theory afloat, submicroscopic pumps were installed across the cell membrane to maintain, for example, the level of Na+ in the cell low and the level of K+ high by the ceaseless pumping activities at the expense of metabolic energy. Forty-five year ago this version of the membrane theory was also experimentally disproved. Despite all these overwhelming evidence against the membrane-pump theory, it is still taught as verified truth in all high-school and biology textbooks known to us today. Meanwhile, almost unnoticed, a new unifying theory of the living cell called the association-induction hypothesis came into being some 40 years ago. Also little noticed was the fact that it has received extensive confirmation worldwide, and has shown an ability to provide self-consistent interpretations of most if not all known experimental observations that are contradicting the membrane-pump theory as well as other observations that seem to support the membrane pump theory."
and that it appears to be the molecule to which Sars-CoV-2 attaches itself to enter the human body, the persistent narrative of it as essential leads the researchers to conclude not that n-6 polyunsaturated fatty acids should be limited, both via consumption and lipolysis, but that their challenge is the development of a pharmaceutical drug which can distort the spike protein of Sars-CoV-2, thus preventing it attaching to the linoleic acid, pointing to similar drugs that have already been developed to avoid rhinovirus attaching themselves to the lungs. (135)
The study authors note that despite colossal investment searching for elusive human immunodeficiency viruses (HIV) vaccines, the medical community relied upon therapeutic anti-viral medications of varying efficacy to decrease disease mortality risk.
Dr Ray Peat (136), in an article titled "fats, functions & malfunctions", discusses both linoleic acid and arachidonic acid, as not only increasing lipid membrane permeability but that the whole cell increases in permeability. This causes structural proteins to bind throughout the cell, which is exhibited in fibrosis seen in both Covid-19/ARDS and septic shock, along with an increased affinity to retain water. This leads to generalised cellular swelling and localised swelling in the mitochondria that reduce oxidative function, and allows increased cellular calcium that activates cellular excitation and initiates a redox shift toward inflammatory states that ultimately leads to inappropriate growth and mass, as seen in fibrosis and cancer, or cell death.
Dr Peat highlights the impact of such cellular environments, and the effects of glycogen restriction, which may occur via increased energy demand, or energy restriction, either intentionally or due to metabolic dysfunction—stating that decreased glycogen stores lead to increases in the secretion of adrenaline that may act to liberate fatty acids from adipose stores. Following chronic dietary consumption of n-6 polyunsaturated fatty acids, the ability to be oxidised or detoxified by the liver is impacted by glycogen availability and thyroid function. (137)
Peat (136), draws awareness to research by Cook et al. (138), Li et al. (139), and Autore et al. (140), and the quite remarkable resistance displayed by animals deficient in so-called “essential fatty acids to shock. This indicates the central role of polyunsaturated fatty acids in the maladaptive, and often chronic adaptions caused by acute shock, such as retention of calcium, cellular leakiness, and energy production inhibition, which bear striking similarities to the markers of many disease pathologies, and so-called “normal” ageing. The abundance of serum free fatty acids and stress hormones that tend in aged subjects to be both chronically higher, and result in poorer outcomes in diseases such as Covid-19 and other respiratory illnesses, alongside reduced tolerance of incidences of stress.
Much research indicates that animals with lower levels of unsaturated fatty acids exhibit higher metabolic rates, and a preference for glucose utilisation, which leads to increased carbon dioxide production (141), and enhanced resistance to toxins such as cobra venom (142), and lipopolysaccharides, commonly known as endotoxins. (139) This correlates with the discussion in Consistent Eating (143), that metabolism decreases in line with energy intake through the lifespan. That susceptibility to stress decreases as metabolism declines, suggesting a lower respiratory quotient due to limited glucose intake and increased consumption of fatty acids and protein.
Despite the associations with ACE2, identified polymorphisms in human ACE2 genes are not correlated with SAR-CoV disease progression. (144; 145)
Functional performance of RAS is evidenced to decrease as part of “normal” physiological processes of ageing, as is exemplified by a progressive inhibition of circulating levels of renin and the plasma activity. (146; 147)
Indeed, ageing is a frequently noted variable in infections related to both SARS-CoV, and SARS-CoV-2 as a significant predictor of poor outcome. (148)
Thus, RAS function in elderly, and groups with co-morbid conditions may lead to worse outcomes regarding ARDS and acute injury due to an overall impairment in RAS activity.
