The CEO of the OneAmerica insurance company publicly disclosed that during the third and fourth quarters of 2021, death in people of working age (18-64) was 40% higher than it was before the pandemic. Significantly, the majority of the deaths were not attributed to COVID. Even a… pic.twitter.com/Hx5EbBjgKn
2020, 2021,2022 Ed Dowd did Under an organization called the Humanities Project compile a history of excess deaths during and after the pandemic and here is what they found.
Question Did more all-cause deaths occur during the first months of the coronavirus disease 2019 (COVID-19) pandemic in the United States compared with the same months during previous years?
Findings 2020 In this cohort study, the number of deaths due to any cause increased by approximately 122 000 from March 1 to May 30, 2020, which is 28% higher than the reported number of COVID-19 deaths.
Meaning Official tallies of deaths due to COVID-19 underestimate the full increase in deaths associated with the pandemic in many states.
Abstract
Importance Efforts to track the severity and public health impact of coronavirus disease 2019 (COVID-19) in the United States have been hampered by state-level differences in diagnostic test availability, differing strategies for prioritization of individuals for testing, and delays between testing and reporting. Evaluating unexplained increases in deaths due to all causes or attributed to nonspecific outcomes, such as pneumonia and influenza, can provide a more complete picture of the burden of COVID-19.
Objective To estimate the burden of all deaths related to COVID-19 in the United States from March to May 2020.
Design, Setting, and Population This observational study evaluated the numbers of US deaths from any cause and deaths from pneumonia, influenza, and/or COVID-19 from March 1 through May 30, 2020, using public data of the entire US population from the National Center for Health Statistics (NCHS). These numbers were compared with those from the same period of previous years. All data analyzed were accessed on June 12, 2020.
Main Outcomes and Measures Increases in weekly deaths due to any cause or deaths due to pneumonia/influenza/COVID-19 above a baseline, which was adjusted for time of year, influenza activity, and reporting delays. These estimates were compared with reported deaths attributed to COVID-19 and with testing data.
Results There were approximately 781 000 total deaths in the United States from March 1 to May 30, 2020, representing 122 300 (95% prediction interval, 116 800-127 000) more deaths than would typically be expected at that time of year. There were 95 235 reported deaths officially attributed to COVID-19 from March 1 to May 30, 2020. The number of excess all-cause deaths was 28% higher than the official tally of COVID-19–reported deaths during that period. In several states, these deaths occurred before increases in the availability of COVID-19 diagnostic tests and were not counted in official COVID-19 death records. There was substantial variability between states in the difference between official COVID-19 deaths and the estimated burden of excess deaths.
Conclusions and Relevance Excess deaths provide an estimate of the full COVID-19 burden and indicate that official tallies likely undercount deaths due to the virus. The mortality burden and the completeness of the tallies vary markedly between states.
Discussion
Monitoring excess deaths has been used as a method for tracking influenza mortality for more than a century. Herein, we used a similar strategy to capture COVID-19 deaths that had not been attributed specifically to the pandemic coronavirus. Monitoring trends in broad mortality outcomes, like changes in all-cause and pneumonia/influenza/COVID-19 mortality, provides a window into the magnitude of the mortality burden missed in official tallies of COVID-19 deaths. Given the variability in testing intensity between states and over time, this type of monitoring provides key information on the severity of the pandemic and the degree to which viral testing might be missing deaths caused by COVID-19. These findings demonstrate that estimates of the death toll of COVID-19 based on excess all-cause mortality may be more reliable than those relying only on reported deaths, particularly in places that lack widespread testing.
Syndromic end points, such as deaths due to pneumonia/influenza/COVID-19, outpatient visits for influenza-like illness, and emergency department visits for fever, can provide a crude but informative measure of the progression of the outbreak.18 These measures themselves can be biased by changes in health-seeking behavior and how conditions are recorded. However, in the absence of widespread and systematic testing for COVID-19, they provide a useful measure of pandemic progression and the impact of interventions.
The gap between reported COVID-19 deaths and excess deaths can be influenced by several factors, including the intensity of testing; guidelines on the recording of deaths that are suspected to be related to COVID-19 but do not have a laboratory confirmation; and the location of death (eg, hospital, nursing home, or unattended death at home). For instance, deaths that occur in nursing homes might be more likely to be recognized as part of an epidemic and correctly recorded as due to COVID-19. As the pandemic has progressed, official statistics have become better aligned with excess mortality estimates, perhaps due to enhanced testing and increased recognition of the clinical features of COVID-19. In New York City, official COVID-19 death counts were revised after careful inspection of death certificates, adding an extra 5048 probable deaths to the 13 831 laboratory-confirmed deaths.19 As a result, the all-cause excess mortality burden from March 11 to May 2, 2020, is only 27% higher than official COVID-19 statistics.19 This aligns well with our estimate of 26% for a similar period in New York City, using a slightly different modeling approach.
Many European countries have experienced sharp increases in all-cause deaths associated with the pandemic. Real-time all-cause mortality data from the EuroMomo project (https://www.euromomo.eu/) demonstrate gaps between the official COVID-19 death toll and excess deaths that echo findings in our study. These gaps are more pronounced in countries that were affected more and earlier by the pandemic and had weak testing. Very limited excess mortality information is available from Asia, Africa, the Middle East, and South America thus far; these data will be important to fully capture the heterogeneity of death rates related to the COVID-19 pandemic across the world. Prior work on the 1918 and 2009 pandemics has shown substantial heterogeneity in mortality burden between countries, in part related to health care.8,20
Humanities Project Excess Deaths USA by Year and Vaccination Status
Horowitz Possible Explanation from Pfizer Databank
A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence and study indicate that group 2b viruses encoding the SHC014 spike in a wild-type backbone can efficiently use multiple orthologs of the SARS receptor human angiotensin converting enzyme II (ACE2), replicate efficiently in primary human airway cells and achieve in vitro titers equivalent to epidemic strains of SARS-CoV. Repost w emphasis on spike used by Baric and Daszak.
Associated Revelation. Wuhan Institute of Virology Shao Cao admits they Tested Coronavirus Variants for the Best Adeherent to ACE2 Receptor
Abstract
The emergence of severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome (MERS)-CoV underscores the threat of cross-species transmission events leading to outbreaks in humans. Here we examine the disease potential of a SARS-like virus, SHC014-CoV, which is currently circulating in Chinese horseshoe bat populations1. Using the SARS-CoV reverse genetics system2, we generated and characterized a chimeric virus expressing the spike of bat coronavirus SHC014 in a mouse-adapted SARS-CoV backbone. The results indicate that group 2b viruses encoding the SHC014 spike in a wild-type backbone can efficiently use multiple orthologs of the SARS receptor human angiotensin converting enzyme II (ACE2), replicate efficiently in primary human airway cells and achieve in vitro titers equivalent to epidemic strains of SARS-CoV. Additionally, in vivo experiments demonstrate replication of the chimeric virus in mouse lung with notable pathogenesis. Evaluation of available SARS-based immune-therapeutic and prophylactic modalities revealed poor efficacy; both monoclonal antibody and vaccine approaches failed to neutralize and protect from infection with CoVs using the novel spike protein. On the basis of these findings, we synthetically re-derived an infectious full-length SHC014 recombinant virus and demonstrate robust viral replication both in vitro and in vivo. Our work suggests a potential risk of SARS-CoV re-emergence from viruses currently circulating in bat populations.
Supplementary information
The online version of this article (doi:10.1038/nm.3985) contains supplementary material, which is available to authorized users.
Subject terms: Policy and public health in microbiology, Viral infection, SARS virus, Translational research
SPIKE PROTEIN CLOTTING PROBLEM
Dr. McCullough: The COVID Vaccines Are Causing the ‘Largest Blood Clots We’ve Ever Seen’
“My experience with these blood clots are they’re enormously resistant to blood thinners,” disclosed Dr. @P_McCulloughMD. “Wuhan spike protein is inside the blood clots, and it’s folding,… pic.twitter.com/UIawzXBToH
The emergence of SARS-CoV heralded a new era in the cross-species transmission of severe respiratory illness with globalization leading to rapid spread around the world and massive economic impact3,4. Since then, several strains—including influenza A strains H5N1, H1N1 and H7N9 and MERS-CoV—have emerged from animal populations, causing considerable disease, mortality and economic hardship for the afflicted regions5. Although public health measures were able to stop the SARS-CoV outbreak4, recent metagenomics studies have identified sequences of closely related SARS-like viruses circulating in Chinese bat populations that may pose a future threat1,6. However, sequence data alone provides minimal insights to identify and prepare for future prepandemic viruses. Therefore, to examine the emergence potential (that is, the potential to infect humans) of circulating bat CoVs, we built a chimeric virus encoding a novel, zoonotic CoV spike protein—from the RsSHC014-CoV sequence that was isolated from Chinese horseshoe bats1—in the context of the SARS-CoV mouse-adapted backbone. The hybrid virus allowed us to evaluate the ability of the novel spike protein to cause disease independently of other necessary adaptive mutations in its natural backbone. Using this approach, we characterized CoV infection mediated by the SHC014 spike protein in primary human airway cells and in vivo, and tested the efficacy of available immune therapeutics against SHC014-CoV. Together, the strategy translates metagenomics data to help predict and prepare for future emergent viruses.
