For those who may be disappointed by some of our postings, those postings that discuss a potential worsening of the Covid scamdemic, one word of clarification. We do not in the least suggest that such a possibility could be a natural development of a virus out of control. Rather, such posts are meant to warn the public of the real possibility of an escalation of the scamdemic by the same means that made it possible in the first place. The same agenda that triggered the phase one of the plandemic continues against the public, only at a more heightened level.
By Peter Andrews, Irish science journalist and writer based in London. He has a background in the life sciences, and graduated from the University of Glasgow with a degree in genetics
It has been revealed that the standard tests being used in the US to diagnose Covid-19 cases are far too sensitive, with the vast majority of people marked down as being positive actually turning out to be negative.
Top US virologists have been stunned by revelations about the laxity of the US Covid testing regimen. It turns out that tests that deliver a simple binary“positive or negative” result are not fit for purpose, as they tell us nothing about the contagiousness of each person.
Data from three US states – New York, Nevada and Massachusetts – shows that when the amount of the virus found in a person is taken into account, up to 90 percent of people who have tested positive should actually have been negative, as they are carrying only tiny amounts of the virus, are not contagious, pose no risk to others, and have no need to isolate.
This means that only a fraction of the daily “cases” being reported so hysterically in the mainstream media are actual, bona fide Covid-19 sufferers, and need treatment and to separate themselves from others.
It’s a sensitive issue
So how could this have happened? The answer has to do with the sensitivity of PCR (Polymerase chain reaction) tests for Covid, which it turns out can be ramped up according to the taste of the testing companies. Most testing companies have chosen the outrageously high sensitivity limit of 40 PCR cycles – meaning that the DNA in a sample is exponentially increased 40 times in order to amplify its signal.
But using such a ridiculously sensitive test means that the faintest traces of a dead virus, or even leftovers from previous infections, can result in a positive. Professor Juliet Morrison, a University of California virologist, said that even a limit of 35 PCR cycles is too high, let alone 40. She said she was “shocked that people would think that 40 could represent a positive.”But apparently, pretty much everyone in the US Covid brain trust took exactly that on faith.
So the scale of the pandemic ‘problem’ is actually much smaller than we’ve been led to believe – about a tenth of what all the politicians and media have been using to justify the lockdowns, the quarantines, the mass testing. Some may be shocked that the scale of the problem is so much smaller than assumed. But for a seasoned ignorer of any and all statistics that contain Covid ‘cases’, there are no surprises here. The truth is, there was never any reason to be confident in such figures. The FDA has only now been forced to concede that they have no idea how different testing companies determine which the positive and negative tests are: they just accept whatever data they are given.
What these findings bring is absolute assurance that the testing to this point has been an utter waste of time, and that not one statistic concerning this pandemic – from cases to deaths to infection rates – can be believed. But it should not have taken some journalist to ask the right question to discover this: a bit of common sense would have been enough. What is it going to take for these professional virologists to drop their assumptions and models, and just start acting based on the facts at hand?
Scrap test and trace
It’s a virus so deadly, you need a test to tell whether you have it or not. So goes the refrain of many lockdown skeptics, Covidiots and anti-maskers, of whom I am an indignant supporter. Something has gone… not just wrong, but totally haywire… when the might of the world’s scientific establishment is trained with the zeal of a Witchfinder General on one particular microscopic particle. Not even a particularly dangerous particle; the latest data show it is the eighth most common cause of death in England, and it doesn’t make the top ten in Wales.
Meanwhile, in Wuhan, the original source of this disease, the pool partiesare in full swing. They don’t seem to be too worried about PCR tests or contact tracing, or even the virus itself. The Chinese government says that their supreme lockdown was so awesome that they now have zero Covid: a biological impossibility. Maybe they just stopped testing, and decided to get on with their lives. Everyone else should take a leaf out of their book.
By Peter Andrews, Irish science journalist and writer based in London. He has a background in the life sciences, and graduated from the University of Glasgow with a degree in genetics.
A widely circulated scientific study reported that Covid-19 causes long-term heart problems. Its authors have been forced to issue major corrections after they wildly miscalculated the risk, but the damage has already been done.
The scientific establishment wields a lot of power these days. The emergence of the novel coronavirus has elevated many career scientists and academics to positions of great influence, acting as advisors and commissars to governments on all things Covid-related. Which, it turns out, is everything. That is why it is so important that they conduct rational, unbiased research, and analyse all findings with great scepticism, taking nothing for granted.
Weird science
Alas, that was never going to happen. Unless you follow the right Twitter accounts (such as Alex Berenson who has been indefatigable in his criticism of shoddy Covid-19 ‘science’), you won’t read about this anywhere else. But what should be a pretty big scandal resulting in a major inquiry into publishing practices is currently underway in the field of cardiology.
Just over a month ago, a paper from Germany entitled, ‘Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19)’, was published in the journal JAMA Cardiology. It was based on 100 people recently recovered from Covid-19, who underwent MRI scans to find factors associated with damage to their hearts.
The article quickly became a smash hit, going viral, inasmuch as academic research can. It racked up hundreds of thousands of interactions on its Altmetric score, a tool that tracks how much a piece of research is being clicked, shared and talked about online. No doubt, this was owing to the paper’s bombshell conclusions. If Covid-19 was strongly linked to long-lasting heart disease in a significant proportion of those who survive it, that would be a hugely important thing to know.
A comedy of errors
The only problem with the conclusion of the paper is that almost every piece of data given to support it was wrong. As more and more media breathlessly reported that Covid-19 will eventually kill everyone with heart attacks, the mathematically minded on Twitter – including Darrel Francis, a Professor of Cardiology at the National Heart and Lung Institute – began topoint out obvious miscalculations and mismatches in the results of the study.
The authors appeared to confuse medians for means, and data points present in the graphs were absent elsewhere. In essence, the paper was riddled with remedial mistakes that the first few hundreds of thousands of people who read it (or scan the last few sentences) failed to notice.
But Professor Francis is still not happy with the reissued article, launching another scathing attack on his Twitter account. He has more than the layman’s knowledge of statistics, but he lays out in no uncertain terms that the authors are still, even after their extraordinary climb down, fudging the numbers. He is adamant that the corrected figures show that while people who have recovered from Covid-19 do show markers of heart disease in their MRI scans, so do people of similar health profiles who have not had the virus. That is, Covid-19 had absolutely nothing to do with the heart damage seen in the people in the study.
The authors of the study, meanwhile, have not taken kindly to the egg on their faces. They have lashed out at Twitter’s dismantling of their less-accredited math skills, (not sure people outside UK will know what these are) griping that a letter to the editor “would indeed be more appropriate.” It only took them a month to correct their substandard article, but by that point the damage was done. Just the other day I actually had someone casually inform me that “Covid causes heart damage.” Clearly the study’s reach has been wide. Whether its debunking will have as wide a reach remains to be seen.
Denis Rancourt, PhD, has published over 100 peer-reviewed studies in his career, but ResearchGate choose to censor and remove this paper because it didn’t fit the narrative of the Great Panic of 2020 over COVID-19. Such censorship proves the existence of an alternative agenda.
Again, this underscores the Technocrat methodology of shaming, ridiculing and censoring anybody that comes forth with real science that refutes their pseudo-science. ⁃ TN Editor
Masks and respirators do not work.
There have been extensive randomized controlled trial (RCT) studies, and meta-analysis reviews of RCT studies, which all show that masks and respirators do not work to prevent respiratory influenza-like illnesses, or respiratory illnesses believed to be transmitted by droplets and aerosol particles.
Furthermore, the relevant known physics and biology, which I review, are such that masks and respirators should not work. It would be a paradox if masks and respirators worked, given what we know about viral respiratory diseases: The main transmission path is long-residence-time aerosol particles (< 2.5 μm), which are too fine to be blocked, and the minimum-infective dose is smaller than one aerosol particle.
The present paper about masks illustrates the degree to which governments, the mainstream media, and institutional propagandists can decide to operate in a science vacuum, or select only incomplete science that serves their interests. Such recklessness is also certainly the case with the current global lockdown of over 1 billion people, an unprecedented experiment in medical and political history.