That coronavirus activates inflammatory systems, particularly RAS, and with available medications to act as both angiotensin receptor blockers and inhibit ACE. Angiotensin converting enzyme enables the production of inflammatory proteins which increase blood pressure, and the correlation between angiotensin and serotonin is well established in regards to age-related inflammation. As lifespan increases, exposure to and production of angiotensin occurs, increasing blood vessel contraction, which creates greater clotting risk and increases fatigue, alongside inhibiting energy production. (149; 150)
The class one viral fusion spike protein, which while unique to coronaviruses, is a feature that mediates attachment to the host receptor in all species of CoV. (151) The N-glycosylated spike protein varies abundantly between the CoV species with lengths between 1100 to 1600 residues, and an estimation of molecular mass ranging to <220 kDa. The spike protein features trimers that form the spikes evident on the surface of the CoV particle, which may be between 18–23-nm, a factor which may cause issues in the reliance on reverse transcriptase-polymerase chain reaction (RT-PCR) testing. (152; 153; 154)
Reverse transcription-polymerase chain reaction (RT-PCR) is an established laboratory technique used to identify specific genetic materials present in a sample via a biochemical amplification process. The test has been lauded as a scientific advance of great importance to the field of molecular biology, with the foundation of PCR revolutionising DNA study and gaining its creator, Kary B. Mullis, the 1993 Nobel Prize for Chemistry. It uses primers to sequences the encoding and may involve a cross-reaction with the spike protein that detects SARS-CoV-2 and other hCoV during the sample collection (155), as well as other respiratory viruses. As discussed, some degree of immunity is conferred by previous exposure to similar viruses. (156)
Reported variances in illnesses range from mild symptoms to severe, and well-documented occurrences of death since SARS-CoV-2 was first confirmed and reported in humans.
The Centre for Disease Control (CDC) initially suggested the following symptoms “may” appear 2-14 days after exposure.
Shortness of breath (156)
Covid-19 was described as having a mortality rate of 2-3.48 per cent, depending on the source (157), which may be a statistical distortion due to issues with test validity, continuity and availability, as well as a lack of diagnostic testing in those that are suggested to be infected but asymptomatic and therefore do not report for testing. As is the case in any well documented global pandemic, patients that become critical standout, and with no clear evidence on actual rates of those infected, or the actual rate of mortality in the population.
Variances and confusion seem evident in the testing protocol, with many citing initial failures in test validity (158; 159; 160; 161), with nucleic acid tests (NATs) that are widely utilised for diagnosis of new cases being suggested to increase the likelihood that many such infections may remain undocumented. Presumably where false negatives are a possibility, so to must be false positives. Whilst relatively cheap, and potentially abundant, the use of NATs as one of the two primary methods for confirming Covid-19 presence in humans subjects involves collecting patient samples that are then tested for specific molecules relevant to the Covid-19 genetic material.
Under previous criteria, a diagnosis of Covid-19 needed to be confirmed by lab tests, specifically a nucleic acid test performed on swabs from a patient’s respiratory tract or blood. Yet issues exist in nucleic acid testing, with “false negatives” created by tests that are not sensitive enough requiring greater amplification (cycle threshold), problems in transporting and handling samples, and questions over the quality of sample collection. (162)
A nucleic acid test (NAT) is a procedure for the detection of a specific nucleic acid sequence to detect virus or bacteria via the genetic materials RNA (ribonucleic acid)/DNA (deoxyribonucleic acid), as opposed to antigens/antibodies. As the amounts of genetic material are typically small, techniques are used to amplify genetic materials, namely nucleic acid amplification tests (NAATs), such as a strand displacement assay (SDA), or transcription-mediated assay (TMA), as seems to be utilised in the specific Covid-19 polymerase chain reaction (PCR) test.
PCR typically involves a process of 20–40 repeated cycles of thermal temperature variation. (163)
Initialisation: Consisting of heating to between 94–96 °C (201–205 °F), or 98 °C (208 °F) for 1–10 minutes.
Denaturation: Heating to 94–98 °C (201–208 °F) for 20–30 seconds.
Annealing: Lowered temperature to 50–65 °C (122–149 °F) for 20–40 seconds.
Extension/elongation: The temperature typically raised to approximately 75–80 °C (167–176 °F), but can be as low as 72 °C (162 °F)
This represents a single cycle, which is repeated to amplify the DNA
Final elongation: May be performed between 70–74 °C (158–165 °F) for 5–15 minutes.
Final hold: Cools to 4–15 °C (39–59 °F) for indefinite periods, including short-term storage.
Which brings about doubts in procedural effects, and assumptions made from studies involving the use of once-living intact organisms that are highly treated, potentially rendering data meaningless, and potentially creating conflict due to entropic changes. (164)
That the medical community has rallied to develop reliable molecular diagnostic tests has been aided by numerous research groups working to identify and sequence the viral genomes via open databases. As infections are suggested to increase, authorities sought methods to diagnose and reliable document cases accurately. Clinically, access to robust, and accurate data was dependent upon the isolation and cultivation of coronavirus from the broncho-alveolar lavage fluid via three patients classified as a probable outbreak source.
Electron microscopy, a technique fraught with issues previously discussed by Hillman (164), allowed observations of "typical" coronavirus morphology, whilst more classic use of light microscopy demonstrated a cytopathic effect upon epithelial cells in the human airway. From this, various international groups worked utilising this sequence data to produce primers for PCR tests that would support public health laboratories in the absence of an available commercial Covid-19 test.