The sequences of SHC014 and the related RsWIV1-CoV show that these CoVs are the closest relatives to the epidemic SARS-CoV strains (Fig. 1a,b); however, there are important differences in the 14 residues that bind human ACE2, the receptor for SARS-CoV, including the five that are critical for host range: Y442, L472, N479, T487 and Y491 (ref. 7). In WIV1, three of these residues vary from the epidemic SARS-CoV Urbani strain, but they were not expected to alter binding to ACE2 (Supplementary Fig. 1a,b and Supplementary Table 1). This fact is confirmed by both pseudotyping experiments that measured the ability of lentiviruses encoding WIV1 spike proteins to enter cells expressing human ACE2 (Supplementary Fig. 1) and by in vitro replication assays of WIV1-CoV (ref. 1). In contrast, 7 of 14 ACE2-interaction residues in SHC014 are different from those in SARS-CoV, including all five residues critical for host range (Supplementary Fig. 1c and Supplementary Table 1). These changes, coupled with the failure of pseudotyped lentiviruses expressing the SHC014 spike to enter cells (Supplementary Fig. 1d), suggested that the SHC014 spike is unable to bind human ACE2. However, similar changes in related SARS-CoV strains had been reported to allow ACE2 binding7,8, suggesting that additional functional testing was required for verification. Therefore, we synthesized the SHC014 spike in the context of the replication-competent, mouse-adapted SARS-CoV backbone (we hereafter refer to the chimeric CoV as SHC014-MA15) to maximize the opportunity for pathogenesis and vaccine studies in mice (Supplementary Fig. 2a). Despite predictions from both structure-based modeling and pseudotyping experiments, SHC014-MA15 was viable and replicated to high titers in Vero cells (Supplementary Fig. 2b). Similarly to SARS, SHC014-MA15 also required a functional ACE2 molecule for entry and could use human, civet and bat ACE2 orthologs (Supplementary Fig. 2c,d). To test the ability of the SHC014 spike to mediate infection of the human airway, we examined the sensitivity of the human epithelial airway cell line Calu-3 2B4 (ref. 9) to infection and found robust SHC014-MA15 replication, comparable to that of SARS-CoV Urbani (Fig. 1c). To extend these findings, primary human airway epithelial (HAE) cultures were infected and showed robust replication of both viruses (Fig. 1d). Together, the data confirm the ability of viruses with the SHC014 spike to infect human airway cells and underscore the potential threat of cross-species transmission of SHC014-CoV.
SARS-like viruses replicate in human airway cells and produce in vivo pathogenesis.
(a) The full-length genome sequences of representative CoVs were aligned and phylogenetically mapped as described in the Online Methods. The scale bar represents nucleotide substitutions, with only bootstrap support above 70% being labeled. The tree shows CoVs divided into three distinct phylogenetic groups, defined as α-CoVs, β-CoVs and γ-CoVs. Classical subgroup clusters are marked as 2a, 2b, 2c and 2d for the β-CoVs and as 1a and 1b for the α-CoVs. (b) Amino acid sequences of the S1 domains of the spikes of representative β-CoVs of the 2b group, including SARS-CoV, were aligned and phylogenetically mapped. The scale bar represents amino acid substitutions. (c,d) Viral replication of SARS-CoV Urbani (black) and SHC014-MA15 (green) after infection of Calu-3 2B4 cells (c) or well-differentiated, primary air-liquid interface HAE cell cultures (d) at a multiplicity of infection (MOI) of 0.01 for both cell types. Samples were collected at individual time points with biological replicates (n = 3) for both Calu-3 and HAE experiments. (e,f) Weight loss (n = 9 for SARS-CoV MA15; n = 16 for SHC014-MA15) (e) and viral replication in the lungs (n = 3 for SARS-CoV MA15; n = 4 for SHC014-MA15) (f) of 10-week-old BALB/c mice infected with 1 × 104 p.f.u. of mouse-adapted SARS-CoV MA15 (black) or SHC014-MA15 (green) via the intranasal (i.n.) route. (g,h) Representative images of lung sections stained for SARS-CoV N antigen from mice infected with SARS-CoV MA15 (n = 3 mice) (g) or SHC014-MA15 (n = 4 mice) (h) are shown. For each graph, the center value represents the group mean, and the error bars define the s.e.m. Scale bars, 1 mm.
To evaluate the role of the SHC014 spike in mediating infection in vivo, we infected 10-week-old BALB/c mice with 104 plaque-forming units (p.f.u.) of either SARS-MA15 or SHC014-MA15 (Fig. 1e–h). Animals infected with SARS-MA15 experienced rapid weight loss and lethality by 4 d post infection (d.p.i.); in contrast, SHC014-MA15 infection produced substantial weight loss (10%) but no lethality in mice (Fig. 1e). Examination of viral replication revealed nearly equivalent viral titers from the lungs of mice infected with SARS-MA15 or SHC014-MA15 (Fig. 1f). Whereas lungs from the SARS-MA15–infected mice showed robust staining in both the terminal bronchioles and the lung parenchyma 2 d.p.i. (Fig. 1g), those of SHC014-MA15–infected mice showed reduced airway antigen staining (Fig. 1h); in contrast, no deficit in antigen staining was observed in the parenchyma or in the overall histology scoring, suggesting differential infection of lung tissue for SHC014-MA15 (Supplementary Table 2). We next analyzed infection in more susceptible, aged (12-month-old) animals. SARS-MA15–infected animals rapidly lost weight and succumbed to infection (Supplementary Fig. 3a,b). SHC014-MA15 infection induced robust and sustained weight loss, but had minimal lethality. Trends in the histology and antigen staining patterns that we observed in young mice were conserved in the older animals (Supplementary Table 3). We excluded the possibility that SHC014-MA15 was mediating infection through an alternative receptor on the basis of experiments using Ace2−/− mice, which did not show weight loss or antigen staining after SHC014-MA15 infection (Supplementary Fig. 4a,b and Supplementary Table 2). Together, the data indicate that viruses with the SHC014 spike are capable of inducing weight loss in mice in the context of a virulent CoV backbone.
Given the preclinical efficacy of Ebola monoclonal antibody therapies, such as ZMApp10, we next sought to determine the efficacy of SARS-CoV monoclonal antibodies against infection with SHC014-MA15. Four broadly neutralizing human monoclonal antibodies targeting SARS-CoV spike protein had been previously reported and are probable reagents for immunotherapy11,12,13. We examined the effect of these antibodies on viral replication (expressed as percentage inhibition of viral replication) and found that whereas wild-type SARS-CoV Urbani was strongly neutralized by all four antibodies at relatively low antibody concentrations (Fig. 2a–d), neutralization varied for SHC014-MA15. Fm6, an antibody generated by phage display and escape mutants11,12, achieved only background levels of inhibition of SHC014-MA15 replication (Fig. 2a). Similarly, antibodies 230.15 and 227.14, which were derived from memory B cells of SARS-CoV–infected patients13, also failed to block SHC014-MA15 replication (Fig. 2b,c). For all three antibodies, differences between the SARS and SHC014 spike amino acid sequences corresponded to direct or adjacent residue changes found in SARS-CoV escape mutants (fm6 N479R; 230.15 L443V; 227.14 K390Q/E), which probably explains the absence of the antibodies’ neutralizing activity against SHC014. Finally, monoclonal antibody 109.8 was able to achieve 50% neutralization of SHC014-MA15, but only at high concentrations (10 μg/ml) (Fig. 2d). Together, the results demonstrate that broadly neutralizing antibodies against SARS-CoV may only have marginal efficacy against emergent SARS-like CoV strains such as SHC014.
SARS-CoV monoclonal antibodies have marginal efficacy against SARS-like CoVs.
(a–d) Neutralization assays evaluating efficacy (measured as reduction in the number of plaques) of a panel of monoclonal antibodies, which were all originally generated against epidemic SARS-CoV, against infection of Vero cells with SARS-CoV Urbani (black) or SHC014-MA15 (green). The antibodies tested were fm6 (n = 3 for Urbani; n = 5 for SHC014-MA15)11,12 (a), 230.15 (n = 3 for Urbani; n = 2 for SHC014-MA15) (b), 227.15 (n = 3 for Urbani; n = 5 for SHC014-MA15) (c) and 109.8 (n = 3 for Urbani; n = 2 for SHC014-MA15)13 (d). Each data point represents the group mean and error bars define the s.e.m. Note that the error bars in SARS-CoV Urbani–infected Vero cells in b,c are overlapped by the symbols and are not visible.