Review of the Medical Literature
Here are key anchor points to the extensive scientific literature that establishes that wearing surgical masks and respirators (e.g., “N95”) does not reduce the risk of contracting a verified illness:
Jacobs, J. L. et al. (2009) “Use of surgical face masks to reduce the incidence of the common cold among health care workers in Japan: A randomized controlled trial,” American Journal of Infection Control, Volume 37, Issue 5, 417 – 419. https://www.ncbi.nlm.nih.gov/pubmed/19216002
N95-masked health-care workers (HCW) were significantly more likely to experience headaches. Face mask use in HCW was not demonstrated to provide benefit in terms of cold symptoms or getting colds.
None of the studies reviewed showed a benefit from wearing a mask, in either HCW or community members in households (H). See summary Tables 1 and 2 therein.
“There were 17 eligible studies. … None of the studies established a conclusive relationship between mask/respirator use and protection against influenza infection.”
Smith, J.D. et al. (2016) “Effectiveness of N95 respirators versus surgical masks in protecting health care workers from acute respiratory infection: a systematic review and meta-analysis,” CMAJ Mar 2016 https://www.cmaj.ca/content/188/8/567
“We identified six clinical studies … . In the meta-analysis of the clinical studies, we found no significant difference between N95 respirators and surgical masks in associated risk of (a) laboratory-confirmed respiratory infection, (b) influenza-like illness, or (c) reported work-place absenteeism.”
Offeddu, V. et al. (2017) “Effectiveness of Masks and Respirators Against Respiratory Infections in Healthcare Workers: A Systematic Review and Meta-Analysis,” Clinical Infectious Diseases, Volume 65, Issue 11, 1 December 2017, Pages 1934–1942, https://academic.oup.com/cid/article/65/11/1934/4068747
Self-reported assessment of clinical outcomes was prone to bias. Evidence of a protective effect of masks or respirators against verified respiratory infection (VRI) was not statistically significant”; as per Fig. 2c therein:
Radonovich, L.J. et al. (2019) “N95 Respirators vs Medical Masks for Preventing Influenza Among Health Care Personnel: A Randomized Clinical Trial,” JAMA. 2019; 322(9): 824–833. https://jamanetwork.com/journals/jama/fullarticle/2749214
“Among 2862 randomized participants, 2371 completed the study and accounted for 5180 HCW-seasons. … Among outpatient health care personnel, N95 respirators vs medical masks as worn by participants in this trial resulted in no significant difference in the incidence of laboratory-confirmed influenza.”
“A total of six RCTs involving 9,171 participants were included. There were no statistically significant differences in preventing laboratory-confirmed influenza, laboratory-confirmed respiratory viral infections, laboratory-confirmed respiratory infection, and influenza-like illness using N95 respirators and surgical masks. Meta-analysis indicated a protective effect of N95 respirators against laboratory-confirmed bacterial colonization (RR = 0.58, 95% CI 0.43-0.78). The use of N95 respirators compared with surgical masks is not associated with a lower risk of laboratory-confirmed influenza.”
Conclusion Regarding That Masks Do Not Work
No RCT study with verified outcome shows a benefit for HCW or community members in households to wearing a mask or respirator. There is no such study. There are no exceptions.
Likewise, no study exists that shows a benefit from a broad policy to wear masks in public (more on this below).
Furthermore, if there were any benefit to wearing a mask, because of the blocking power against droplets and aerosol particles, then there should be more benefit from wearing a respirator (N95) compared to a surgical mask, yet several large meta-analyses, and all the RCT, prove that there is no such relative benefit.
Masks and respirators do not work.
Precautionary Principle Turned on Its Head with Masks
In light of the medical research, therefore, it is difficult to understand why public-health authorities are not consistently adamant about this established scientific result, since the distributed psychological, economic, and environmental harm from a broad recommendation to wear masks is significant, not to mention the unknown potential harm from concentration and distribution of pathogens on and from used masks. In this case, public authorities would be turning the precautionary principle on its head (see below).
Physics and Biology of Viral Respiratory Disease and of Why Masks Do Not Work
In order to understand why masks cannot possibly work, we must review established knowledge about viral respiratory diseases, the mechanism of seasonal variation of excess deaths from pneumonia and influenza, the aerosol mechanism of infectious disease transmission, the physics and chemistry of aerosols, and the mechanism of the so-called minimum-infective-dose.
In addition to pandemics that can occur anytime, in the temperate latitudes there is an extra burden of respiratory-disease mortality that is seasonal, and that is caused by viruses. For example, see the review of influenza by Paules and Subbarao (2017). This has been known for a long time, and the seasonal pattern is exceedingly regular. (Publisher’s note: All links to source references to studies here forward are found at the end of this article.)
For example, see Figure 1 of Viboud (2010), which has “Weekly time series of the ratio of deaths from pneumonia and influenza to all deaths, based on the 122 cities surveillance in the US (blue line). The red line represents the expected baseline ratio in the absence of influenza activity,” here:
The seasonality of the phenomenon was largely not understood until a decade ago. Until recently, it was debated whether the pattern arose primarily because of seasonal change in virulence of the pathogens, or because of seasonal change in susceptibility of the host (such as from dry air causing tissue irritation, or diminished daylight causing vitamin deficiency or hormonal stress). For example, see Dowell (2001).
In a landmark study, Shaman et al. (2010) showed that the seasonal pattern of extra respiratory-disease mortality can be explained quantitatively on the sole basis of absolute humidity, and its direct controlling impact on transmission of airborne pathogens.
Lowen et al. (2007) demonstrated the phenomenon of humidity-dependent airborne-virus virulence in actual disease transmission between guinea pigs, and discussed potential underlying mechanisms for the measured controlling effect of humidity.
The underlying mechanism is that the pathogen-laden aerosol particles or droplets are neutralized within a half-life that monotonically and significantly decreases with increasing ambient humidity. This is based on the seminal work of Harper (1961). Harper experimentally showed that viral-pathogen-carrying droplets were inactivated within shorter and shorter times, as ambient humidity was increased.
Harper argued that the viruses themselves were made inoperative by the humidity (“viable decay”), however, he admitted that the effect could be from humidity-enhanced physical removal or sedimentation of the droplets (“physical loss”): “Aerosol viabilities reported in this paper are based on the ratio of virus titre to radioactive count in suspension and cloud samples, and can be criticized on the ground that test and tracer materials were not physically identical.”
The latter (“physical loss”) seems more plausible to me, since humidity would have a universal physical effect of causing particle/droplet growth and sedimentation, and all tested viral pathogens have essentially the same humidity-driven “decay.” Furthermore, it is difficult to understand how a virion (of all virus types) in a droplet would be molecularly or structurally attacked or damaged by an increase in ambient humidity. A “virion” is the complete, infective form of a virus outside a host cell, with a core of RNA or DNA and a capsid. The actual mechanism of such humidity-driven intra-droplet “viable decay” of a virion has not been explained or studied.
In any case, the explanation and model of Shaman et al. (2010) is not dependent on the particular mechanism of the humidity-driven decay of virions in aerosol/droplets. Shaman’s quantitatively demonstrated model of seasonal regional viral epidemiology is valid for either mechanism (or combination of mechanisms), whether “viable decay” or “physical loss.”
The breakthrough achieved by Shaman et al. is not merely some academic point. Rather, it has profound health-policy implications, which have been entirely ignored or overlooked in the current coronavirus pandemic.
In particular, Shaman’s work necessarily implies that, rather than being a fixed number (dependent solely on the spatial-temporal structure of social interactions in a completely susceptible population, and on the viral strain), the epidemic’s basic reproduction number (R0) is highly or predominantly dependent on ambient absolute humidity.
For a definition of R0, see HealthKnowlege-UK (2020): R0 is “the average number of secondary infections produced by a typical case of an infection in a population where everyone is susceptible.” The average R0 for influenza is said to be 1.28 (1.19–1.37); see the comprehensive review by Biggerstaff et al. (2014).
