MonthOctober 2020

The utter unreliability of PCR testing

Excerpt of a SARS-CoV-2 PCR KIT Data Sheet

I’ve written already on why there is abundant reason not to trust PCRs for diagnosis of the pandemic status of SARS-CoV-2. I’ve added that over-reliance on these methods can easily lead to psuedo-epidemics.

This time I want to present you with other factual sources on PCR.

First, the picture above shows you part of a data sheet of a PCR kit for SARS-CoV-2. Notice the highlights:

  • the test can suffer interference from a host of other common seasonal viruses
  • the test should not be used as a sole evidence for clinical diagnosis and treatment

Second, article in the British Medical Journal clearly states:

RT-PCR tests can detect viral SARS-CoV-2 RNA in the upper respiratory tract for a mean of 17 days; however, detection of viral RNA does not necessarily equate to infectiousness, and viral culture from PCR positive upper respiratory tract samples has been rarely positive beyond nine days of illness.

Third, the Oxford Centre for Evidence Based Medicine’s article clearly explains that testing positive to PCR does not equate to infection:

A PCR test might find the virus it was looking for. This results in a PCR positive, but a crucial question remains: is this virus active, i.e. infectious, or virulent? The PCR alone cannot answer this question. The CEBM explains why culturing the virus is needed to answer this question:

“In viral culture, viruses are injected in the laboratory cell lines to see if they cause cell damage and death, thus releasing a whole set of new viruses that can go on to infect other cells.”

H1N1: the pandemic that wasn’t

Original article on Forbes. Copying as Forbes has been deleting its old articles that give support to the idea that WHO is faking this pandemic, too.

Mar 11, 2010,12:00pm EST, Henry I. Miller

The H1N1 swine flu outbreak appears to have ended less like the rogue wild boar that United Nations bureaucrats predicted and more like roasted pork tenderloin with apples and sage. From the beginning the World Health Organization’s actions have ranged from the dubious to the flagrantly incompetent.

Last June the WHO boosted the pandemic alert to the highest level, Phase 6. That meant that, according to the WHO, a pandemic was under way–the first time in 41 years that the organization had made such a declaration. But the WHO must have been suffering from four decades of amnesia because ordinary seasonal flu, which sweeps the world annually–and which is far more lethal than the currently circulating low-virulence H1N1 swine flu–certainly meets the organization’s definition of a pandemic: infections over a wide geographic area that affect a large proportion of the population.

Ironically, one might even consider the emergence of the H1N1 flu during the past year a net public health benefit, since it appears to have suppressed, or at least supplanted, the far more virulent and lethal seasonal flu strains. During the second week of January, 3.7% of Americans tested positive for the seasonal flu, compared with 11.5% during the same week last year. The death toll in the U.S. from H1N1 is estimated by the Centers for Disease Control and Prevention to be around 3,900, while in an average year seasonal flu kills about 36,000.

The WHO’s April 2009 decision to raise the pandemic flu threat to the penultimate level, Phase 5, “Pandemic Imminent,” was unwarranted and far outpaced the data accumulated. Even worse was the June declaration that a pandemic was under way, which exposed the WHO’s flawed fundamental paradigm. A warning system based solely on how widely a virus has spread, but that does not consider the nature, severity and impact of the illness it causes, is prone to false positives; it would classify not only seasonal flu but also the frequent but largely inconsequential outbreaks of virus-caused colds and gastroenteritis as “pandemics.” WHO has never offered any explanation for why these examples that seem to fit its definition of a pandemic do not meet its criteria.

False alarms make the “pandemic under way” designation almost meaningless, and they diminish its usefulness, which, in turn, has important consequences. As Dr. Jack Fisher, a professor of surgery at the University of California, San Diego, School of Medicine, observed, “Keep crying ‘wolf,’ and WHO can expect lower than customary compliance with flu vaccine advisories next fall.” Not only next fall, but also at some future time when we encounter a genuinely dangerous new pathogen such as a strain of H5N1 avian flu (which in its present form boasts a mortality rate more than 100 fold higher than the H1N1 swine flu) that is easily transmissible between humans.

The U.N.’s false alarms have had more immediate, negative effects. Matthew Hingerty, managing director of Australia’s Tourism Export Council, lamented that the country lost thousands of tourists because of the WHO’s pandemic declaration. Egyptian public health authorities overreacted and summarily ordered the slaughter of all the pigs in the country. In addition to the devastating economic losses, garbage filled the streets of Cairo and the numbers of rodents rose to fearsome levels because the pigs were no longer available to consume much of the garbage produced in the city. The U.N. indicted by the Law of Unintended Consequences.

The publicity and resulting panic surrounding the WHO’s announcement of Phase 5 and 6 alerts–especially since the vaccine was not widely available until December–also brought out the fraudulent peddling of all sorts of ineffective and possibly dangerous protective gear and nostrums, including gloves, masks, dietary supplements, shampoo, a nasal sanitizer and a spray that supposedly coats the hands with a layer of anti-microbial “ionic silver.”