To evaluate the efficacy of existing vaccines against infection with SHC014-MA15, we vaccinated aged mice with double-inactivated whole SARS-CoV (DIV). Previous work showed that DIV could neutralize and protect young mice from challenge with a homologous virus14; however, the vaccine failed to protect aged animals in which augmented immune pathology was also observed, indicating the possibility of the animals being harmed because of the vaccination15. Here we found that DIV did not provide protection from challenge with SHC014-MA15 with regards to weight loss or viral titer (Supplementary Fig. 5a,b). Consistent with a previous report with other heterologous group 2b CoVs15, serum from DIV-vaccinated, aged mice also failed to neutralize SHC014-MA15 (Supplementary Fig. 5c). Notably, DIV vaccination resulted in robust immune pathology (Supplementary Table 4) and eosinophilia (Supplementary Fig. 5d–f). Together, these results confirm that the DIV vaccine would not be protective against infection with SHC014 and could possibly augment disease in the aged vaccinated group.
In contrast to vaccination of mice with DIV, the use of SHC014-MA15 as a live, attenuated vaccine showed potential cross-protection against challenge with SARS-CoV, but the results have important caveats. We infected young mice with 104 p.f.u. of SHC014-MA15 and observed them for 28 d. We then challenged the mice with SARS-MA15 at day 29 (Supplementary Fig. 6a). The prior infection of the mice with the high dose of SHC014-MA15 conferred protection against challenge with a lethal dose of SARS-MA15, although there was only a minimal SARS-CoV neutralization response from the antisera elicited 28 d after SHC014-MA15 infection (Supplementary Fig. 6b, 1:200). In the absence of a secondary antigen boost, 28 d.p.i. represents the expected peak of antibody titers and implies that there will be diminished protection against SARS-CoV over time16,17. Similar results showing protection against challenge with a lethal dose of SARS-CoV were observed in aged BALB/c mice with respect to weight loss and viral replication (Supplementary Fig. 6c,d). However, the SHC014-MA15 infection dose of 104 p.f.u. induced >10% weight loss and lethality in some aged animals (Fig. 1 and Supplementary Fig. 3). We found that vaccination with a lower dose of SHC014-MA15 (100 p.f.u.), did not induce weight loss, but it also failed to protect aged animals from a SARS-MA15 lethal dose challenge (Supplementary Fig. 6e,f). Together, the data suggest that SHC014-MA15 challenge may confer cross-protection against SARS-CoV through conserved epitopes, but the required dose induces pathogenesis and precludes use as an attenuated vaccine.
Having established that the SHC014 spike has the ability to mediate infection of human cells and cause disease in mice, we next synthesized a full-length SHC014-CoV infectious clone based on the approach used for SARS-CoV (Fig. 3a)2. Replication in Vero cells revealed no deficit for SHC014-CoV relative to that for SARS-CoV (Fig. 3b); however, SHC014-CoV was significantly (P < 0.01) attenuated in primary HAE cultures at both 24 and 48 h after infection (Fig. 3c). In vivo infection of mice demonstrated no significant weight loss but showed reduced viral replication in lungs of full-length SHC014-CoV infection, as compared to SARS-CoV Urbani (Fig. 3d,e). Together, the results establish the viability of full-length SHC014-CoV, but suggest that further adaptation is required for its replication to be equivalent to that of epidemic SARS-CoV in human respiratory cells and in mice.
Full-length SHC014-CoV replicates in human airways but lacks the virulence of epidemic SARS-CoV.
(a) Schematic of the SHC014-CoV molecular clone, which was synthesized as six contiguous cDNAs (designated SHC014A, SHC014B, SHC014C, SHC014D, SHC014E and SHC014F) flanked by unique BglI sites that allowed for directed assembly of the full-length cDNA expressing open reading frames (for 1a, 1b, spike, 3, envelope, matrix, 6–8 and nucleocapsid). Underlined nucleotides represent the overhang sequences formed after restriction enzyme cleavage. (b,c) Viral replication of SARS-CoV Urbani (black) or SHC014-CoV (green) after infection of Vero cells (b) or well-differentiated, primary air-liquid interface HAE cell cultures (c) at an MOI of 0.01. Samples were collected at individual time points with biological replicates (n = 3) for each group. Data represent one experiment for both Vero and HAE cells. (d,e) Weight loss (n = 3 for SARS-CoV MA15, n = 7 for SHC014-CoV; n = 6 for SARS-Urbani) (d) and viral replication in the lungs (n = 3 for SARS-Urbani and SHC014-CoV) (e) of 10-week-old BALB/c mice infected with 1 × 105 p.f.u. of SARS-CoV MA15 (gray), SHC014-CoV (green) or SARS-CoV Urbani (black) via the i.n. route. Each data point represents the group mean, and error bars define the s.e.m. **P < 0.01 and ***P < 0.001 using two-tailed Student’s t-test of individual time points.
During the SARS-CoV epidemic, links were quickly established between palm civets and the CoV strains that were detected in humans4. Building on this finding, the common emergence paradigm argues that epidemic SARS-CoV originated as a bat virus, jumped to civets and incorporated changes within the receptor-binding domain (RBD) to improve binding to civet Ace2 (ref. 18). Subsequent exposure to people in live-animal markets permitted human infection with the civet strain, which, in turn, adapted to become the epidemic strain (Fig. 4a). However, phylogenetic analysis suggests that early human SARS strains appear more closely related to bat strains than to civet strains18. Therefore, a second paradigm argues that direct bat-human transmission initiated SARS-CoV emergence and that palm civets served as a secondary host and reservoir for continued infection (Fig. 4b)19. For both paradigms, spike adaptation in a secondary host is seen as a necessity, with most mutations expected to occur within the RBD, thereby facilitating improved infection. Both theories imply that pools of bat CoVs are limited and that host-range mutations are both random and rare, reducing the likelihood of future emergence events in humans.
Coronavirus strains are maintained in quasi-species pools circulating in bat populations. (a,b) Traditional SARS-CoV emergence theories posit that host-range mutants (red circle) represent random and rare occurrences that permit infection of alternative hosts. The secondary-host paradigm (a) argues that a nonhuman host is infected by a bat progenitor virus and, through adaptation, facilitates transmission to humans; subsequent replication in humans leads to the epidemic viral strain. The direct paradigm (b) suggests that transmission occurs between bats and humans without the requirement of an intermediate host; selection then occurs in the human population with closely related viruses replicating in a secondary host, permitting continued viral persistence and adaptation in both. (c) The data from chimeric SARS-like viruses argue that the quasi-species pools maintain multiple viruses capable of infecting human cells without the need for mutations (red circles). Although adaptations in secondary or human hosts may be required for epidemic emergence, if SHC014 spike–containing viruses recombined with virulent CoV backbones (circles with green outlines), then epidemic disease may be the result in humans. Existing data support elements of all three paradigms.
Although our study does not invalidate the other emergence routes, it does argue for a third paradigm in which circulating bat CoV pools maintain ‘poised’ spike proteins that are capable of infecting humans without mutation or adaptation (Fig. 4c). This hypothesis is illustrated by the ability of a chimeric virus containing the SHC014 spike in a SARS-CoV backbone to cause robust infection in both human airway cultures and in mice without RBD adaptation. Coupled with the observation of previously identified pathogenic CoV backbones3,20, our results suggest that the starting materials required for SARS-like emergent strains are currently circulating in animal reservoirs. Notably, although full-length SHC014-CoV probably requires additional backbone adaption to mediate human disease, the documented high-frequency recombination events in CoV families underscores the possibility of future emergence and the need for further preparation.
To date, genomics screens of animal populations have primarily been used to identify novel viruses in outbreak settings21. The approach here extends these data sets to examine questions of viral emergence and therapeutic efficacy. We consider viruses with the SHC014 spike a potential threat owing to their ability to replicate in primary human airway cultures, the best available model for human disease. In addition, the observed pathogenesis in mice indicates a capacity for SHC014-containing viruses to cause disease in mammalian models, without RBD adaptation. Notably, differential tropism in the lung as compared to that with SARS-MA15 and attenuation of full-length SHC014-CoV in HAE cultures relative to SARS-CoV Urbani suggest that factors beyond ACE2 binding—including spike processivity, receptor bio-availability or antagonism of the host immune responses—may contribute to emergence. However, further testing in nonhuman primates is required to translate these finding into pathogenic potential in humans. Importantly, the failure of available therapeutics defines a critical need for further study and for the development of treatments. With this knowledge, surveillance programs, diagnostic reagents and effective treatments can be produced that are protective against the emergence of group 2b–specific CoVs, such as SHC014, and these can be applied to other CoV branches that maintain similarly heterogeneous pools.