In fact, Shaman et al. showed that R0 must be understood to seasonally vary between humid-summer values of just larger than “1” and dry-winter values typically as large as “4” (for example, see their Table 2). In other words, the seasonal infectious viral respiratory diseases that plague temperate latitudes every year go from being intrinsically mildly contagious to virulently contagious, due simply to the bio-physical mode of transmission controlled by atmospheric humidity, irrespective of any other consideration.
Therefore, all the epidemiological mathematical modeling of the benefits of mediating policies (such as social distancing), which assumes humidity-independent R0 values, has a large likelihood of being of little value, on this basis alone. For studies about modeling and regarding mediation effects on the effective reproduction number, see Coburn (2009) and Tracht (2010).
To put it simply, the “second wave” of an epidemic is not a consequence of human sin regarding mask wearing and hand shaking. Rather, the “second wave” is an inescapable consequence of an air-dryness-driven many-fold increase in disease contagiousness, in a population that has not yet attained immunity.
If my view of the mechanism is correct (i.e., “physical loss”), then Shaman’s work further necessarily implies that the dryness-driven high transmissibility (large R0) arises from small aerosol particles fluidly suspended in the air; as opposed to large droplets that are quickly gravitationally removed from the air.
Such small aerosol particles fluidly suspended in air, of biological origin, are of every variety and are everywhere, including down to virion-sizes (Despres, 2012). It is not entirely unlikely that viruses can thereby be physically transported over inter-continental distances (e.g., Hammond, 1989).
More to the point, indoor airborne virus concentrations have been shown to exist (in day-care facilities, health centers, and on-board airplanes) primarily as aerosol particles of diameters smaller than 2.5 μm, such as in the work of Yang et al. (2011):
“Half of the 16 samples were positive, and their total virus −3 concentrations ranged from 5800 to 37 000 genome copies m . On average, 64 per cent of the viral genome copies were associated with fine particles smaller than 2.5 μm, which can remain suspended for hours. Modeling of virus concentrations indoors suggested a source strength of 1.6 ± 1.2 × 105 genome copies m−3 air h−1 and a deposition flux onto surfaces of 13 ± 7 genome copies m−2 h−1 by Brownian motion. Over one hour, the inhalation dose was estimated to be 30 ± 18 median tissue culture infectious dose (TCID50), adequate to induce infection. These results provide quantitative support for the idea that the aerosol route could be an important mode of influenza transmission.”
Such small particles (< 2.5 μm) are part of air fluidity, are not subject to gravitational sedimentation, and would not be stopped by long-range inertial impact. This means that the slightest (even momentary) facial misfit of a mask or respirator renders the design filtration norm of the mask or respirator entirely irrelevant. In any case, the filtration material itself of N95 (average pore size ~0.3−0.5 μm) does not block virion penetration, not to mention surgical masks. For example, see Balazy et al. (2006).
Mask stoppage efficiency and host inhalation are only half of the equation, however, because the minimal infective dose (MID) must also be considered. For example, if a large number of pathogen-laden particles must be delivered to the lung within a certain time for the illness to take hold, then partial blocking by any mask or cloth can be enough to make a significant difference.
On the other hand, if the MID is amply surpassed by the virions carried in a single aerosol particle able to evade mask-capture, then the mask is of no practical utility, which is the case.
Yezli and Otter (2011), in their review of the MID, point out relevant features:
Most respiratory viruses are as infective in humans as in tissue culture having optimal laboratory susceptibility
It is believed that a single virion can be enough to induce illness in the host
The 50-percent probability MID (“TCID50”) has variably been found to be in the range 100−1000 virions
There are typically 10 to 3rd power − 10 to 7th power virions per aerolized influenza droplet with diameter 1 μm − 10 μm
The 50-percent probability MID easily fits into a single (one) aerolized droplet
For further background:
A classic description of dose-response assessment is provided by Haas (1993).
Zwart et al. (2009) provided the first laboratory proof, in a virus-insect system, that the action of a single virion can be sufficient to cause disease.
Baccam et al. (2006) calculated from empirical data that, with influenza A in humans,“we estimate that after a delay of ~6 h, infected cells begin producing influenza virus and continue to do so for ~5 h. The average lifetime of infected cells is ~11 h, and the half-life of free infectious virus is ~3 h. We calculated the [in-body] basic reproductive number, R0, which indicated that a single infected cell could produce ~22 new productive infections.”
Brooke et al. (2013) showed that, contrary to prior modeling assumptions, although not all influenza-A-infected cells in the human body produce infectious progeny (virions), nonetheless, 90 percent of infected cell are significantly impacted, rather than simply surviving unharmed.
All of this to say that: if anything gets through (and it always does, irrespective of the mask), then you are going to be infected. Masks cannot possibly work. It is not surprising, therefore, that no bias-free study has ever found a benefit from wearing a mask or respirator in this application.
Therefore, the studies that show partial stopping power of masks, or that show that masks can capture many large droplets produced by a sneezing or coughing mask-wearer, in light of the above-described features of the problem, are irrelevant. For example, such studies as these: Leung (2020), Davies (2013), Lai (2012), and Sande (2008).
Why There Can Never Be an Empirical Test of a Nation-Wide Mask-Wearing Policy
As mentioned above, no study exists that shows a benefit from a broad policy to wear masks in public. There is good reason for this. It would be impossible to obtain unambiguous and bias-free results [because]:
Any benefit from mask-wearing would have to be a small effect, since undetected in controlled experiments, which would be swamped by the larger effects, notably the large effect from changing atmospheric humidity.
Mask compliance and mask adjustment habits would be unknown.
Mask-wearing is associated (correlated) with several other health behaviors; see Wada (2012).
The results would not be transferable, because of differing cultural habits.
Compliance is achieved by fear, and individuals can habituate to fear-based propaganda, and can have disparate basic responses.
Monitoring and compliance measurement are near-impossible, and subject to large errors.
Self-reporting (such as in surveys) is notoriously biased, because individuals have the self-interested belief that their efforts are useful.
Progression of the epidemic is not verified with reliable tests on large population samples, and generally relies on non-representative hospital visits or admissions.
Several different pathogens (viruses and strains of viruses) causing respiratory illness generally act together, in the same population and/or in individuals, and are not resolved, while having different epidemiological characteristics.
Unknown Aspects of Mask Wearing
Many potential harms may arise from broad public policies to wear masks, and the following unanswered questions arise:
Do used and loaded masks become sources of enhanced transmission, for the wearer and others?
Do masks become collectors and retainers of pathogens that the mask wearer would otherwise avoid when breathing without a mask?
Are large droplets captured by a mask atomized or aerolized into breathable components? Can virions escape an evaporating droplet stuck to a mask fiber?
What are the dangers of bacterial growth on a used and loaded mask?
How do pathogen-laden droplets interact with environmental dust and aerosols captured on the mask?
What are long-term health effects on HCW, such as headaches, arising from impeded breathing?
Are there negative social consequences to a masked society?
Are there negative psychological consequences to wearing a mask, as a fear-based behavioral modification?
What are the environmental consequences of mask manufacturing and disposal?
Do the masks shed fibers or substances that are harmful when inhaled?
Conclusion
By making mask-wearing recommendations and policies for the general public, or by expressly condoning the practice, governments have both ignored the scientific evidence and done the opposite of following the precautionary principle.
In an absence of knowledge, governments should not make policies that have a hypothetical potential to cause harm. The government has an onus barrier before it instigates a broad social-engineering intervention, or allows corporations to exploit fear-based sentiments.
Furthermore, individuals should know that there is no known benefit arising from wearing a mask in a viral respiratory illness epidemic, and that scientific studies have shown that any benefit must be residually small, compared to other and determinative factors.
Otherwise, what is the point of publicly funded science?
The present paper about masks illustrates the degree to which governments, the mainstream media, and institutional propagandists can decide to operate in a science vacuum, or select only incomplete science that serves their interests. Such recklessness is also certainly the case with the current global lockdown of over 1 billion people, an unprecedented experiment in medical and political history.