The lab of Christian Drosten, of the Institute of Virology, Charité University Hospital, Berlin, and academic collaborators in Europe and Hong Kong (165), verified and assessed the test validity in the absence of both isolates of SARS-CoV-2 or indeed patient samples. Upon this basis, 250,000 kits, were dispatched by the World Health Organization (WHO), to 159 laboratories globally.
A Hong Kong University group developed two quantitative RT reverse transcription PCR tests (166), that target viral genome sequences deposited with GenBank, then validated against two clinical specimens via SARS-CoV-2/Covid-19 infected patients.
The RT-PCR test is suggested to be highly sensitive if used correctly, but notably when the cycle threshold (amplification) is increased. This produces significant problems in high-pressure settings. It remains unclear on the optimal type of clinical specimen, suggesting that the nasopharyngeal swabs give greater consistency than sputum samples. (167) Questions are also raised concerning consistency in cycle threshold between test (with variances in assays), and the cut-off point at which cycle threshold becomes too sensitive and detects dead viral fragments from previous infections.
These early lab tests are suggested to "buy-time,' and give public health authorities some diagnostic tools before commercial products and kits become available at scale. In China, genome sequencing firm BGI Group of Shenzhen had distributed over 50,000 test kits across China by the end of January. On the 5th February, it opened an emergency test laboratory in Wuhan that processed 10,000 samples per day. Other companies developed their tests more slowly.
Not all were relying on primer designs and protocols specified by academic laboratories or public health authorities. Rather than develop bespoke PCR tests, IDbyDNA was one of a handful of companies employing metagenomic nucleic acid analysis as a routine diagnostic and surveillance tool. Its existing Explify Respiratory test was a laboratory-developed test, able to identify over 900 respiratory pathogens, including viruses, bacteria, fungi and parasites, by comparing unbiased metagenomic data obtained from patient samples with a large repository of sequence data.
It was suggested that it could already detect the SARS-CoV-2 strain.
"We have now updated our data with the new coronavirus and are in the process of revalidating,"
Said co-founder and chief medical officer Robert Schlaberg.
"The modifications are all on the data analysis side."
That was, he stated, a more straightforward process than updating the physical assay. The actual data analysis took less than an hour, giving a total turnaround time from receipt of sample to test result of 36 hours. Although more expensive than PCR testing, the falling costs of sequencing could help to democratise this approach. The company is selling the technology as well as its testing services.
The suggestion that NAT tests falsely produce negative results in patients with the infection is complicated by suggestions that Computerised Tomography scans are able to clearly identify signs of viral infection, even though radiation creates tissue disturbances. (168)
The enactment of emergency measures created a situation in which large biotech and medical testing laboratories can develop and validate their tests. Yet, various sources are compiled to generate the data which becomes publicly available. Interestingly, despite the seeming fragility to the stock market, certain biotech companies' value seems to be increasing. (169)
As described above regarding testing, these probabilistic inferences rely upon clusters of so-called empirical evidence, which can be seen to lack validity. As discussed in Mandel (170), a problem discussed by Eddy (171), explains that the following problem is encountered concerning the accuracy of a medical test in aiding probability assessment;
"The probability of breast cancer is one per cent for a woman at age 40 who participates in routine screening. If a woman has breast cancer, the probability is 80 per cent that she will get a positive mammography. If a woman does not have breast cancer, the probability is 9.6 per cent that she will also get a positive mammography. A woman in this age group had a positive mammography in a routine screening. What is the probability that she has breast cancer? __ per cent."
which is shown by Casscells, Schoenberger, and Graboys (172), amongst others, that physicians frequently incorrectly interpret the actual probability. Using bayesian reasoning, as discussed by Mandel (170), physicians fare better when all the information is considered rationally. The proportion of patients in the scenario initially suggested to have breast cancer would be referred to as the prior probability. The possibility that those with breast cancer receive a positive mammogram and a positive mammogram will be received by an individual who has not got breast cancer are both known as conditional probabilities. This information would collectively be referred to as priors. Through its use, we could estimate the likelihood of breast cancer.
If a sample of 10,000 female participants is utilised, and 100 of those have breast cancer, of which just 80 have received a positive mammogram. Nine thousand nine hundred do not have breast cancer, yet 950 of them will also receive a positive mammogram. From this data, we can assess that 1,030 females out of the original 10,000 participants received a positive mammogram, yet only 80 will have cancer, just 7.8 per cent of the total group.
This gives us four groups:
80 females have both breast cancer and a mammogram that is positive.
20 females that have breast cancer mammogram that is negative.
950 females that do not have breast cancer but have a mammogram that is positive.
8,950 females that do not have breast cancer and also have a mammogram that is negative.
Most physicians, and indeed most people make a common error and ignore both the fractions of females with breast cancer and those without breast cancer that have a false-positive diagnosis. Instead, it focuses only upon those with breast cancer and a positive mammogram, commonly assuming that breast cancer's probability must be 80 per cent due to the positive mammogram evidence. Reliance upon one single data point ignores three available pieces of data, and relies upon the prior probability, disregarding the available conditional probabilities. If one utilises all known data or even searches for further data to estimate the probability, then we can revise knowledge.