In addition to offering preparation against future emerging viruses, this approach must be considered in the context of the US government–mandated pause on gain-of-function (GOF) studies22. On the basis of previous models of emergence (Fig. 4a,b), the creation of chimeric viruses such as SHC014-MA15 was not expected to increase pathogenicity. Although SHC014-MA15 is attenuated relative to its parental mouse-adapted SARS-CoV, similar studies examining the pathogenicity of CoVs with the wild-type Urbani spike within the MA15 backbone showed no weight loss in mice and reduced viral replication23. Thus, relative to the Urbani spike–MA15 CoV, SHC014-MA15 shows a gain in pathogenesis (Fig. 1). On the basis of these findings, scientific review panels may deem similar studies building chimeric viruses based on circulating strains too risky to pursue, as increased pathogenicity in mammalian models cannot be excluded. Coupled with restrictions on mouse-adapted strains and the development of monoclonal antibodies using escape mutants, research into CoV emergence and therapeutic efficacy may be severely limited moving forward. Together, these data and restrictions represent a crossroads of GOF research concerns; the potential to prepare for and mitigate future outbreaks must be weighed against the risk of creating more dangerous pathogens. In developing policies moving forward, it is important to consider the value of the data generated by these studies and whether these types of chimeric virus studies warrant further investigation versus the inherent risks involved.
Overall, our approach has used metagenomics data to identify a potential threat posed by the circulating bat SARS-like CoV SHC014. Because of the ability of chimeric SHC014 viruses to replicate in human airway cultures, cause pathogenesis in vivo and escape current therapeutics, there is a need for both surveillance and improved therapeutics against circulating SARS-like viruses. Our approach also unlocks the use of metagenomics data to predict viral emergence and to apply this knowledge in preparing to treat future emerging virus infections.
Viruses, cells, in vitro infection and plaque assays.
Wild-type SARS-CoV (Urbani), mouse-adapted SARS-CoV (MA15) and chimeric SARS-like CoVs were cultured on Vero E6 cells (obtained from United States Army Medical Research Institute of Infectious Diseases), grown in Dulbecco’s modified Eagle’s medium (DMEM) (Gibco, CA) and 5% fetal clone serum (FCS) (Hyclone, South Logan, UT) along with antibiotic/antimycotic (Gibco, Carlsbad, CA). DBT cells (Baric laboratory, source unknown) expressing ACE2 orthologs have been previously described for both human and civet; bat Ace2 sequence was based on that from Rhinolophus leschenaulti, and DBT cells expressing bat Ace2 were established as described previously8. Pseudotyping experiments were similar to those using an HIV-based pseudovirus, prepared as previously described10, and examined on HeLa cells (Wuhan Institute of Virology) that expressed ACE2 orthologs. HeLa cells were grown in minimal essential medium (MEM) (Gibco, CA) supplemented with 10% FCS (Gibco, CA) as previously described24. Growth curves in Vero E6, DBT, Calu-3 2B4 and primary human airway epithelial cells were performed as previously described8,25. None of the working cell line stocks were authenticated or tested for mycoplasma recently, although the original seed stocks used to create the working stocks are free from contamination. Human lungs for HAE cultures were procured under University of North Carolina at Chapel Hill Institutional Review Board–approved protocols. HAE cultures represent highly differentiated human airway epithelium containing ciliated and non-ciliated epithelial cells as well as goblet cells. The cultures are also grown on an air-liquid interface for several weeks before use, as previously described26. Briefly, cells were washed with PBS and inoculated with virus or mock-diluted in PBS for 40 min at 37 °C. After inoculation, cells were washed three times and fresh medium was added to signify time ‘0’. Three or more biological replicates were harvested at each described time point. No blinding was used in any sample collections nor were samples randomized. All virus cultivation was performed in a biosafety level (BSL) 3 laboratory with redundant fans in the biosafety cabinets, as described previously by our group2. All personnel wore powered air purifying respirators (Breathe Easy, 3M) with Tyvek suits, aprons and booties and were double-gloved.
Sequence clustering and structural modeling.
The full-length genomic sequences and the amino acid sequences of the S1 domains of the spike of representative CoVs were downloaded from Genbank or Pathosystems Resource Integration Center (PATRIC), aligned with ClustalX and phylogenetically compared by using maximum likelihood estimation using 100 bootstraps or by using the PhyML (https://code.google.com/p/phyml/) package, respectively. The tree was generated using maximum likelihood with the PhyML package. The scale bar represents nucleotide substitutions. Only nodes with bootstrap support above 70% are labeled. The tree shows that CoVs are divided into three distinct phylogenetic groups defined as α-CoVs, β-CoVs and γ-CoVs. Classical subgroup clusters are marked as 2a, 2b, 2c and 2d for β-CoVs, and 1a and 1b for the α-CoVs. Structural models were generated using Modeller (Max Planck Institute Bioinformatics Toolkit) to generate homology models for SHC014 and Rs3367 of the SARS RBD in complex with ACE2 based on crystal structure 2AJF (Protein Data Bank). Homology models were visualized and manipulated in MacPyMol (version 1.3).
Construction of SARS-like chimeric viruses.
Both wild-type and chimeric viruses were derived from either SARS-CoV Urbani or the corresponding mouse-adapted (SARS-CoV MA15) infectious clone (ic) as previously described27. Plasmids containing spike sequences for SHC014 were extracted by restriction digest and ligated into the E and F plasmid of the MA15 infectious clone. The clone was designed and purchased from Bio Basic as six contiguous cDNAs using published sequences flanked by unique class II restriction endonuclease sites (BglI). Thereafter, plasmids containing wild-type, chimeric SARS-CoV and SHC014-CoV genome fragments were amplified, excised, ligated and purified. In vitro transcription reactions were then preformed to synthesize full-length genomic RNA, which was transfected into Vero E6 cells as previously described2. The medium from transfected cells was harvested and served as seed stocks for subsequent experiments. Chimeric and full-length viruses were confirmed by sequence analysis before use in these studies. Synthetic construction of chimeric mutant and full-length SHC014-CoV was approved by the University of North Carolina Institutional Biosafety Committee and the Dual Use Research of Concern committee.
Ethics statement.
This study was carried out in accordance with the recommendations for the care and use of animals by the Office of Laboratory Animal Welfare (OLAW), NIH. The Institutional Animal Care and Use Committee (IACUC) of The University of North Carolina at Chapel Hill (UNC, Permit Number A-3410-01) approved the animal study protocol (IACUC #13-033) used in these studies.
Mice and in vivo infection.
Female, 10-week-old and 12-month-old BALB/cAnNHsD mice were ordered from Harlan Laboratories. Mouse infections were done as previously described20. Briefly, animals were brought into a BSL3 laboratory and allowed to acclimate for 1 week before infection. For infection and live-attenuated virus vaccination, mice were anesthetized with a mixture of ketamine and xylazine and infected intranasally, when challenged, with 50 μl of phosphate-buffered saline (PBS) or diluted virus with three or four mice per time point, per infection group per dose as described in the figure legends. For individual mice, notations for infection including failure to inhale the entire dose, bubbling of inoculum from the nose, or infection through the mouth may have led to exclusion of mouse data at the discretion of the researcher; post-infection, no other pre-established exclusion or inclusion criteria are defined. No blinding was used in any animal experiments, and animals were not randomized. For vaccination, young and aged mice were vaccinated by footpad injection with a 20-μl volume of either 0.2 μg of double-inactivated SARS-CoV vaccine with alum or mock PBS; mice were then boosted with the same regimen 22 d later and challenged 21 d thereafter. For all groups, as per protocol, animals were monitored daily for clinical signs of disease (hunching, ruffled fur and reduced activity) for the duration of the experiment. Weight loss was monitored daily for the first 7 d, after which weight monitoring continued until the animals recovered to their initial starting weight or displayed weight gain continuously for 3 d. All mice that lost greater than 20% of their starting body weight were ground-fed and further monitored multiple times per day as long as they were under the 20% cutoff. Mice that lost greater than 30% of their starting body weight were immediately sacrificed as per protocol. Any mouse deemed to be moribund or unlikely to recover was also humanely sacrificed at the discretion of the researcher. Euthanasia was performed using an isoflurane overdose and death was confirmed by cervical dislocation. All mouse studies were performed at the University of North Carolina (Animal Welfare Assurance #A3410-01) using protocols approved by the UNC Institutional Animal Care and Use Committee (IACUC).