Denis G. Rancourt is a researcher at the Ontario Civil Liberties Association (OCLA.ca) and is formerly a tenured professor at the University of Ottawa, Canada. This paper was originally published at Rancourt’s account on ResearchGate.net. As of June 5, 2020, this paper was removed from his profile by its administrators at Researchgate.net/profile/D_Rancourt. At Rancourt’s blog ActivistTeacher.blogspot.com,he recounts the notification and responses he received from ResearchGate.net and states, “This is censorship of my scientific work like I have never experienced before.”
The original April 2020 white paper in .pdf format is available here, complete with charts that have not been reprinted in the Reader print or web versions.
Endnotes:
Baccam, P. et al. (2006) “Kinetics of Influenza A Virus Infection in Humans”, Journal of Virology Jul 2006, 80 (15) 7590-7599; DOI: 10.1128/JVI.01623-05 https://jvi.asm.org/content/80/15/7590
Balazy et al. (2006) “Do N95 respirators provide 95% protection level against airborne viruses, and how adequate are surgical masks?”, American Journal of Infection Control, Volume 34, Issue 2, March 2006, Pages 51-57. doi:10.1016/j.ajic.2005.08.018 http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.488.4644&rep=rep1&type=pdf
Biggerstaff, M. et al. (2014) “Estimates of the reproduction number for seasonal, pandemic, and zoonotic influenza: a systematic review of the literature”, BMC Infect Dis 14, 480 (2014). https://doi.org/10.1186/1471-2334-14-480
Brooke, C. B. et al. (2013) “Most Influenza A Virions Fail To Express at Least One Essential Viral Protein”, Journal of Virology Feb 2013, 87 (6) 3155-3162; DOI: 10.1128/JVI.02284-12 https://jvi.asm.org/content/87/6/3155
Coburn, B. J. et al. (2009) “Modeling influenza epidemics and pandemics: insights into the future of swine flu (H1N1)”, BMC Med 7, 30. https://doi.org/10.1186/1741-7015-7-30
Davies, A. et al. (2013) “Testing the Efficacy of Homemade Masks: Would They Protect in an Influenza Pandemic?”, Disaster Medicine and Public Health Preparedness, Available on CJO 2013 doi:10.1017/dmp.2013.43 http://journals.cambridge.org/abstract_S1935789313000438
Despres, V. R. et al. (2012) “Primary biological aerosol particles in the atmosphere: a review”, Tellus B: Chemical and Physical Meteorology, 64:1, 15598, DOI: 10.3402/tellusb.v64i0.15598 https://doi.org/10.3402/tellusb.v64i0.15598
Dowell, S. F. (2001) “Seasonal variation in host susceptibility and cycles of certain infectious diseases”, Emerg Infect Dis. 2001;7(3):369–374. doi:10.3201/eid0703.010301 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2631809/
Hammond, G. W. et al. (1989) “Impact of Atmospheric Dispersion and Transport of Viral Aerosols on the Epidemiology of Influenza”, Reviews of Infectious Diseases, Volume 11, Issue 3, May 1989, Pages 494–497, https://doi.org/10.1093/clinids/11.3.494
HealthKnowlege-UK (2020) “Charter 1a – Epidemiology: Epidemic theory (effective & basic reproduction numbers, epidemic thresholds) & techniques for analysis of infectious disease data (construction & use of epidemic curves, generation numbers, exceptional reporting & identification of significant clusters)”, HealthKnowledge.org.uk, accessed on 2020-04-10. https://www.healthknowledge.org.uk/public-health-textbook/research-methods/1a- epidemiology/epidemic-theory
Lai, A. C. K. et al. (2012) “Effectiveness of facemasks to reduce exposure hazards for airborne infections among general populations”, J. R. Soc. Interface. 9938–948 http://doi.org/10.1098/rsif.2011.0537
Leung, N.H.L. et al. (2020) “Respiratory virus shedding in exhaled breath and efficacy of face masks”, Nature Medicine (2020). https://doi.org/10.1038/s41591-020-0843-2
Lowen, A. C. et al. (2007) “Influenza Virus Transmission Is Dependent on Relative Humidity and Temperature”, PLoS Pathog 3(10): e151. https://doi.org/10.1371/journal.ppat.0030151
Sande, van der, M. et al. (2008) “Professional and Home-Made Face Masks Reduce Exposure to Respiratory Infections among the General Population”, PLoS ONE 3(7): e2618. doi:10.1371/journal.pone.0002618 https://doi.org/10.1371/journal.pone.0002618
Shaman, J. et al. (2010) “Absolute Humidity and the Seasonal Onset of Influenza in the Continental United States”, PLoS Biol 8(2): e1000316. https://doi.org/10.1371/journal.pbio.1000316
Tracht, S. M. et al. (2010) “Mathematical Modeling of the Effectiveness of Facemasks in Reducing the Spread of Novel Influenza A (H1N1)”, PLoS ONE 5(2): e9018. doi:10.1371/journal.pone.0009018 https://doi.org/10.1371/journal.pone.0009018
Viboud C. et al. (2010) “Preliminary Estimates of Mortality and Years of Life Lost Associated with the 2009 A/H1N1 Pandemic in the US and Comparison with Past Influenza Seasons”, PLoS Curr. 2010; 2:RRN1153. Published 2010 Mar 20. doi:10.1371/currents.rrn1153 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2843747/
Wada, K. et al. (2012) “Wearing face masks in public during the influenza season may reflect other positive hygiene practices in Japan”, BMC Public Health 12, 1065 (2012). https://doi.org/10.1186/1471-2458-12-1065
Yang, W. et al. (2011) “Concentrations and size distributions of airborne influenza A viruses measured indoors at a health centre, a day-care centre and on aeroplanes”, Journal of the Royal Society, Interface. 2011 Aug;8(61):1176-1184. DOI: 10.1098/rsif.2010.0686. https://royalsocietypublishing.org/doi/10.1098/rsif.2010.0686
Yezli, S., Otter, J.A. (2011) “Minimum Infective Dose of the Major Human Respiratory and Enteric Viruses Transmitted Through Food and the Environment”, Food Environ Virol 3, 1–30. https://doi.org/10.1007/s12560-011-9056-7
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Professor Giuseppe Tritto, an internationally known expert in biotechnology and nanotechnology, says that the China Virus definitely wasn’t a freak of nature that happened to cross the species barrier from bat to man.Prof. Giuseppe Tritto in a March 2020
August 10, 2020 (LifeSiteNews) – It will not be possible for the Dr. Fauci’s of the world to dismiss Professor Giuseppe Tritto as a crank. Not only is he an internationally known expert in biotechnology and nanotechnology who has had a stellar academic career, but he is also the president of the World Academy of Biomedical Sciences and Technologies (WABT), an institution founded under the aegis of UNESCO in 1997.
In other words, he is a man of considerable stature in the global scientific community. Equally important, one of the goals of WABT is to analyze the effect of biotechnologies—like genetic engineering—on humanity.
In his new book, this world-class scientist does exactly that. And what he says is that the China Virus definitely wasn’t a freak of nature that happened to cross the species barrier from bat to man. It was genetically engineered in the Wuhan Institute of Virology’s P4 (high-containment) lab in a program supervised by the Chinese military.
Prof. Tritto’s book, which at present is available only in Italian, is called Cina COVID 19: La Chimera che ha cambiato il Mondo(China COVID 19: The chimera that changed the world). It was published on August 4 by a major Italian press, Edizioni Cantagalli, which coincidently also published the Italian edition of one of my books, Population Control (Controllo Demografico in Italian)several years ago.
What sets Prof. Tritto’s book apart is the fact that it demonstrates—conclusively, in my view—the pathway by which a PLA-owned coronavirus was genetically modified to become the China Virus now ravaging the world. His account leaves no doubt that it is a “chimera”, an organism created in a lab.
He also connects the dots linking the Wuhan lab to France and the United States, showing how both countries provided financial and scientific help to the Chinese as they began to conduct ever more dangerous bioengineering experiments. Although neither American nor French virologists are responsible for the end result—a highly infectious coronavirus and a global pandemic—their early involvement may explain why so many insist that the “chimera” must have come from nature. The last thing they want to admit is that they might have had a hand in it.