Priors may be true. They may indeed reflect the reality, but without effective judgement against all available data, or if priors are held as defined and facts that are unchallengeable, beliefs may be given unsubstantiated credibility.
This highlights that Covid-19 testing accuracy is not known, that multiple variants of tests may have been utilised globally, nationally, and indeed across state-lines. Indeed, all diagnoses may not be via tests, with less severe cases that are self-isolated and reported as Covid-19. That said, so-called asymptomatic carriers of the infection may remain undiagnosed. Thus suggestions regarding mortality/fatality rates remain questionable.
We can draw out some data that helps from the cases in Wuhan, China. In Zhang et al. (173), we see that from a total of 140 cases, other comorbidity's were present, indeed from all instances the most prevalent underlying health issue was hypertension.
64.3 per cent of those in the Zhang et al. research had underlying health conditions representing 90 people.
Of those 90;
42 (30%) suffered hypertension
17 (12.1%) suffered diabetes
8 (5.7%) suffered fatty liver disease
7 (5%) chronic gastritis
7 (5%) coronary heart disease
5 (3.6%) thyroid disease
We can even delve into the severity of these conditions and get the nuanced data,
In non-severe cases 82 cases were split by;
20 (24.4% ) hypertension
9 (11%) diabetes
4 (5%) fatty liver diesese
5 (6.1%) chronic gastritis
3 (3.7%) coronary heart disease
1 (1.2%) thyroid disease
And in severe cases (58 people);
22 (37.9%) hypertension
8 (13.8%) diabetes
4 (6.9%) fatty liver disease
2 (3.4%) chronic gastritis
4 (6.9%) coronary heart disease
4 (6.9%) thyroid disease
Giving p-values of
Hypertension - 0.85
Diabetes - 0.615
Fatty liver disease - 0.718
Chronic gastritis - 0.700
Coronary heart disease - 0.448
Thyroid disease - 1.60
A p-value less than 0.05 (typically ≤ 0.05) is statistically significant. However, I often take odds with p-values (124) for data skewing, p hacking et cetera, and I would also be curious about the incidence of thyroid disease due to poor diagnostic terms within orthodox medicine.
The endemic spread of hCoV’s that produce the so-called common-cold enables some degree of immunity, not only to those specific viruses but also to those closely related, with SARS-CoV-2 being one such virus. The evidence that SARS and SARS-CoV-2 are approximately 80 to 85 per cent identical at the genome sequence (67) should indicate that some degree of immunity cross-over could be expected to be demonstrated in contamination of results indicating SARS-CoV-2 infection being due to other hCoV types.
A systematic review by Jefferson et al. (174) suggests that the RT-PCR test is so sensitive that it is susceptible to picking up other hCoV contaminants and that it potentially detects post-infection fragments of SARS-CoV-2 (or other hCoV) that are no longer live. According to the team, this may lead to over-diagnosis of Covid-19 that has occurred, specifically in the so-called second wave of the pandemic.
One of the authors of the study, Professor Heneghan suggests that the findings should be used to classify whether test outcomes that are currently "positive or negative" depending on detection of "the virus", could be refined with a viral cut-off point. In which viral amounts are considered regarding how much trigger what would classically be called a case, indicated by symptoms and illness, not the current definition of a case which is simply a positive result.
The team, including Heneghan, reviewed evidence collected from 25 studies in which viral specimens from samples of positive tests were virally cultured to test whether they were able to grow. This indicates whether a positive test contains an active viral sample that is able to reproduce and transmit or just viral fragments that are dead and unable to grow either in the laboratory setting or presumably in an individual.
The diagnosis of Covid-19 involves an RT-PCR swab test as the standard diagnostic method in both clinical and community-wide settings. It uses numerous processes and chemicals that amplify the genetic material of the virus to aid its study. As discussed previously, "cycles" that occur to recover sufficient viral material to identify it could be utilised to indicate how much virus is evident. The more replication cycles needed, the more infectious an individual may be, which presents an unquantified risk for false positives. Jefferson et al. (174), suggest that while every sample cannot be cultured in a laboratory, an indication of a samples viral content could be deduced from knowledge of the number of threshold cycles required to identify the virus which could provide evidence of whether it is indeed an active infection. (175)
Gniazdowski et al. (176), suggest that even when SARS-CoV-2 was detected molecularly, acknowledgement of the number of cycle thresholds provided increased accuracy in infection diagnosis, particularly in combination with RT-PCR test results, and in those presenting with clinical symptoms. One hundred sixty-one cases indicated positive by RT-PCR exhibited a wide range of values for cycle threshold, which is suggested to reflect variance in viral load despite all sharing a positive test that confirms their status as a Covid-19 case by orthodox means.
In viral samples found to be infectious by culture study, the mean cycle threshold value was indicated to be 18.8 ± 3.4, with a median value of 18.7. In samples that could not be cultured, indicating samples to be non-infectious, a mean cycle threshold value of 27.1 ± 5.7, with a median of 27.5 was indicated.