Histological analysis.
The left lung was removed and submerged in 10% buffered formalin (Fisher) without inflation for 1 week. Tissues were embedded in paraffin and 5-μm sections were prepared by the UNC Lineberger Comprehensive Cancer Center histopathology core facility. To determine the extent of antigen staining, sections were stained for viral antigen using a commercially available polyclonal SARS-CoV anti-nucleocapsid antibody (Imgenex) and scored in a blinded manner by for staining of the airway and parenchyma as previously described20. Images were captured using an Olympus BX41 microscope with an Olympus DP71 camera.
Virus neutralization assays.
Plaque reduction neutralization titer assays were performed with previously characterized antibodies against SARS-CoV, as previously described11,12,13. Briefly, neutralizing antibodies or serum was serially diluted twofold and incubated with 100 p.f.u. of the different infectious clone SARS-CoV strains for 1 h at 37 °C. The virus and antibodies were then added to a 6-well plate with 5 × 105 Vero E6 cells/well with multiple replicates (n ≥ 2). After a 1-h incubation at 37 °C, cells were overlaid with 3 ml of 0.8% agarose in medium. Plates were incubated for 2 d at 37 °C, stained with neutral red for 3 h and plaques were counted. The percentage of plaque reduction was calculated as (1 − (no. of plaques with antibody/no. of plaques without antibody)) × 100.
Statistical analysis.
All experiments were conducted contrasting two experimental groups (either two viruses, or vaccinated and unvaccinated cohorts). Therefore, significant differences in viral titer and histology scoring were determined by a two-tailed Student’s t-test at individual time points. Data was normally distributed in each group being compared and had similar variance.
Biosafety and biosecurity.
Reported studies were initiated after the University of North Carolina Institutional Biosafety Committee approved the experimental protocol (Project Title: Generating infectious clones of bat SARS-like CoVs; Lab Safety Plan ID: 20145741; Schedule G ID: 12279). These studies were initiated before the US Government Deliberative Process Research Funding Pause on Selected Gain-of-Function Research Involving Influenza, MERS and SARS Viruses (http://www.phe.gov/s3/dualuse/Documents/gain-of-function.pdf). This paper has been reviewed by the funding agency, the NIH. Continuation of these studies was requested, and this has been approved by the NIH.
SARS-CoV is a select agent. All work for these studies was performed with approved standard operating procedures (SOPs) and safety conditions for SARS-CoV, MERs-CoV and other related CoVs. Our institutional CoV BSL3 facilities have been designed to conform to the safety requirements that are recommended in the Biosafety in Microbiological and Biomedical Laboratories (BMBL), the US Department of Health and Human Services, the Public Health Service, the Centers for Disease Control (CDC) and the NIH. Laboratory safety plans were submitted to, and the facility has been approved for use by, the UNC Department of Environmental Health and Safety (EHS) and the CDC. Electronic card access is required for entry into the facility. All workers have been trained by EHS to safely use powered air purifying respirators (PAPRs), and appropriate work habits in a BSL3 facility and active medical surveillance plans are in place. Our CoV BSL3 facilities contain redundant fans, emergency power to fans and biological safety cabinets and freezers, and our facilities can accommodate SealSafe mouse racks. Materials classified as BSL3 agents consist of SARS-CoV, bat CoV precursor strains, MERS-CoV and mutants derived from these pathogens. Within the BSL3 facilities, experimentation with infectious virus is performed in a certified Class II Biosafety Cabinet (BSC). All members of the staff wear scrubs, Tyvek suits and aprons, PAPRs and shoe covers, and their hands are double-gloved. BSL3 users are subject to a medical surveillance plan monitored by the University Employee Occupational Health Clinic (UEOHC), which includes a yearly physical, annual influenza vaccination and mandatory reporting of any symptoms associated with CoV infection during periods when working in the BSL3. All BSL3 users are trained in exposure management and reporting protocols, are prepared to self-quarantine and have been trained for safe delivery to a local infectious disease management department in an emergency situation. All potential exposure events are reported and investigated by EHS and UEOHC, with reports filed to both the CDC and the NIH.
Research in this manuscript was supported by grants from the National Institute of Allergy & Infectious Disease and the National Institute of Aging of the US National Institutes of Health (NIH) under awards U19AI109761 (R.S.B.), U19AI107810 (R.S.B.), AI085524 (W.A.M.), F32AI102561 (V.D.M.) and K99AG049092 (V.D.M.), and by the National Natural Science Foundation of China awards 81290341 (Z.-L.S.) and 31470260 (X.-Y.G.), and by USAID-EPT-PREDICT funding from EcoHealth Alliance (Z.-L.S.). Human airway epithelial cultures were supported by the National Institute of Diabetes and Digestive and Kidney Disease of the NIH under award NIH DK065988 (S.H.R.). We also thank M.T. Ferris (Dept. of Genetics, University of North Carolina) for the reviewing of statistical approaches and C.T. Tseng (Dept. of Microbiology and Immunology, University of Texas Medical Branch) for providing Calu-3 cells. Experiments with the full-length and chimeric SHC014 recombinant viruses were initiated and performed before the GOF research funding pause and have since been reviewed and approved for continued study by the NIH. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
V.D.M. designed, coordinated and performed experiments, completed analysis and wrote the manuscript. B.L.Y. designed the infectious clone and recovered chimeric viruses; S.A. completed neutralization assays; L.E.G. helped perform mouse experiments; T.S. and J.A.P. completed mouse experiments and plaque assays; X.-Y.G. performed pseudotyping experiments; K.D. generated structural figures and predictions; E.F.D. generated phylogenetic analysis; R.L.G. completed RNA analysis; S.H.R. provided primary HAE cultures; A.L. and W.A.M. provided critical monoclonal antibody reagents; and Z.-L.S. provided SHC014 spike sequences and plasmids. R.S.B. designed experiments and wrote manuscript.
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Quote Dr. David Martin said Peter Daszak wrote in 2015 ‘they needed the media to hype up the need for coronavirus vaccines to sell them’. The very next year Dr Ralf Baric wrote in 2016: ‘..’the (WIV) virus was human ready’ a clear indication a weapon was being readied for human transmission. Seems to me J. Jyrkkanen ‘Collusion and Conspiracy to commit a crime for profit’.
These folks woked together with a large team under the funding of Fauci, the Government and even President Biden to craft a deadly population whacking killer bioweapon and even created technology to hide the fact. The NoSeeUm Technology of Baric.
(Left to right): Ralph Baric, Peter Daszak, Shi Zhengli.
A group of Chinese scientists lobbied to rename ‘SARS-CoV-2’ to ‘2019-nCoV’. In the correspondence, the scientists feared that the virus would become known as ‘Wuhan Coronavirus’ or ‘Wuhan Pneumonia’.
The truth behind the science around the origin of the SARS-CoV-2 lies with Ralph Baric of the University of North Carolina, Peter Daszak of EcoHealth Alliance and Prof Shi Zhengli of the Wuhan Institute of Virology (WIV).
According to the email obtained by the US Right To Know organization, on January 13, 2020, in an email to Peter Daszak at 6.50 pm, Ralph Baric, states:
“Hi Peter, I have to participate in an NIH call tomorrow at 10. I believe it’s a strategic meeting designed to help craft a NIH response plan to the WU-CoV. Hope things are going well. Looks like we found our highly variable SARS-like CoV! Ralph”
In reply to Ralph Baric’s email, Peter Daszak at 7.55 pm states:
“It sounds like we’re on the same call! And my exact thoughts are of the highly variable SARS-like CoV. I’ve told journalists about it, but it’s a complicated story for them to get across.”
On 13 January 2020, before China or the World Health Organisation (WHO) made any official statement on the nature of the coronavirus, both Ralph Baric and Peter Daszak in their emails appear to be confident that the coronavirus in China is a “highly variable SARS-like CoV”. Most importantly, Ralph Baric refers to the coronavirus as “Our highly variable SARS-like COV”, displaying a familiarity with the virus.
Reportedly, in 2013, the American virologist Ralph Baric approached Zhengli Shi at a meeting. Shi had detected the genome of a new virus, called SHC014, that was one of the two closest relatives to the original SARS virus, but her team had not been able to culture it in the laboratory. Baric had developed a way around that problem—a technique termed as “reverse genetics” in coronaviruses. Not only did it allow him to bring an actual virus to life from its genetic code, but he could mix and match parts of multiple viruses. He wanted to take the “spike” gene from SHC014 and move it into a genetic copy of the SARS virus he already had in his laboratory. The spike molecule is what lets a coronavirus open a cell and get inside it. The resulting chimera would demonstrate whether the spike of SHC014 would attach to human cells.