Those of us who, early on, argued for a laboratory origin were dismissed as conspiracy theorists. Our articles were censored as “fake news,” often by American virologists who knew perfectly well what the truth was, but preferred to protect China, and themselves, from scrutiny lest they themselves be implicated.
Dr. Tritto’s 272 pages of names, dates, places, and facts leaves such apologists with no place to hide. The story begins following the SARS epidemic of 2003, as the Chinese attempt to develop vaccines to combat the deadly disease. Dr. Shi Zhengli, about whom I have previously written, was in charge of the program at the Wuhan Institute of Virology.
In vaccine development, reverse genetics is used to create viral strains that have reduced pathogenicity but to which the immune system responds by creating antibodies against the virus. But reverse genetics can also be used to create viral strains that have increased pathogenicity. That is what Dr. Shi, encouraged by PLA bioweapons experts, began increasingly to focus her research on, according to Prof. Tritto.
Dr. Shi first solicited help from the French government, which built the P4 lab, and from the country’s Pasteur institute, which showed her how to manipulate HIV genomes. The gene insertion method used is called “reverse genetics system 2.” Using this method, she inserted an HIV segment into a coronavirus discovered in horseshoe bats to make it more infectious and lethal.
The U.S. was involved as well, particularly Prof Ralph S. Baric, of the University of North Carolina, who was on the receiving end of major grants from the National Institute of Allergy and Infectious Disease. This is, of course, Dr. Anthony Fauci’s shop. Fauci was a big proponent of “gain of function” research, and when this was prohibited at Baric’s lab because it was considered to be too dangerous, the research was shifted to China.
Prof. Tritto believes that, while Dr. Shi’s research began as an effort to develop a vaccine against SARS, it gradually morphed into an effort to use “reverse genetics” to build lethal biological weapons. This was the reason that the Wuhan lab became China’s leading center for virology research in recent years, attracting major funding and support from the central government.
I would add that the rule in Communist-controlled China is “let the civilian support the military,” which means that as soon as Dr. Shi’s research showed any potential military uses the PLA would have begun exercising control of the research. This came out in the open with the outbreak, when China’s leading expert on bioweapons, People’s Liberation Army Major General Chen Wei, was immediately placed in charge of the Wuhan Institute of Virology. As for Dr. Shi Zheng-Li, she seems to have disappeared.
As Dr. Tritto explained in an interview with Italian media:
In 2005, after the SARS epidemic, the Wuhan Institute of Virology was born, headed by Dr. Shi Zheng-Li, who collects coronaviruses from certain bat species and recombines them with other viral components in order to create vaccines. In 2010 she came into contact with American researchers led by Prof. Ralph Baric, who in turn works on recombinant viruses based on coronaviruses. Thanks to the matrix viruses provided by Shi, Baric created in 2015 a mouse Sars-virus chimera, which has a pathogenic effect on human cells analyzed in vitro.
At that point, the China-US collaboration becomes competition. Shi wants to work on a more powerful virus to make a more powerful vaccine: it combines a bat virus with a pangolin virus in vitro and in 2017 publishes the results of this research in some scientific articles.
Her research attracts the interest of the Chinese military and medical-biological sector which deals with biological weapons used as a deterrent for defensive and offensive purposes. Thus Shi is joined by doctors and biologists who belong to the political-military sphere, such as Guo Deyin, a scholar of anti-AIDS and anti-viral hepatitis vaccines and expert in genetic recombination techniques. The introduction of the new engineered inserts into the virus genome is the result of the collaboration between the Shi team and that of Guo Deyin. The realization of this new chimera, from a scientific point of view, is a success. So much so that, once the epidemic has broken out, the two researchers ask WHO to register it as a new virus, H-nCoV-19 (Human new Covid 19), and not as another virus derived from SARS. It is reasonable to think that Shi acted only from the point of view of scientific prestige, without however taking into account the risks in terms of security and the political-military interests that her research would have aroused.
When asked why China has refused to provide the complete genome of the China Virus to the WHO or to other countries, Dr. Tritto explained that “providing the matrix [source] virus would have meant admitting that SARS-CoV-2 [China Virus] was created in the laboratory. In fact, the incomplete genome made available by China lacks some inserts of AIDS amino acids, which itself is a smoking gun.”
The key question, for those of us who are living through the pandemic, concerns the development of a vaccine. On this score, Prof. Tritto is not optimistic:
Given the many mutations of SARS-CoV-2, it is extremely unlikely that a single vaccine that blocks the virus will be found. At the moment 11 different strains have been identified: the A2a genetic line which developed in Europe and the B1 genetic line which took root in North America are more contagious than the 0 strain originating in Wuhan. I therefore believe that, at the most, a multivalent vaccine can be found effective on 4-5 strains and thus able to cover 70-75% of the world’s population.
In other words, by withholding from the world the original genetic code of the China Virus that it created, the Chinese Communist Party is ensuring that no completely effective vaccine will ever be developed by the West.
Steven W. Mosher is the President of the Population Research Institute and the author of Bully of Asia: Why China’s “Dream” is the New Threat to World Order.
In 2013, scientists investigating deaths in a disused mine found a coronavirus remarkably similar to that behind the pandemic. They took samples to their lab 1,000 miles away
In the monsoon season of August 2012 a small team of scientists travelled to southwest China to investigate a new and mysteriously lethal illness. After driving through terraced tea plantations, they reached their destination: an abandoned copper mine where — in white hazmat suits and respirator masks — they ventured into the darkness.
Instantly, they were struck by the stench. Overhead, bats roosted. Underfoot, rats and shrews scurried through thick layers of their droppings. It was a breeding ground for mutated micro-organisms and pathogens deadly to human beings. There was a reason to take extra care. Weeks earlier, six men who had entered the mine had been struck down by an illness that caused an uncontrollable pneumonia. Three of them died.
Today, as deaths from the Covid-19 pandemic exceed half a million and economies totter, the bats’ repellent lair has taken on global significance.
Evidence seen by The Sunday Times suggests that a virus found in its depths — part of a faecal sample that was frozen and sent to a Chinese laboratory for analysis and storage — is the closest known match to the virus that causes Covid-19.
It came from one of the last droppings collected in the year-long quest, during which the six researchers sent hundreds of samples back to their home city of Wuhan. There, experts on bat viruses were trying to identify the source of the Sars — severe acute respiratory syndrome — pandemic 10 years earlier.
The virus was a huge discovery. It was a “new strain” of a Sars-type coronavirus that, surprisingly, received only a passing mention in an academic paper. The six sick men were not referred to at all.
What happened to the virus in the years between its discovery and the eruption of Covid-19? Why was its existence tucked away in obscure records, and its link to three deaths not mentioned?
Nobody can deny the bravery of the scientists who risked their lives by harvesting the highly infectious virus. But did their courageous detective work lead inadvertently to a global disaster?
ONE
Where flowers bloom all year
The first victims of a new virus
Kunming, the capital of Yunnan province in southwest China, is known as “the city of eternal spring” because its unique climate encourages flowers to bloom all year. The sprawling high-rise buildings of the First Affiliated Hospital tower over the ancient city.
On Tuesday April 24, 2012, a 45-year-old man with the surname of Guo was admitted to the hospital’s intensive care unit suffering from severe pneumonia.
The next day a 42-year-old man with the surname Lv was taken to the hospital with the same life-threatening symptoms, and by Thursday three more cases — Zhou, 63, Liu, 46, and Li, 32 — had joined him in intensive care. A sixth man called Wu, 30, was taken into intensive care the following Wednesday.
All the men were linked. They had been given the task of clearing out piles of bat faeces in an abandoned copper mine in the hills south of the town of Tongguan in the Mojiang region. Some had worked for two weeks before falling ill, and others just a few days.
The illness confounded the doctors. The men had raging fevers of above 39C, coughs and aching limbs. All but one had severe difficulty in breathing.
After the first two men died, the remaining four underwent a barrage of tests for haemorrhagic fever, dengue fever, Japanese encephalitis and influenza, but they all came back negative. They were also tested for Sars, the outbreak that had erupted in southern China in 2002, but that also proved negative.