For all these reasons, the declaration of a pandemic cannot be a prognostication but rather should be a real-time snapshot, and it must only be made when science and common sense support it.

WHO’s performance has been widely criticized. Most flu experts believe that the WHO’s actions were overly alarmist and precipitous and the Parliamentary Assembly of the Council of Europe announced that it plans to debate “false pandemics, a threat to health.”

And yet WHO officials continue to defend their actions. In a Jan. 14 conference call with reporters, Keiji Fukuda, special adviser to the WHO’s director general for pandemic flu, remonstrated that the organization had not overplayed the dangers but “prepared for the worst and hoped for the best.” Other communications were more strident. “The world is going through a real pandemic. The description of it as a fake is wrong and irresponsible,” the WHO said on Jan. 25. A particularly problematic statement came from WHO spokesman Greg Hartl, who said, “We cannot control how people react to” WHO announcements concerning pandemics. He would benefit from tutoring in risk communication.

The WHO’s dubious decisions demonstrate that its officials are too rigid or too incompetent (or both) to make needed adjustments in the pandemic warning system–deficiencies we have come to expect from an organization that is scientifically challenged, self-important and unaccountable. The WHO may be able to perform and report worldwide surveillance–i.e., count numbers of cases and fatalities–but its policy role should be drastically limited.

U.N. bureaucrats pose as authorities on all manner of products, public policy and human activities, from desertification and biodiversity to the regulation of chemicals, uses of the ocean and the testing of genetically engineered plants. However, the U.N.’s regulatory policies, requirements and standards often defy scientific consensus and common sense. Its officials are no friends of commerce, public health or environmental protection. The result is a more precarious, more dangerous and less resilient world. When it comes to pestilence, the U.N. may be the greatest plague of all.

Henry I. Miller, a physician, molecular biologist and former flu researcher, is a fellow at Stanford University’s Hoover Institution and at the Competitive Enterprise Institute. He was an official at the National Institutes of Health and Food & Drug Administration.


Yes, you read it. Pseudo-epidemics. They are a real thing.

Though I am scientist by training, I am not a medical scientist or anything closely related. But I remain a scientist. The scientific method that underpins all the sciences doesn’t change.

That’s what allowed to have a critical eye on all this pandemic business.

Now, all the recent posts on this blog are there to point out one simple thing: the Covid-19 pandemic has ended in May. What we’re seeing now is what many scientists and medical doctors are calling a casedemic.

In short, due to pre-existing T-cell immunity and the now endemic nature of the virus, the over-reliance on PCR testing is causing a overwhelming high number of false positives. These false positives are what they call asymptomatic people. Unlike what the people in the media tell you, the reality about these people is that they are not actually sick.

A few days ago I found out that there’s an established term to refer to what’s happening right now with SARS-CoV-2. It’s called a pseudo-epidemic.

A sample of articles that talk about this phenomenon:

From the latter I quote:

Given current definitions COVID-19 will never end. People will be dying of it forever, even if the virus disappears completely. Worse still, the system is locked in a series of feedback loops — if something causes test numbers to rise then so will case numbers, which in turn will cause a further increase in testing, causing the rise to continue, triggering local lockdowns and pointless evidence free rituals, until people get depressed and stop trying to do things causing numbers being tested to fall again.

A medic’s case against another lockdown

If lockdowns were a prescription drug for Covid-19 treatment, the FDA would never have approved it. The seminal Imperial College London paper and other mathematical models like it were used to justify their use, but clinicians would never prescribe a drug or propose a surgery based on such modelling. The now well-publicised failure of these models to accurately predict Covid-19 outcomes proves the rule.

In medical science, we rely on epidemiologists to take all the available data from all the countries and perform statistical analyses to correct for as many different variables as possible.

This has now been done for lockdowns. In August, the Lancet published an analysis of data from 50 countries. The researchers found that full lockdowns were ‘not associated’ with decreased mortality from Covid-19. These are hard outcome data; reality cannot be waved away with theories or projections.

Covid-19: Do many people have pre-existing immunity?

I have already talked about the mounting evidence supporting widespread T-cell immunity against SARS-CoV-2 (Covid-19).