Baric asked Shi Zhengli if he could have the genetic data for SHC014. “She was gracious enough to send us those sequences almost immediately,” he told media. His team introduced the virus modified with that code into mice and into a petri dish of human airway cells. Sure enough, the chimera exhibited “robust replication” in the human cells—evidence that nature was full of coronaviruses ready to leap directly to people.
It is no surprise that a group of Chinese scientists lobbied through US Professor of the University of North Carolina Ralph Baric to rename «SARS-CoV-2» given by the Coronavirus Study Group (CSG) of the International Committee on Virus Taxonomy (ICTV) to “2019-nCoV”. In the correspondence, the Chinese scientists feared that the virus would become known as “Wuhan Coronavirus” or “Wuhan Pneumonia”. In an email dated 13/2/2020, Professor Shi Zhengli wrote to Ralph Baric. The subject of the email was “Virus Name”. The email had an attached document titled, “A unique and unified name for the novel coronavirus from Wuhan SJ clean”.
The email stated:
“Dear Ralph,
We heard that the 2019-nCoV was renamed as SARS-CoV-2. We had a fierce discussion among Chinese virologists. We have some comments on this name, I’m wondering if the CoV study group would consider a revision.
I attached the comments from me and my Chinese colleague.”
The document from Prof. Shi Zhengli to Prof. Ralph Baric states:
“A unique and unified name is needed for the novel coronavirus identified from Wuhan. An outbreak of unusual pneumonia of unknown cause in Wuhan, China, was first reported in December 2019. By 5 January 2020, Chinese scientists had quickly identified the causative agent a new type of coronavirus (CoV) belonging to the Betacoronaviruses genus of the Coronavirdae family that also includes severe acute respiratory syndrome (SARS)-CoV and the Middle East respiratory syndrome (MERS)- CoV.
On 12 January 2020, the World Health Organization (WHO) temporarily named the virus as 2019 novel coronavirus (2019-nCoV). On 30 January, WHO recommended naming the disease as “2019-nCoV acute respiratory disease”. On 8 February 2020, the China National Health Commission (CNHC) announced naming the disease as “Novel CoronavirusPneumonia” (NCP). On 11 February 2020, WHO renamed the disease “coronavirus disease2019” (COVID-19). On 7 February 2020, the Coronavirus Study Group (CSG) of the International Committee on Virus Taxonomy (ICTV) posted a manuscript at bioRxiv and suggested designating the novel coronavirus as “severe acute respiratory syndrome coronavirus 2(SA RS-CoV-2)” based on the phylogenetic analysis of related coronaviruses.
Zhengli further in her document to Ralph Baric says, “By 11th February 2020, the new coronavirus had caused more than 40,000 confirmed infections and more than 1000 deaths, mostly in mainland China, despite efforts by the Chinese government and its people to contain the spread of the virus in past weeks. lt goes without saying that the effects of the epidemic on all the aspects of Chinese life are devastating and, possibly, irreversible. Consequently, appropriately naming the virus and disease becomes a matter of importance to the Chinese people, in general, and virologists, in specific, and the issue has been fervently discussed and debated among scientists with the outcome, so far, as noted above. We fully agree that the new virus and SARS-CoV belong to the same virus species by classification. However, the consensus opinion of Chinese virologists is that none of the currently proposed names reflects the uniqueness and characteristics of the novel virus and that more consideration is needed for naming the virus. Based on the following reasons, we propose giving a unique and unified name to the new virus.”
Prof Shi Zhengli, also known as the “Batwoman”, continues to impress upon Ralph Baric on behalf of the group of Chinese scientists. She says, “All proposed names are either too generic, or too similar, to previously well-known viruses, or contain an Arabic number. This makes it hard to remember or recognize, leading to a tendency among the general population and scientists alike to use a shorthand term such as ‘Wuhan coronavirus’ or ‘Wuhan pneumonia’. This has, in fact. been the case since it was named as 2019-nCoV. This practice would, however, stigmatize and insult the people in Wuhan, who are still suffering from the outbreak.”
The document sent by Prof Zhengli to Ralph Baric, further states, “The new virus is still evolving, and it is still too early to predict the outcome of the current outbreak. However, it is already clear that the infection of the new virus has diverse symptoms, from asymptomatic infection to severe pneumonia and even death. It has less case-fatality rate and higher transmissibility than SARS-CoV, indicating its clear difference from SARS-CoV. Again. therefore, it is not appropriate to designate the new virus as SARS-CoV-2 before we know more properties of the virus.”
Baric, Daszak and Zhengli were working together on the gain-of-function research. Scientists have posited that SARS-CoV-2 may be a product of WIV’s experiments on an unpublished bat coronavirus that is more closely related to SARS-CoV-2 than RaTG13. “First, SARS-CoV-2 may have evolved in bats, which are known reservoirs of immense coronavirus diversity, and then spread directly, or indirectly via an intermediate host, to humans through natural mechanisms. The degree of anticipated but undiscovered natural diversity clearly lends support to this scenario, as well as support to other scenarios. Second, SARS-CoV-2 or a recent ancestor virus may have been collected by humans from a bat or other animal and then brought to a laboratory where it was stored knowingly or unknowingly, propagated and perhaps manipulated genetically to understand its biological properties and then released accidentally.“
Wuhan Institute of Virology authorities shut down outside access to its virus database in September 2019, thereby making it difficult to verify that “The Wuhan lab has many bat samples not yet worked out or results published. There are some concerns that some of their samples may not have been handled properly and leaked out of the lab.”
Savio Rodrigues is the founder and editor-in-chief of Goa Chronicle.
Lab-made coronavirus related to SARS can infect human cells.
An experiment that created a hybrid version of a bat coronavirus — one related to the virus that causes SARS (severe acute respiratory syndrome) — has triggered renewed debate over whether engineering lab variants of viruses with possible pandemic potential is worth the risks.
In an article published in Nature Medicine1 on 9 November, scientists investigated a virus called SHC014, which is found in horseshoe bats in China. The researchers created a chimaeric virus, made up of a surface protein of SHC014 and the backbone of a SARS virus that had been adapted to grow in mice and to mimic human disease. The chimaera infected human airway cells — proving that the surface protein of SHC014 has the necessary structure to bind to a key receptor on the cells and to infect them. It also caused disease in mice, but did not kill them.
Although almost all coronaviruses isolated from bats have not been able to bind to the key human receptor, SHC014 is not the first that can do so. In 2013, researchers reported this ability for the first time in a different coronavirus isolated from the same bat population2.
The findings reinforce suspicions that bat coronaviruses capable of directly infecting humans (rather than first needing to evolve in an intermediate animal host) may be more common than previously thought, the researchers say.
But other virologists question whether the information gleaned from the experiment justifies the potential risk. Although the extent of any risk is difficult to assess, Simon Wain-Hobson, a virologist at the Pasteur Institute in Paris, points out that the researchers have created a novel virus that “grows remarkably well” in human cells. “If the virus escaped, nobody could predict the trajectory,” he says.
Creation of a chimaera
The argument is essentially a rerun of the debate over whether to allow lab research that increases the virulence, ease of spread or host range of dangerous pathogens — what is known as ‘gain-of-function’ research. In October 2014, the US government imposed a moratorium on federal funding of such research on the viruses that cause SARS, influenza and MERS (Middle East respiratory syndrome, a deadly disease caused by a virus that sporadically jumps from camels to people).
The latest study was already under way before the US moratorium began, and the US National Institutes of Health (NIH) allowed it to proceed while it was under review by the agency, says Ralph Baric, an infectious-disease researcher at the University of North Carolina at Chapel Hill, a co-author of the study. The NIH eventually concluded that the work was not so risky as to fall under the moratorium, he says.
But Wain-Hobson disapproves of the study because, he says, it provides little benefit, and reveals little about the risk that the wild SHC014 virus in bats poses to humans.
Other experiments in the study show that the virus in wild bats would need to evolve to pose any threat to humans — a change that may never happen, although it cannot be ruled out. Baric and his team reconstructed the wild virus from its genome sequence and found that it grew poorly in human cell cultures and caused no significant disease in mice.
“The only impact of this work is the creation, in a lab, of a new, non-natural risk,” agrees Richard Ebright, a molecular biologist and biodefence expert at Rutgers University in Piscataway, New Jersey. Both Ebright and Wain-Hobson are long-standing critics of gain-of-function research.
In their paper, the study authors also concede that funders may think twice about allowing such experiments in the future. “Scientific review panels may deem similar studies building chimeric viruses based on circulating strains too risky to pursue,” they write, adding that discussion is needed as to “whether these types of chimeric virus studies warrant further investigation versus the inherent risks involved”.