The doctors sought the opinion of Professor Zhong Nanshan, a British-educated respiratory specialist and a former president of China’s medical association who had spearheaded his country’s efforts to combat Sars. Aware the men might be suffering from another Sars-related coronavirus, he advised the doctors to test them for antibodies.
The Wuhan Institute of Virology (WIV), a renowned centre of coronavirus expertise, was called in to test the four survivors. These produced a remarkable finding: while none had tested positive for Sars, all four had antibodies against another, unknown Sars-like coronavirus.
Furthermore, two patients who recovered and went home showed greater levels of antibodies than two still in hospital, one of whom later died.
Researchers in China have been unable to find any news reports of this new Sars-like coronavirus and the three deaths. There appears to have been a media blackout. It is, however, possible to piece together what happened in the Kunming hospital from a master’s thesis by a young medic called Li Xu. His supervisor was Professor Qian Chuanyun, who worked in the emergency department that treated the men. Other vital details, including the results of the antibody tests, were found in a PhD paper by a student of the director of the Chinese Centre for Disease Control and Prevention.
Li’s thesis was unable to say what exactly killed the three miners, but indicated that the most likely cause was a Sars-like coronavirus from a bat.
“This makes the research of the bats in the mine where the six miners worked and later suffered from severe pneumonia caused by unknown virus a significant research topic,” Li concluded.
That research was already under way — led by the Wuhan virologist who became known as “Bat Woman” — and it adds to the mystery.
TWO
The bat heroine
The Bat Woman heralded as a hero in China
For historians of the Chinese Communist Party, Wuhan is where the 72-year-old Mao Tse-tung took a symbolic swim in the Yangtze River in 1966 before launching the Cultural Revolution. For generations born since that disastrous era, the modern industrial city is the crossroads of China’s high-speed rail network and was the centre of the Covid-19 pandemic.
For science, however, Wuhan is the centre for research into the coronavirus in bats. Shi Zhengli, nicknamed “Bat Woman” by her colleagues, is heralded as a hero in China and in scientific communities across the world.
But the bats in Yunnan are 1,000 miles from her laboratory, and one of the most extraordinary coincidences of the Covid-19 pandemic is that ground zero happened to be in Wuhan, the world centre for the study and storage of the types of coronavirus the city’s own scientists believe caused the outbreak.
Coronaviruses are a group of pathogens that sometimes have the potential to leap species from animals to humans and appear to have a crown — or corona — of spikes when viewed under a microscope.
Before Covid-19, six types of coronavirus were known to infect humans but mostly they caused mild respiratory symptoms such as the common cold.
The first outbreak of Sars — now known as Sars-Cov-1 to distinguish it from Sars-Cov-2, the virus that causes Covid-19 — is one of the deadly exceptions. It emerged in Guangdong, southern China, in November 2002 and infected 8,096 people in 29 countries. It caused severe pneumonia in some and killed 774 people before petering out eight months later.
A race began to find out how a coronavirus had mutated into something so deadly and jumped from animals to humans. The initial prime suspects were masked palm civet cats, a delicacy in some parts of China. But suspicion shifted to bats, which had also been linked to other deadly viruses such as rabies. Perhaps they were the primary source and civets were just intermediaries that they infected.
Shi and her team from the WIV began hunting among bat colonies in caves in southern China in 2004. In 2012 they were in the midst of a five-year research project centred on caves in remote mountains southwest of Kunming when the call came to investigate the incident in the copper mine about 200 miles away.
They were joined by local disease control experts when they descended into the mine that August with protective equipment and bat-catching nets.
Over the next year, the scientists took faecal samples from 276 bats. The samples were stored at minus 80C in a special solution and dispatched to the Wuhan institute, where molecular studies and analysis were conducted.
These showed that exactly half the bats carried coronaviruses and several were carrying more than one virus at a time — with the potential to cause a dangerous new mix of pathogens.
The results were reported in a scientific paper entitled “Coexistence of multiple coronaviruses in several bat colonies in an abandoned mineshaft” co-authored by Shi and her fellow scientists in 2016.
Notably, the paper makes no mention of why the study had been carried out: the miners, their pneumonia and the deaths of three of them.
The paper does state, however, that of the 152 genetic sequences of coronavirus found in the six species of bats in the mineshaft, two were of the type that had caused Sars. One is classified as a “new strain” of Sars and labelled RaBtCoV/4991. It was found in a Rhinolophus affinis, commonly known as a horseshoe bat. The towering significance of RaBtCov/4991 would not be fully understood for seven years.
THREE
An ordinary coronavirus
The top security lab at the centre of Wuhan
A new facility was taking shape on the virology institute campus on the west side of the Yangtze in Wuhan. Built by a contractor for the People’s Liberation Army under strict secrecy, a top-security laboratory for handling deadly human pathogens was unveiled in 2017.
There were 31 such laboratories in the world at the time but this was China’s first. The new lab had been certified by the Chinese authorities as “biosafety level 4”, or BSL-4, the highest. But it was raising eyebrows internationally.
Scientists and biosafety experts were concerned that the closed nature of the Chinese state and the emphasis on hierarchy would prove incompatible with running such a dangerous facility.
“Diversity of viewpoint, flat structures where everyone feels free to speak up and openness of information are important,” Tim Trevan, a consultant in biosecurity, told the science magazine Nature when it opened.
Laboratory leaks are not uncommon. In the past, ebola and the fatal bat disease Marburg, which kills nine out of 10 people infected, have escaped from BSL-4 laboratories in the US. American health authorities recorded 749 laboratory safety breaches in the six years to 2015. Indeed, several people were infected by Sars in 2004 after an accident at China’s National Institute of Virology in Beijing.
The need for a secure facility in Wuhan was obvious, however. Shi and her team had already collected hundreds of samples of the coronavirus — including RaBtCov/4991 — from their work on bats across Yunnan province, and they were running controversial experiments to find out how they might mutate to become more infectious to humans.
This “gain-of-function” work is described in papers released by the WIV between 2015 and 2017, scientists say. Shi’s team combined snippets of different coronaviruses to see if they could be made more transmissible in what they called “virus infectivity experiments”.
It was controversial because it had the potential to turn bat coronaviruses into human pathogens capable of causing a pandemic. In 2014 the US government issued a ban on funding any endeavour to make a virus more contagious.
Shi’s team argued that gain-of-function work increased its understanding of how an ordinary coronavirus might one day transform into a killer such as Sars.
Others disagreed. “The debate is whether in fact you learn more by helping to develop vaccines or even drugs by replicating a more virulent virus than currently exists, versus not doing that,” explained Deenan Pillay, professor of virology at University College London. “And I think the consensus became that the risk was too much.”
In January 2018 the US embassy in Beijing took the unusual step of sending scientists with diplomatic status to Wuhan to find out what was going on in the institute’s new biosafety laboratories. They met Shi and members of her team.
Details of the diplomats’ findings have been found in US diplomatic cables that were leaked to The Washington Post and others. “Most importantly,” states a cable from January 19, 2018, “the researchers also showed that various Sars-like coronaviruses can interact with ACE2, the human receptor identified for Sars-coronavirus. This finding strongly suggests that Sars-like coronaviruses from bats can be transmitted to humans to cause Sars-like diseases.”
The Americans were evidently worried about safety. “During interactions with scientists at the WIV laboratory, they noted the new lab has a serious shortage of appropriately trained technicians and investigators needed to safely operate this high-containment laboratory,” the cable added.
Shi was in a conference in Shanghai on Monday December 30, 2019, when she received a call to say there was a new coronavirus on the loose — and it had surfaced in Wuhan, of all places. Since her work had established that such viruses were most likely to originate in south China, she found the news puzzling and extremely worrying. “I wondered if [the local health authority] got it wrong,” she told the Scientific American magazine in a rare interview this year. “I had never expected this kind of thing to happen in Wuhan, in central China.”
One of her initial thoughts, as she prepared to return immediately to analyse the virus, was “Could they [the new coronaviruses] have come from our lab?”. It was a natural anxiety, although she said she was later able to dismiss it after examining the lab’s records.
FOUR
Patient Zero
When did Covid-19 really start?
The precise point at which Covid-19 erupted in Wuhan may never be known. Various theories have been discredited.