The research found a general trend that observed an increase in cycle threshold, indicating a reduced viral load. Interestingly, the study found that some patients initially testing negative for SARS-CoV-2, received a positive result on a subsequent test, but that the follow up positive result indicated on a previously negative patient was elicited with a cycle threshold >29.5, and that attempts to recover the infectious virus via culturing these specimens indicated the samples to be negative.
Indeed, Public Health England, acting on behalf of the United Kingdom government (177), state that the cycle threshold provides a value that is semi-quantitative and able to broadly categorise viral concentration within a sample collected by RT PCR. Yet they add the context with regards to samples collected from the upper respiratory tract may be inadequately collected or represent a degraded sample. As such irrespective of the same sample being used to diagnose a case of Covid-19 disease, single same sample cycle threshold values are suggested to be unreliable, noting that values for cycle threshold are not directly comparable due to variances in assays types, not only between laboratories but also within the same laboratory which may have used multiple assays.
The United Kingdom government/SAGE stance is that around six to seven per cent of the population have been infected with SARS-CoV-2 due in part to seroprevalence studies of viral antibodies within the blood. (64), A position that is not supported by Sekine et al. (178), in an investigation of the close family members of patients with “confirmed” Covid-19 infection, finding T cell reactivity in individuals that were asymptomatic or seronegative. Approximately 60 per cent of close family members were evidenced to produce antibodies, yet 90 per cent evidenced T cell response, suggesting that many did not produce or maintain antibodies despite infection. Gallais et al. (179), also concluded that SARS-CoV-2 might induce virus-specific T cell responses without seroconversion, and that reliance upon epidemiological data based upon SARS-CoV-2 detection may be substantial underestimating prior viral exposure within the population. Media attention has maintained a focus on antibody research, and in contrast to the above findings, studies such as Long et al. (180), and Seow et al. (181), that report the waning of SARS-CoV-2 antibodies to at around two to three months fuelled a narrative in both the media and in governmental policy (64; 182), that repeat infection was a plausible risk that necessitated extreme measures to protect not only the 94 per cent that had escaped infection but the minority six per cent that had been theoretically infected already. (183)
Le Bert et al. (184), state that “T cell reactivity was found 17 years after the patients were infected with SARS, which led them to suggest the possibility that T cells generation may protect or reduce the pathology of SARS-CoV-2 infection. This would suggest that the basic premise that antibody data would allow an understanding of whom remained at risk and who was protected is inherently flawed, a fact discussed by Altmann and Boyton. (185)
In reviews (186; 187), of the primary and secondary outcome measures of phase III placebo-controlled trials, T cell reactivity is not considered. Thus, pre-existing immunity levels are not considered either in need to vaccinate previously exposed individuals or in regards to the suggested outcomes that Covid-19 vaccination is currently suggested to confer only short term “immunity”. With studies concluding at 56 days, it is currently impossible to suggest long term immunity is possible, and given that “immunity” is measured by antibodies, one must conclude that it does not look plausible given the above-noted evidence.
“Immunity” via vaccination
The known candidates for Covid-19 vaccine are Pfizer (188), Moderna (189), Johnson & Johnson (190), and AstraZeneca (191), with Pfizer's already being issued emergency authorisation in the United Kingdom at time of writing. Some degree of transparency occurred in publishing vaccine trial protocols. While worthy of praise, the protocols do raise concerns that are seemingly ignored, both by a nation seeking a silver bullet, and government looking for some semblance of success in what has to date been an unmitigated disaster.
The protocols utilised seem to have been specifically designed to prove the vaccines' efficacy, despite minimal measured effects. A trial for a vaccine would typically be expected to have a critical outcome measure, the prevention of infection. As discussed, this would need to occur alongside RT-PCR testing controlled for cycle threshold, serological tests, antibody tests, and more importantly, T cell reactivity measures.
Yet all the trials conducted did not have the prevention of infection as a criterion for effectiveness, or success. for any of these vaccines. In all studies, the primary suggestion of successful outcome was that in those with confirmed infections, the differences in symptom severity between vaccinated and unvaccinated participants were indicated as vaccine effectiveness. Thus, measured differences in symptoms amongst those identified as being infected with SARS-CoV-2 (the accuracy of which may be affected by cycle threshold) determines that the so-called "vaccines" are not effective in preventing infection, or transmission, but theoretically may be effective in modifying symptom in those classed as infected.
In much of society an expectation, and indeed a belief may be that an effective vaccine is one that not only prevents severe disease, but the transmission of the disease/virus to achieve the desired herd immunity. The trials by Pfizer and Moderna that have been indicted for emergency use authorisation in the United Kingdom at the time of writing, and the protocol used by AstraZeneca do not establish that the product prevents serious disease, just that prevention of mild-moderate symptoms are prevented or reduced.
Tests for vaccine efficacy in disease prevention, require large clinical studies that take many years and involve 30-60 thousand participants, rather than the less rigorous protocols that saw manufacturers achieve authorisation for emergency use by the Medicines and Healthcare products Regulatory Authority (MHRA), and seek emergency use authorisation (EUA) from the United States Food and Drug Administration (FDA), via their limited preliminary results.