Useful research
But Baric and others say the research did have benefits. The study findings “move this virus from a candidate emerging pathogen to a clear and present danger”, says Peter Daszak, who co-authored the 2013 paper. Daszak is president of the EcoHealth Alliance, an international network of scientists, headquartered in New York City, that samples viruses from animals and people in emerging-diseases hotspots across the globe.
Studies testing hybrid viruses in human cell culture and animal models are limited in what they can say about the threat posed by a wild virus, Daszak agrees. But he argues that they can help indicate which pathogens should be prioritized for further research attention.
Without the experiments, says Baric, the SHC014 virus would still be seen as not a threat. Previously, scientists had believed, on the basis of molecular modelling and other studies, that it should not be able to infect human cells. The latest work shows that the virus has already overcome critical barriers, such as being able to latch onto human receptors and efficiently infect human airway cells, he says. “I don’t think you can ignore that.” He plans to do further studies with the virus in non-human primates, which may yield data more relevant to humans.
Quote Dr. David Martin said Peter Daszak wrote in 2015 ‘they needed the media to hype up the need for coronavirus vaccines to sell them’. The very next year Dr Ralf Baric wrote in 2016: ‘..’the (WIV) virus was human ready’ a clear indication a weapon was being readied for human transmission. Seems to me J. Jyrkkanen ‘Collusion and Conspiracy to commit a crime for profit’.
: “They took the money that Cheney gave them [from the Patriot Act], $2.2 billion, and they funneled it through NIH, and it all went through Anthony Fauci. So beginning in 2002, Anthony Fauci got a 68% raise from the Pentagon for doing bioweapons development, and he got a raise of billions of dollars a year, and then he started doing all of this gain-of-function. In 2014, three of those bugs escaped in high-profile escapes from different labs in the US. Congress held hearings on it. Everybody was angry, and 300 top scientists sent letters to Obama saying you got to shut down Fauci because he is going to create a pandemic. So, Obama ordered a moratorium, and at that time, Fauci had eighteen different gain-of-function experiments he was doing around the US. He instead moved his stuff offshore to Wuhan, where he could do it out of sight of these 300 scientists and nosy White House officials who were trying to shut him down. And he continued to do it with the same people he was funding here, Ralph Baric and Peter Dazak, and they moved their operation to the Wuhan lab.”
the CIA, DOD, and Tony Fauci taught Chinese military scientists how to build weapons of mass destruction. Then Bill Gates, a former CIA director, and China’s CDC director collaborated on how to censor a lab leak at Event 201 in Oct. 2019:
“Fauci funded the study that taught the Chinese military scientists, everything in China is dual-use, that lab is a military lab, and he taught them cutting-edge technology for building weapons of mass destruction.
In other words, the study for how to create the clones and how to create a spike protein that could attach to a human lung and transplant it onto a coronavirus.
He also funded through Ralph Baric at the University of North Carolina a technique called seamless ligation which is a technique for hiding human tampering on that virus after you’ve done it. Fauci gave Baric $212 million, and Baric developed a technique for hiding the human tampering; (Pic)
Quote Dr. David Martin said Peter Daszak wrote in 2015 ‘they needed the media to hype up the need for coronavirus vaccines to sell them’. The very next year Dr Ralf Baric wrote in 2016: ‘..’the (WIV) virus was human ready’ a clear indication a weapon was being readied for human transmission. Seems to me J. Jyrkkanen ‘Collusion and Conspiracy to commit a crime for profit’.
Baric taught that to Shi Zhengli (BELOW), the Chinese bat lady. Fauci says we were doing this for vaccine development and countermeasures, but there is no justification in the world for funding somebody to create seamless ligation; in fact, it is the inverse of what you would do if your interest was public health. If your interest was bioweapons creation, and he was the czar of bioweapons since 2002, that’s what you would do. USAID gave ten times what Fauci gave. The DOD was there. Why were they in there teaching Chinese scientists how to build weapons of mass destruction?
USAID is a CIA front group. Eco-health Alliance is a CIA front group. The CIA modeled this outbreak in 2019 twice, the second time at Event 201. Who was at Event 201? Avril Haines co-hosted it with Bill Gates, and the head of the Chinese CDC, George Gao, was there. The virus was already circulating in Wuhan, nobody knew it, but George Gao had to know it; he was the head of the Chinese CDC and their number one expert on coronaviruses. He comes to New York in October of 2019 and sits downs with Avril Haines, the former director of the CIA, today the Director of National Intelligence, the top spy in the country, and they do a four-part simulation, and the fourth part is George Gao and Avril Haines talking about how do we get social media to censor people if they say this is from a lab leak.”
.@RobertKennedyJr tells @jimmy_dore the CIA, DOD, and Tony Fauci taught Chinese military scientists how to build weapons of mass destruction. Then Bill Gates, a former CIA director, and China's CDC director collaborated on how to censor a lab leak at Event 201 in Oct. 2019:… pic.twitter.com/qYANxt4ZT2
Bill Gates Crimes Short List. 2023-03-02. Jorma Jyrkkanen, BSc, PDP
Jorma Jyrkkanen
BILL GATES CRIMES: U.S. patents show CDC ownership of Coronavirus. Both China and the U.S. involved in the creation of Wuhan SARS-CoV-2. Gates and CCP controlled WHO appoints criminal Tedros. CDC, FDA, CIA, NIH, Gates, Fauci, Baric, Rockefeller are all involved in Federal Crimes.
Bill Gates and the Rockefeller foundation paid Google, Facebook, Politico, Wikipedia, Fact Checkers in order to censor and control all the information.
GIRLS IN AFRICA VACCINATED FOR DTP HAD 10X THE MORTALITY OF THOSE NOT VACCINATED. GATES WANTED TO VACCINATE 160 MILLION W DTP (Whooping Cough, measles and mumps)
The CIA has been using Operation Mockingbird for years and has over 3,000 agents implanted in Mainstream Media to control the population.
Event 201 was sponsored by Bill Gates, the Johns Hopkins Center for Health Security (CIA) and the World Economic Forum to enforce a worldwide Pandemic response 5 months before the WHO fraudulently declared a global pandemic. It was a planned coordinated criminal effort worldwide.
In January 2017 Anthony Fauci said there will be a surprise virus outbreak before the end of 2020. Bill Gates in 2015 talked of a future pandemic and lied in April 2020 when he said they did not simulate or practice for a pandemic.
Klaus Schwab in his book Covid-19 The Great Reset shows Covid was the Trojan Horse to Reset the World according to the UN 2030 Agenda. Build Back Better slogan is a criminal coordinated effort to remove human rights and institute a one world government.
Bill Gates and the Rockefeller foundation bribes the WHO, NIH, NIAID, CDC, FDA, Medical Schools and Journals to control the health industry and public health policy.
WHO Chief Tedros involved in genocide killing and torture in Ethiopia. Tedros is a known member of the communist party. He is Beijing’s and Bill Gates puppet. As a Health Minister he was accused of covering up three Cholera Epidemics and committing crimes against humanity. The CCP and Bill Gates helped put Tedros in charge of the WHO.
John D. Rockefeller over 100 years ago seized the U.S. Media and took control over public health using toxic petroleum based drugs for profit and controlled the American Medical Association blacklisting and expelling any doctors who practiced natural medicine.
Rockefeller’s poison injections and medicines started causing cancer in early years and to cover it up formed the American Cancer Society. Medical error is the 3rd leading cause of death in America.
Bill Gates used India and Africa as guinea pigs for pharmaceutical companies to make a financial killing while killing a lot of people in the process including killing innocent children and babies with vaccines. Bill Gates controls GAVI The Vaccine Alliance to vaccinate the world with his poisons.
National Security Study Memorandum NSSM 200 Implications of Worldwide Population Growth For U.S. Security and Overseas Interests December 10, 1974 (THE KISSINGER REPORT) shows the intention of governments to reduce the population.
Bill Gates is one of the key funders in the Stratosphere experiment to block out the sun for Climate Change by releasing poisons in the air. Environmental Scientist call it global genocide experiment. Gates has invested over one billion dollars in the Earth Now Global Surveillance project to launch hundreds of satellites to monitor people everywhere 24/7 a day.
In partnership with MIT Bill Gates has developed a new technology that allows vaccines to be injected under your skin along with your medical records. Bill Gates Gates funded genetically modified mosquitoes released in the USA to allow human immunization by means of mosquito bites “Flying Syringes.”
Bill Gates had business dealings and a relationship with Jeffrey Epstein, a convicted child sex criminal. Why would he choose to partner with the world’s most notorious pedophile? To Blackmail?
BILL GATES NAME APPEARS ON THE EPSTEIN ISLAND VISITOR LIST
Bill Gates is the top financial donor of the WHO and CDC. No one person has more power than Gates to influence and control the health and medical freedom of all people. Bill Gates and all mRNA Vaccines must be stopped. This is a global genocide experiment and a takeover of the world.