A study by Harvard University claimed the virus may have started last August. It relied on satellite images in which the car parks of selected Wuhan hospitals looked busier. However, the study’s detractors have pointed to discrepancies in the evidence.
There is also a theory — propagated by the Chinese media — that the virus may have been introduced into the country by foreign athletes competing in the Military World Games in Wuhan last October. They included the French former world champion pentathlete Élodie Clouvel and the Italian Olympic gold medallist fencer Matteo Tagliariol, who were laid low by fever during the Games.
Few of the athletes have been tested to find out whether they carry antibodies to Covid-19, apart from the Swedish team. Melina Westerberg, a Swedish pentathlete, has revealed that while many of her teammates were sick during the Games, they tested negative. “It was just a coincidence,” she said.
It is possible that the virus did start patchily at around the time of the Military World Games. Yu Chuanhua, an epidemiology professor at Wuhan University, has told Chinese media that one man was admitted to hospital on September 29 with Covid-19-like symptoms but it is impossible now to show whether he had the virus because he died. There were two more suspected early carriers of the virus from November 14 and 21 in the city’s 47,000-strong database of cases, but they are unconfirmed.
Probably the first confirmed case was a 70-year-old man with Alzheimer’s disease, whose family had told researchers from Wuhan Jinyintan Hospital that his symptoms had begun on December 1.
From that point it accelerated to about 60 identifiable cases by December 20, according to government research data reported in the South China Morning Post. However, it would not be until a week later that Dr Zhang Jixian, of the Hospital of Integrated Traditional Chinese and Western Medicine in Hubei province, became the first person to report a suspected outbreak to the provincial government.
By then it had already spread as far as Europe, probably via regular flights from Wuhan. The virus may have been in Italy as early as December 18. The country’s National Institute of Health reported finding traces of Covid-19 in sewage water collected in Milan and Turin on that date.
It was certainly in France, as a man called Amirouche Hammar was admitted to Jean-Verdier hospital in Paris on December 27. He had unknown respiratory pneumonia and was coughing blood. His samples later revealed Covid-19. His wife, who had a slight cough, worked at a supermarket used by shoppers leaving Charles de Gaulle airport, where there were direct flights from Wuhan.
Early cases
First Covid-19 cases recorded in Wuhan that were linked to the Huanan seafood market and not linked, by the day that symptoms were first reported
Dec152229Jan0510152025303540MarketclosedJan 1
Chart: The Times and The Sunday Times • Source: The New England Journal of Medicine
In Wuhan itself, the first cluster of cases included traders and shoppers at the Huanan seafood market, a maze of small trading stores opening on to crowded alleys in the centre of the city. Despite its name, the market also sold meat and vegetables, and there was an exotic wildlife section in the west of the market.
On January 1 the Huanan market was closed and scientists found 33 coronavirus samples, nearly all in the area of the market where wild animals were sold.
It seemed like an open and shut case. When the results were released later that month, the Chinese state news agency Xinhua reported: “The results suggest that the novel coronavirus outbreak is highly relevant to the trading of wild animals.”
However, an early study published in The Lancet made clear that of the 41 patients who contracted Covid-19 in Wuhan only 27 had been “exposed” to the market. A third had no connection to the market, including the study’s “patient zero”, who fell ill on December 1.
Months later George Gao, the director of the Chinese Centre for Disease Control and Prevention, revealed that all the samples taken from animals at the market had tested negative for the virus and that those found had been from sewage or other environmental sources. The Chinese health authorities are now working on the theory that the market helped spread the disease but was not where it originated.
FIVE
Mapping the virus
China warns world of deadly new strain
On December 31, the day Shi returned to the WIV to begin work identifying the new coronavirus, the Chinese authorities decided it was time to tell the world there was potentially a problem.
The World Health Organisation (WHO) was notified that a number of people had been struck down with pneumonia but the cause was not stated. On the same day, the Wuhan health authority put out a bland public statement reporting 27 cases of flu-like infection and urged people to seek medical attention if they fell ill. Neither statement indicated that the new illness could be transmitted between humans or that the likely source was already known: a coronavirus.
By the second week in January, desperate scenes were unfolding at Wuhan hospitals. Hopelessly ill-prepared and ill-equipped staff were forced to make life-and-death calls about who they could treat. Within a few days, the lack of beds, equipment and staff made the decisions for them.
Shi’s team managed to identify five cases of the coronavirus from samples taken from patients at Wuhan Jinyintan Hospital using a technique to amplify the virus’s genetic material. The samples were sent to another lab, which completed the whole genomic sequence.
However, the sequence would not be passed to the WHO until January 12 and China would not admit there had been human-to-human transmission until January 20, despite sitting on evidence the virus had been passed to medics.
One of Shi’s other urgent tasks was to check through her laboratory’s records to see if any errors, particularly with disposal of hazardous materials, could have caused a leak from the premises.
She spoke of her relief to discover that the sequences for the new virus were not an exact match with the samples her team had brought back from the bat caves. “That really took a load off my mind,” she told the Scientific American, “I had not slept a wink for days.”
SIX
RaTG13
From bat cave to lab
She then set about writing a paper describing the new coronavirus to the world for the first time. Published in Nature on February 3 and entitled “A pneumonia outbreak associated with a new coronavirus of probable bat origin”, the document was groundbreaking.
It set out a full genomic description of the Covid-19 virus and revealed that the WIV had in storage the closest known relative of the virus, which it had taken from a bat. The sample was named RaTG13. According to the paper, it is a 96.2% match to the Covid-19 virus and they share a common lineage distinct from other Sars-type coronaviruses. The paper concludes that this close likeness “provides evidence” that Covid-19 “may have originated in bats”.
In other words, RaTG13 was the biggest lead available as to the origin of Covid-19. It was therefore surprising that the paper gave only scant detail about the history of the virus sample, stating merely that it was taken from a Rhinolophus affinis bat in Yunnan province in 2013 — hence the “Ra” and the 13.
Inquiries have established, however, that RaTG13 is almost certainly the coronavirus discovered in the abandoned mine in 2013, which had been named RaBtCoV/4991 in the institute’s earlier scientific paper. For some reason, Shi and her team appear to have renamed it.
The clearest evidence is in a database of bat viruses published by the Chinese Academy of Sciences — the parent body of the WIV — which lists RaTG13 and the mine sample as the same entity. It says it was discovered on July 24, 2013, as part of a collection of coronaviruses that were described in the 2016 paper on the abandoned mine.
In fact, researchers in India and Austria have compared the partial genome of the mine sample that was published in the 2016 paper and found it is a 100% match with the same sequence for RaTG13. The same partial sequence for the mine sample is a 98.7% match with the Covid-19 virus.
Peter Daszak, a close collaborator with the Wuhan institute, who has worked with Shi’s team hunting down viruses for 15 years, has confirmed to The Sunday Times that RaTG13 was the sample found in the mine. He said there was no significance in the renaming. “The conspiracy folks are saying there’s something suspicious about the change in name, but the world has changed in six years — the coding system has changed,” he said.
He recalled: “It was just one of the 16,000 bats we sampled. It was a faecal sample, we put it in a tube, put it in liquid nitrogen, took it back to the lab. We sequenced a short fragment.”
In 2013 the Wuhan team had run the sample through a polymerase chain reaction process to amplify the amount of genetic material so it could be studied, Daszak said. But it did no more work on it until the Covid-19 outbreak because it had not been a close match to Sars.
Other scientists find the initial indifference about a new strain of the coronavirus hard to understand. Nikolai Petrovsky, professor of medicine at Flinders University in Adelaide, South Australia, said it was “simply not credible” that the WIV would have failed to carry out any further analysis on RaBtCoV/4991, especially as it had been linked to the deaths of three miners.
“If you really thought you had a novel virus that had caused an outbreak that killed humans then there is nothing you wouldn’t do — given that was their whole reason for being [there] — to get to the bottom of that, even if that meant exhausting the sample and then going back to get more,” he said.
“I would expect people to be as clear as they can be about the history of the isolates of their sequencing,” said Professor Wendy Barclay, head of Imperial College London’s infectious disease department and a member of the UK government’s Sage advisory committee. “Most of us would have reported the entire history of the isolate, [back] to where all that came from, at the time.”