The protocols also set out rather mild symptoms as the stated requirements for diagnosis that an individual has contracted Covid-19. Minimum criteria to be included as a Covid-19 case is a positive PCR test, which has already been discussed in regards to issues with accuracy, are either one or two symptoms including fever, headache, mild nausea, or a cough. All symptoms that are notable as common cold symptoms, side effects following vaccination and more astonishingly are amongst some of the symptoms indicated for injection of sodium chloride, which is used in the placebo vaccine. (192; 193) Criteria for approval is indicated to be the variance in symptoms displayed in control and vaccine groups that are “infected”, with no use of measures of infection between groups.
For many holding out hope that a vaccine will have an ability to both prevent infection, severe illness and death, particularly in those with known preexisting conditions, or older members of society, the vaccine is hoped to allow social interaction to occur once again. Yet severe illness and death outcomes are listed as secondary objectives. The prevention of death and even hospitalisation from SARS-CoV-2 infection are not critical to the phase III trials satisfactory conclusion.
In being deemed effective in the United Kingdom, and as is expected, in other nations, the trials conducted today have simply been set out so that products can be established as effective by measures that are presumably the lowest barriers to success. Whether this is yet again for political aplomb by a government in crisis, or simply part of an industry race to meet demand and beat the competition remains to be seen. As things stand, work remains incomplete in establishing vaccine efficacy. Questions arise as to whether such detailed research will be completed, or if this “emergency response” will become the new normal in bringing pharmaceutical to market in global pandemics.
Pandemic Parlour Tricks
As has been discussed in this text and both Consistent Eating (143), and Controlling Intuitive Appetite (124), science and particularly research remains at risk of data hacking and other scientific attempts to skew evidence to maintain a hypothesis.
As has been discussed, increased amplification or cycle thresholds have been identified as having the potential to increase false positive, to diagnose cases of Covid-19 in individuals who may not have active infections. The much fated second wave of Covid-19 in the United Kingdom saw a paradox in which “cases” grew exponentially in relation to “deaths with Covid-19”, which may have occurred due to several factors;
Increased test availability when compared to early 2020
A less lethal strain but with increased virulence
Increased cycle threshold
The discussed issue with cycle threshold provides a plausible possibility that post-vaccination, tests could be conducted with lower amplifications which would naturally lower cases by omitting positive samples that are prior infections and simply fragments of dead virus.
This effect, whilst being plausibly deniable as either “conspiracy theory”, is, in fact, possible given that numbers of cases could be dialled up and down at will via sleight of hand parlour tricks that manipulate the data to suit the desired outcome. Such underhand tactics may seem far fetched; one needs only consider previous activities both within the industrial-medical complex, and government, particularly in the United States and the United Kingdom concerning historical and recent manipulations. (7; 124)
Globally the establishment of RT-PCR testing as the Covid-19 gold standard has been flawed, indeed, without the availability of viral material, reliance was put upon the specific genetic sequence initially published by Chinese scientists (194)
Test protocols both globally and even within nations have utilised RT-PCR testing that requires two primer matches, instead of the preferred three. A potential “oversight” that may render such test protocols inaccurate in their ability to both delivery results, and in their use in comparing data against other variations of test protocols, with Borger (195), suggesting that the use of such a poor PCR test protocols, combined with a high cycle threshold (>35), as is common both in the United States and throughout Europe. Leads to a probability of infection in a positively diagnosed person is <three per cent, suggesting the probability of a false-positive result is, therefore, 97 per cent.
Even the United States own Dr Fauci is evidenced on video stating that; "If you get a cycle threshold of 35 or more…the chances of it being replication-competent are minuscule…you almost never can culture virus from a 37 threshold cycle…even 36… it's just dead nucleotides, period." (196)
As the virus apparently spreads rapidly with a drastically increasing number of cases appearing despite the introduction of many measures (masks, social distancing et cetera), many have noted that a significant majority are free from what may be classified as severe symptoms. This led to the warning initially that specific groups such as infants through to adolescents may be asymptomatic superspreaders (197). While not evidently sick, it did help transmit the virus amongst the community.
This narrative changed; specifically, it seemed to alter when the government required schooling facilities to reopen, so that the economy may also be opened by allowing parents and caregivers to outsource childcare once again. Around this period spread amongst younger people was partially dismissed as irrelevant, and asymptomatic spread was thus positioned as a community-wide problem with the potential for anyone without symptoms to spread SARS-CoV-2.