This study on the British Medical Journal (Covid-19: Do many people have pre-existing immunity?) is interesting because it’s one of the few places where a similar situation from 2009 is recalled. In fact, in 2009 we experienced a casedemic with H1N1, that is, a growing number of cases which however did not lead to an actual high mortality rate. I quote:

Swine flu déjà vu

In late 2009, months after the World Health Organization declared the H1N1 “swine flu” virus to be a global pandemic, Alessandro Sette was part of a team working to explain why the so called “novel” virus did not seem to be causing more severe infections than seasonal flu.12

Their answer was pre-existing immunological responses in the adult population: B cells and, in particular, T cells, which “are known to blunt disease severity.”12 Other studies came to the same conclusion: people with pre-existing reactive T cells had less severe H1N1 disease.1314 In addition, a study carried out during the 2009 outbreak by the US Centers for Disease Control and Prevention reported that 33% of people over 60 years old had cross reactive antibodies to the 2009 H1N1 virus, leading the CDC to conclude that “some degree of pre-existing immunity” to the new H1N1 strains existed, especially among adults over age 60.15

The data forced a change in views at WHO and CDC, from an assumption before 2009 that most people “will have no immunity to the pandemic virus”16 to one that acknowledged that “the vulnerability of a population to a pandemic virus is related in part to the level of pre-existing immunity to the virus.”17 But by 2020 it seems that lesson had been forgotten.

Structural stability of SARS-CoV-2 3CLpro and identification of quercetin as an inhibitor by experimental screening – ScienceDirect

Structural stability of SARS-CoV-2 3CLpro and identification of quercetin as an inhibitor by experimental screening – ScienceDirect
— Read on

This is on top of Quercetin also being a Zinc ionophore, which helps increasing the amount of intracellular elemental zinc, which in turns inhibits replication of RNA viruses.

Potential interventions for SARS‐CoV‐2 infections: Zinc showing promise – Brewer – – Journal of Medical Virology – Wiley Online Library

Intracellular elemental zinc (Zn) inhibits various RNA viruses including coronaviruses.2 In a 2010 study, Zn coupled with an Zn ionophore (pyrithione), showed potent inhibition of SARS‐CoV replication (even at very low micromolar concentrations). Zn directly inhibited the coronaviral RNA‐dependent RNA polymerase, which functions as the core enzyme of the RNA viral synthesizing machinery.2 Zn also inhibits SARS‐CoV papain‐like protease 2, which is also a key enzyme for viral replication and assembly of functional viral proteins.3 Zn and several Zn chelates were shown to inhibit furin (proprotein convertase) which is important in the pathogenesis of many viruses.4 The furin proteases have been proposed as therapeutic targets for several viral pathogens.5 Specifically, the spike glycoprotein of SARS‐CoV‐2 contains a unique furin cleavage site that is not found in SARS‐CoV.6 This furin activation mechanism increases the infectivity and pathogenicity of viruses.6 Zn inhibition of host furin in SARS‐CoV‐2 infection may be an important antiviral mechanism unique to this novel strain.

Chloroquine has been shown to be a potent Zn ionophore and transports Zn through the cell membrane substantially increasing intracellular levels of Zn, especially in the endosomal‐lysosomal compartment.7 These same ionophore properties presumably apply to the closely related molecule, hydroxychloroquine (HCQ).
— Read on

Trajectory of COVID-19 epidemic in Europe and herd immunity

From this study (not yet peer-reviewed), we read:

«Whatever value is specified for the infection fatality ratio, a model that allows for heterogeneity has better fit to the data than the homogeneity model and supports herd immunity as the main factor underlying the reversal of the epidemic.»

This is compatible with the mounting evidence of pre-existing T-cell immunity against SARS-CoV-2.

Immune cells for common cold may recognize SARS-CoV-2

More on cross-reactive T-cell immunity.

They found that of the SARS-CoV-2 and “common cold” coronavirus fragments that were most similar (at least 67% genetic similarity) 57% showed cross-reactivity by memory T cells.

The evidence for pre-existing T-cell immunity against Covid-19 keeps piling up, hence the case for a much lower threshold for herd immunity becomes stronger. Conversely, the case for a vaccine becomes way weaker.

Lockdown responsible for excess deaths more than Covid-19?

There’s a lot of analysis on excess deaths, and I have no intention to cover everything. But one thing is clear: the way deaths by Covid-19 have been counted is wrong in most countries. Also, the excess deaths is comparable to that of a bad flu year. Anyhow, this post is about something else: there’s now emerging evidence of something that, to me and many others, is pretty obvious; that is, that the lockdown has caused more excess deaths than the “pandemic” itself.

This study (Coronial autopsies identify the indirect effects of COVID-19) says:

Of the 67 autopsies done at our hospital during the first 2 months of lockdown, only two autopsies identified COVID-19 that was undiagnosed before death. More frequently, reduced access to health-care systems associated with lockdown was identified as a probable contributory factor (six cases) or possible contributory factor (eight cases) to death.

These causes included potentially preventable out-of-hospital deaths such as acute myocardial infarction and diabetic ketoacidosis, in which patients contacted the health services by telephone and were advised to self-isolate at home rather than attending hospital.

Direct reference to financial or work pressures caused by COVID-19 was identified in three of ten cases of suicide.

Deaths from drug and alcohol misuse significantly increased during the lockdown period in comparison to the same period in 2018 (appendix), but it was not possible to identify whether individual cases were influenced by COVID-19 movement restrictions

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