According to Daszak, the mine sample had been stored in Wuhan for six years. Its scientists “went back to that sample in 2020, in early January or maybe even at the end of last year, I don’t know. They tried to get full genome sequencing, which is important to find out the whole diversity of the viral genome.”
However, after sequencing the full genome for RaTG13 the lab’s sample of the virus disintegrated, he said. “I think they tried to culture it but they were unable to, so that sample, I think, has gone.”
In recent weeks, academics are said to have written to Nature asking for the WIV to write an erratum clarifying the sample’s provenance, but the Chinese lab has maintained a stony silence. A spokesman for Nature said: “Concerns relating to this paper have been brought to Nature’s attention and are being considered at the moment. We cannot comment further at this time.”
SEVEN
Ski holidays
The contagion spread through Europe
The director of the WIV, Wang Yanyi, gave an interview in May in which she described suggestions that Covid-19 might have leaked from the lab as “pure fabrication”. She said that the institute managed to sequence the genome of RaTG13 but had not been able to return it to a live virus. “Thus, there is no possibility of us leaking RaTG13,” she said.
Shi’s interview with the Scientific American mentions the discovery of a coronavirus that 96% matches the Covid-19 virus, and has a reference to the miners dying in a cave she investigated. However, the two things are not linked and Shi downplays the significance of the miners’ deaths by claiming they succumbed to a fungus.
Experts consulted by this newspaper thought it was significant the men had tested positive for antibodies against Sars. Professor Martin Hibberd, a professor of emerging infectious diseases at the London School of Hygiene & Tropical Medicine, said the antibodies provided “a good clue” that the cause of death was “a proper coronavirus”, which “most likely” was Sars-related.
“[RaTG13] is so similar to all the other Sars coronaviruses and so I’d imagine all of that family can cause similar disease, so it makes good sense to me that if the miners caught it they would end up with something that looks similar.”
On January 23 Wuhan became the first city in the world to go into lockdown and it would later suffer nearly 4,000 deaths, according to official figures that some people believe are too low.
Britain’s first official cases — a Chinese student studying in York and a relative — would not emerge for another week, but it is highly likely the virus was already in the country. There were 901 flights from China to the UK between December 1, when the first known patient fell ill, and January 24. Of those, 23 flights brought thousands of passengers directly from Wuhan to Heathrow.
There is also evidence that Britons were bringing back the virus from Europe. Professor Tim Spector, an epidemiologist at King’s College London, who runs the Covid Symptom Study app, says he was contacted by up to 500 people who had returned to the UK between Christmas and January with symptoms.
Many were returning from ski resorts, notably in Austria. In April, 42% of residents in the town of Ischgl were found to have antibodies. “I was interested in the Austrian surveys done in Tyrol because I was quite struck by the stories of all the people that came back from Austrian ski holidays in January, predominantly, feeling ill. It was very convincing because a lot of the stories were the same from different people,” he said.
EIGHT
The investigation
How did this happen?
The origin of Covid-19 is one of the most pressing questions facing humanity. Scientists worldwide are trying to understand how it evolved, which could help stop such a crisis happening again.
The suggestion that well-intentioned scientists may have introduced Covid-19 to their own city is vehemently denied by the WIV, and its work on the origin of the virus has become an x-rated topic in China. Its leadership has taken strict control of new studies and information about where the virus may have come from.
A directive from the education ministry’s science and technology department in the spring stipulated that such work had to be read by a taskforce directly under the state council — comprising China’s president, Xi Jinping, and top ministers — before it can be published.
The secrecy has only increased as the origin of Covid-19 has become politicised as a weapon of aggressive foreign policy. President Donald Trump has described the virus as a “kung flu” and has delighted in claiming it is a Chinese disease. Scientists are dismayed and fear China will retreat further into its shell.
Professor Richard Ebright, of Rutgers University’s Waksman Institute of Microbiology in New Jersey, believes there is now less than a 50:50 chance China will allow a transparent investigation into the origin of the pandemic. “That’s unfortunate,” he said. “And that largely reflects the poor handling of the matter by the US president, who chose to push this in a way that made it unlikely that there could be an open investigation.”
Over the next few days, WHO scientists will be allowed to fly into China to begin an investigation into the origins of the virus after two months of negotiations. Many experts such as Daszak believe the source of the virus will be found in a bat in the south of China.
“It didn’t emerge in the market, it emerged somewhere else,” said Daszak. He said the “best guess right now” is that the virus started within a “cluster” on the Chinese border that includes the area where RaTG13 was found and an area just south of the mineshaft, where another bat pathogen with a 93% likeness to Covid-19 was discovered recently.
As for how the virus travelled to Wuhan, Daszak said: “Fair assumption is that it spilt into animals in southern China and was then shipped in, via infected people, or animals associated with trade, to Wuhan.”
But how could such an infectious virus avoid causing a single noticeable outbreak during the 1,000-mile journey from Yunnan to the city?
Hibberd said it was feasible the virus could have travelled in an animal such as a pangolin, which passed it to a human wildlife trader when it was being transported for sale in the market. “Maybe a young guy moves a pangolin and sold it on and may have had a mild infection but didn’t have any disease,” he said. “It’s not impossible for that scenario to happen.”
On the other hand, Hibberd believes it is possible the virus could have been brought back by one of the scientists, who were frequent travellers between the caves and Wuhan. “If you imagine these researchers who probably did this are students — who are probably quite young — it’s entirely possible that a researcher might become infected through the study of bats.”
The WIV was not the only body of scientists from the city delving into virus-laden caves. On December 10 last year a Chinese state media outlet published an extraordinary video lionising the bravery of a researcher called Tian Junhua, who is said to have caught 10,000 bats in studies for Wuhan’s disease control centre.
Tian admitted that he knew little about bats when he first started visiting the caves eight years ago, and once had to isolate himself for 14 days after being showered with bat urine while wearing inadequate protection. On occasions bat blood spilt onto his hands but he says he has never been infected.
The young researcher aroused suspicion because one of the offices of the disease control centre is about 300 yards from the Huanan seafood market. He has refused to talk to reporters, but his friends have firmly denied that he was “patient zero”.
The final and trickiest question for the WHO inspectors is whether the virus might have escaped from a laboratory in Wuhan. Is it possible, for example, that RaTG13 or a similar virus turned into Covid-19 and then leaked into the population after infecting one of the scientists at the Wuhan institute?
This seriously divides the experts. The Australian virologist Edward Holmes has estimated that RaTG13 would take up to 50 years to evolve the extra 4% that would make it a 100% match with the Covid-19 virus. Hibberd is slightly less conservative and believes it might take less than 20 years to morph naturally into the virus driving the current pandemic.
But others say such arguments are based on the assumption the virus develops at a constant rate, along lines that have been monitored over the past six months. “That is not a valid assumption,” said Ebright. “When a virus changes hosts and adapts to a new host the rate of evolutionary change is much higher. And so it is possible that RaTG13, particularly if it entered humans prior to November 2019, may have undergone adaptation in humans at a rate that would allow it to give rise to Sars-Cov-2. I think that is a distinct possibility.”
Ebright believes an even more controversial theory should not be ruled out. “It also, of course, is a distinct possibility that work done in the laboratory on RaTG13 may have resulted in artificial in-laboratory adaptation that erased those three to five decades of evolutionary distance.”
It is a view Hibberd does not believe is possible. “Sars-Cov-2 and RaTG13 are not the same virus and I don’t think you can easily manipulate one into the other. It seems exceptionally difficult,” he said.
Ebright alleges, however, that the type of work required to create Covid-19 from RaTG13 was “identical” to work the laboratory had done in the past. “The very same techniques, the very same experimental strategies using RaTG13 as the starting point, would yield a virus essentially identical to Sars-Cov-2.”
The Sunday Times put a series of questions to the WIV. They included why it had failed for months to acknowledge the closest match to the Covid-19 virus was found in a mine where people had died from a coronavirus-like illness. The questions were met with silence.
Prof. Giuseppe Tritto in a March 2020