Remembering, as discussed in Controlling Intuitive Appetite (124), diseases are similar to language, and definitions alter as culture or industry manipulates its usage. Polio's apparent eradication through vaccination is due primarily to manipulating the classes of symptoms classified as polio. Jonas Salk's miracle polio vaccine is a story perpetuated in current orthodox media, particularly in light of the announcement of Covid-19 vaccine availability. Polio, a disease often linked with dichlorodiphenyltrichloroethane (DDT) poisoning. (198) Before introducing the vaccine in 1955 >50,000 people within the United States contracted polio per year, by 1955, a 45 per cent decline was evident, and in 1955 the figure was 28,985. (199)
Dr Bernard Greenberg, the head of the University of Carolina School of Public Health's Department of Biostatistics stated that; qualification for diagnosis of paralytic poliomyelitis required a patient to be exhibit symptoms of paralytic state for at least 60 days following the diseases onset from 1955 onwards. Before the availability of vaccination (<1954), symptoms needed to be exhibited for just 24 hours with no need for confirmation from either laboratory testing, or the residual presence of paralysis. Such changes in defined terms alter reporting and often lead to symptoms being attributed to other disease classifications. In 1955 we started reporting new diseases, "polio-like" illnesses such as transverse myelitis, acute flaccid paralyses, and aseptic meningitis which seem to be increasing in prevalence. (200; 201)
While some "polio" cases result in temporary paralysis, some present with no paralysis and symptoms range from fever, headache, sore throat, vomiting, fatigue, muscle aches/weakness, pain and stiffness in the back, neck or limbs, to meningitis. (202)
By redefining diagnostic criteria, this contributes to a downward shift in documented cases and a rise in other disease pathologies. Similar effects may be apparent in Covid-19 with similarity in pathology to other diseases, alterations in defined symptoms as time advances, with initial reports of symptoms for mild disease as;
Presenting with uncomplicated upper respiratory tract viral infection and may exhibit common non-specific symptoms;
cough (both with or without production of sputum production)
anorexia (medically described as lack of appetite/disinterest in food.
dyspnea (difficulty or laboured breathing)
(4; 7; 203; 204; 205)
Indeed, as documented in Controlling Intuitive Appetite (124), science seems to be for sale to the highest bidder, with industry seemingly able to pay for desirable results to be both published and receive peer review. Yet a replication crisis seems apparent when others attempt to reproduce the same results. (206)
This replication/reproducibility crisis is a methodological effect evident in numerous scientific studies and fields where the findings are either difficult or impossible to reproduce. Within the field of medicine Ioannidis (207), found that from a total of 49 studies conducted between the years 1990 to 2003, accounting for >1000 citations, 45 of the studies claimed effective therapeutic effect, yet further studies subsequently contradicted 16 per cent of the studies.
Baker (208), surveyed>1,500 researchers, with >70 per cent stating they had attempted to reproduced the experiments of other scientists and failed to replicate the findings.
Again Ioannidis (209), highlights this problem, suggesting a need for research to become patient-centred, rather than focusing upon the “needs of physicians, investigators, or sponsors.” Despite this crisis in academia, and the industrial pace at which Covid-19 research occurred, both under time pressures, but free from formal peer review, we are told the government are following “the science” and that we should trust the experts.
Scientific credibility is achieved by research and by establishing further with evidence via their replicability with newly acquired data. This stands alone from retesting scientific “evidence” using the same data and analyses (reproducibility), and retesting existing data with various types of analyses (robustness), in such situations outcomes that were consistent with the prior findings increase confidence, and inconsistent results decrease the confidence.
In Covid-19, it seems there is no exact replication occurring in testing and diagnosis, with every test potentially utilising different cycle thresholds amongst other factors such as assay variability. As such generalisability in data decreases the confidence in the findings as the potentially unique conditions applied to RT-PCR tests can not be considered a replication study.
The inability to validate the test data to support either the number of presenting cases, or the much-queried number of deaths “with Covid-19” (remember that preventable deaths should indeed be considered tragic losses, even if not due to SARS-CoV-2), skewed data does not present an accurate picture of either the scale of the problem, or whether measures are appropriate or effective.
This coupled with the suggestion that antibody production remains low following infection, a process entirely expected in younger and or “healthy” populations that rather than diverting energy generation to a complex, slow and energy-intensive process of antibodies production, utilises what is termed the innate immune system, which works via a far more efficient process involving T-cells that defend against future infections. A such, one would expect to see little or no evidence of antibodies as timespan progresses. Its use by SAGE to guide the proportion of infection amongst the population is either an error due to inadequate qualifications amongst a SAGE team primary constituting mathematicians, modellers and behaviourists, with a government also lacking in biological knowledge. Or due to some degree of malice by those seeking to maintain an unproven narrative that is undoubtedly failing.
Estimating SARS-CoV-2 infection rates within the United Kingdom population may be achieved using the known infection fatality ratio (IFR), which is imperfect, given that deaths with Covid-19 may still be falsely positive. However, theoretically, this is less problematic than the opposing stance of utilising antibody data in all cases, including those codified asymptomatic.
Despite government confidence, the current policy leaves us with this "known unknown" that both seriously hampers understanding of the crisis and damages that response. This effect has been seen by many as the pandemic rages in. The Imperial College team (38), led by Professor Ferguson, suggests that <7 per cent of the United Kingdom population have been infected, which powerfully justifies prolonging lockdowns, social restrictions, and early vaccination rollout. Relaxation of measures such as social distancing are suggested to risks millions of individuals becoming infected, and the already depleted national health service becomes overwhelmed, as it does each winter. (210)
The model suggested excess deaths of circa 510,000 without precautions, and approximately 250,000 using a mitigation strategy, dropping to 20,000 if the plan was to suppress the virus. This suggests that a policy of lockdown would prevent 230,000 excess and unnecessary deaths occurring.
As this paper has sought to establish, the model propagated by Professor Ferguson seems to have drastically underestimated infection rates amongst the population. A paper by Lourenço et al. (211), led by Professor Gupta from Oxford University, suggests that various estimates are suggested for a percentage of infected (both current and prior) population within the United Kingdom, with figures as high as 68 per cent. Critics claimed that Professor Gupta's work was too "speculative" with little "empirical justification", yet the Imperial model also falls foul of the same accusation. The previously discussed estimates are based upon assumptions built into the Imperial model, which created an implausible view of a novel virus. One would assume that models could be updated and coded to work with newly available data, such as cycle thresholds for RT-PCR tests (for example >30 cycle threshold positive tests could be weighed more towards being indicative of prior infection), T-Cell reactivity et cetera.
Being able to increase the accuracy in gauging rate of infection helps not only guides and justifies policy interventions but helps to establish the infection fatality rate (IFR) which is vastly different from the case fatality rate (CFR), that uses the number individuals that tested positive (ignoring false positive and negative results) and is divided by the total deaths (ignoring questions about whether SARS-CoV-2 was the specific cause of death or a co-factor). Variability in CFR occurs between country due to multiple variables, including testing availability et cetera.
Ioannidis (212), led a team to assess the actual infection rates in Santa Clara County, California, using serology testing for antibodies, which as noted performs poorly in documenting longterm exposure rates, specifically in younger/“healthier”. The team looked at the data of 3,300 Santa Clara County residents in the United States and found rates of infection to be 50 to 85 times the amount of cases officially documented (956 at the time of the study).
Loss of antibodies, while biologically expected due previously explained reasons (antibodies production is energetically expensive, while T-cell reactivity which is part of innate immune function is less so), is suggested as a reason for caution within communities (lockdown et cetera) do to the “known unknown” regarding whether re-infection is plausible. (213)
A Japanese woman (214), was suggested to have been re-infected but was classified as being “immunocompromised.”
In considering this we must rationalise many aspects, firstly considering the terms, being classified as suffering from Covid-19 may not necessarily be due to being evidenced SARS-CoV-2 as was clear early in the pandemic within many nations, diagnostic testing was not available to many, as such symptoms were utilised and quarantine necessary. It must be noted that such symptoms are shared by many other pathologies, including the common-cold, which of course can be due to specific coronaviruses. We must also differentiate between the two actual positive results; one may indicate a live virus evident by an RT-PCR utilising a low cycle threshold. The second may be a test procured due to the onset of similar symptoms and the positive result produced using a much higher cycle threshold. Without the availability of data on test protocols, we can not accurately consider whether reinfection is plausible. Indeed, in a case report by Prado-Vivar et al. (215), they put forward evidence including epidemiological data, clinical findings, the positive RT-PCR re-test, two different virus clades and the antibody response as being compatible with reinfection, but admit a critical limitation of the study was the failure to culture the virus, as such we are unable to conclusively state whether it was reinfection to fragments of prior infectious viral material that is no longer live or presenting a risk to others.
Viruses do mutate, and as noted tend to become more easily transmissible, but less dangerous. As discussed, it is implausible that as suggested by the Ferguson Imperial College model, that it presented a novel pathogen. The nature of evolution means it has ancestors and will continue to do so. However, our exposure to one strain should confer some immunity to further, specifically weaker strains. Access to cycle threshold data and T-Cell reactivity studies could re-code the current epidemiological models and provide better-guided governance and strategic planning in tackling the virus, restoring public confidence and creating a plan that allows the economy to reopen. Without such data, and in the hands of leadership relying upon so-called super-forecasters (216), the country seems destined for regular lockdowns and cyclical vaccination programs to “protect” against reinfections of new strains. Undoubtedly, the country (and many other nations) are in the grips or a pandemic that is straining health care provisions beyond their capabilities, but it is essential to gain context. In the United Kingdom, austerity and poor management have not only limited the resources of the National Health Service, which is annually at breaking point each flu season, but staffing levels have suffered due to insufficient funding for students aiming to enter the health care industry, and poor retention of staff due to wage freezes and poor working conditions.
In Controlling Intuitive Eating (124), I wrote that intelligence might be better measured by the ability to observe, analyse, and update beliefs. At this, we are failing, while an emerging pathogen causes fear and reactionary strategies, as timespan increases “the science” could and should be updated rather than moulded to fit the policy. That this continues alongside issues of cronyism in government contracts for personal protective equipment (PPE), testing, and vaccination causes a further degree of distrust in the political strategies utilised to date.
Science needs to be utilised to its full capacity, not coopted to justify policies that meet industrial and political desires.
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