CRIMINAL INDICTMENTS: The U.S. Department of Defense along with Fauci, Gates, Tedros, Moderna, Pfizer, FDA, CDC, WEF, CIA and others willfully and criminally engaged in racketeering, illegal advertising, fraud and mass premeditated murder of millions of innocent people worldwide. pic.twitter.com/WWQePRTYrd
GOVERNMENT CRIMES: They paid doctors and nurses to murder innocent patients. They faked Covid cases and deaths to instill fear in the population. They denied safe early treatments murdering millions of innocent people. They forced ineffective toxic Covid vaccines on the world. They Censored anyone sharing life saving early treatment information and anyone who warned about the dangers of the Covd vaccines. The Governments willfully committed crimes against humanity.
Biden-US Govt DOD Funded ECOHEALTH In Wuhan and 46 others in Ukraine 2023-01-30, Jorma Antero Jyrkkanen BSc, PDP
The Iowa senator introduced legislation to permanently defund EcoHealth Alliance.
WASHINGTON – U.S. Senator Joni Ernst (R-Iowa) is calling on Congress to put an immediate and permanent end to taxpayer funding of EcoHealth Alliance following the release of an investigation today that found the organization mismanaged coronavirus experiments in Wuhan, China.
Senator Ernst requested the investigation by the Department of Health and Human Services’ (HHS) Office of Inspector General (OIG) upon learning that EcoHealth was spending tax dollars on dangerous coronaviruses in Communist China’s Wuhan Institute of Virology (WIV) and was not disclosing information about those projects to the public, as required by law.
The investigation found EcoHealth, WIV, and the National Institutes of Health (NIH) were all at fault for mismanagement:
EcoHealth did not immediately notify NIH when a coronavirus was enhanced to become more lethal, as required; and, when it did, NIH did not quickly act to have the pathogen reviewed for pandemic potential.
EcoHealth misspent tens of thousands of tax dollars on bonuses, junkets, and other unallowable costs.
China’s WIV did not cooperate.</b>
The OIG suggests that WIV should be permanently barred from receiving U.S. taxpayer dollars, EcoHealth should return misspent taxpayer money, and NIH should increase oversight of EcoHealth and other projects involving pathogens with pandemic potential.
Ernst’s response to the HHS investigation:
“While NIH certainly shares in the blame, EcoHealth Alliance is ultimately at fault for failing to tell the world what was really going on at China’s Wuhan Institute. They are guilty of either complacency or a cover-up, or maybe a little of both,” said Ernst.“EcoHealth was paid millions, promising their hunt for bat viruses would protect the world from a pandemic…well, the world got a pandemic, and EcoHealth keeps getting millions. We can’t afford any more of EcoHealth’s ‘prevention’ efforts. That’s why we mustpermanently ban them from receiving taxpayer dollars ever again.”
Since the world learned of the COVID-19 pandemic at the beginning of 2020 – including the role EcoHealth might have played in a potential lab leak— EcoHealth has been given more than $40 million in taxpayer dollars. Just last month, the Biden administration awarded the group $3 million out of the Department of Defense (DOD) budget.
Ernst’s response to the administration’s latest check to EcoHealth:
“The Biden administration is funding EcoHealth to search for risky viruses in places all across the globe, except where they might actually find them: in their own lab experiments! Washington is looking for ways to trim spending, so let’s start by cutting the millions of dollars flowing to EcoHealth’s batty experiments,” said Ernst.
IRS whistleblower Gary Shapley’s opening statement on Department of Justice Corruption and the Biden Family’s Crimes: “I’m here to tell you that the Delaware US Attorney’s Office and Department of Justice’s handling of the Hunter Biden tax investigation was very different from any other case my 14 years at the IRS. At every stage decisions were made that benefited the subject of this investigation. For example, prosecutors conceal contents of Hunter Biden’s laptop from investigators. DOJ slow walked steps to include interviews, serving document requests, and executing search warrants. Warrents that we’re ready as early as April of 2020, but were delayed until after the November 2020 election, and never pursued. Investigators were not allowed to follow up on WhatsApp messages from Hunter Biden’s Apple iCloud backup, where he suggested he was sitting next to his father. Assistant United States Attorney Leslie Wolf cited the optics of executing a search warrant at President Biden’s residence as a deciding factor for not allowing it even though she agreed that probable cause existed. Prosecutors instructed investigators not to ask about the big guy or dad when conducting interviews. The Biden transition team was tipped off about interviews the night before the investigation went over. A fact that my FBI counterpart confirmed to this committee in recent testimony where the result was only one witness spoke to investigators that day. These are just some of the examples of how our investigation was stymied. I’m not here to support partisan agendas on either side. I’m here because our tax system relies on the American people having confidence it is administered fairly and equally for everyone, regardless of your last name, or political connections… After our investigation largely concluded by the end of 2021, the IRS recommended charging Hunter Biden with multiple felonies and several misdemeanors for the tax years of 2014 through 2019. The Delaware assistance United States Attorneys and tax evasion trial attorneys supported charging the felonies and misdemeanors listed in Exhibit two of my interview transcripts… Attorney General Garland led Congress to believe the case was insulated from improper political influence because all decisions were being made exclusively by Delaware US Attorneey David Weiss, but that was not true. The Justice Department allowed the President’s political appointees to weigh in on whether they charged the president’s son. After US Attorney for DC, Mathew Graves, appointed by President Biden refused to bring charges in March 2022, I watched US Attorney Weiss tell a roomful of senior FBI and IRS leaders on October 7, 2022, that he was not the deciding person on whether charges were filed. That was my red line. I had already seen a pattern of preferential treatment and obstruction. Now, US Attorney Weiss was admitting that what the American people believed based on the Attorney General’s sworn statement was false. I could no longer stay silent…”
2. Yesterday Russia claimed Labs in Ukraine created the covid problem.
3. Zelensky Ordered Destruction of All State Docs Associated with METABIOTA on 02/24/22. WAS METABIOTA DOING ILLEGAL STUFF regarding covid in Ukraine and why would Selensky order Dept of Defense Records on METABIOTA destroyed??
Legal Ramifications of Conducting Secret Research on biowarfare capable pathogens stem from an International Convention on Pathogensx for the purpose of military use. The Biological Weapons Convention (BWC), or Biological and Toxin Weapons Convention (BTWC), is a disarmament treaty that effectively bans biological and toxin weapons by prohibiting their development, production, acquisition, transfer, stockpiling and use.
The Convention Articles Biological Weapons Convention
Preamble
Convention on the Prohibition of the Development, Production and Stockpiling of Bacteriological (Biological) and Toxin Weapons and on their Destruction
The States Parties to this Convention,
Determined to act with a view to achieving effective progress towards general and complete disarmament, including the prohibition and elimination of all types of weapons of mass destruction, and convinced that the prohibition of the development, production and stockpiling of chemical and bacteriological (biological) weapons and their elimination, through effective measures, will facilitate the achievement of general and complete disarmament under strict and effective international control,
Recognizing the important significance of the Protocol for the Prohibition of the Use in War of Asphyxiating, Poisonous or Other Gases, and of Bacteriological (Pathogens) Methods of Warfare, signed at Geneva on 17 June 1925, and conscious also of the contribution which the said Protocol has already made and continues to make, to mitigating the horrors of war,
Reaffirming their adherence to the principles and objectives of that Protocol and calling upon all States to comply strictly with them,
Recalling that the General Assembly of the United Nations has repeatedly condemned all actions contrary to the principles and objectives of the Geneva Protocol of 17 June 1925,
Desiring to contribute to the strengthening of confidence between peoples and the general improvement of the international atmosphere,
Desiring also to contribute to the realization of the purposes and principles of the Charter of the United Nations,
Convinced of the importance and urgency of eliminating from the arsenals of States, through effective measures, such dangerous weapons of mass destruction as those using chemical or bacteriological (biological) agents,
Recognizing that an agreement on the prohibition of bacteriological (biological) and toxin weapons represents a first possible step towards the achievement of agreement on effective measures also for the prohibition of the development, production and stockpiling of chemical weapons, and determined to continue negotiations to that end,
Determined, for the sake of all mankind, to exclude completely the possibility of bacteriological (biological) agents and toxins being used as weapons,
Convinced that such use would be repugnant to the conscience of mankind and that no effort should be spared to minimize this risk,
Have agreed as follows: Article I
Each State Party to this Convention undertakes never in any circumstances to develop, produce, stockpile or otherwise acquire or retain:
(1) microbial or other biological agents, or toxins whatever their origin or method of production, of types and in quantities that have no justification for prophylactic, protective or other peaceful purposes;
(2) weapons, equipment or means of delivery designed to use such agents or toxins for hostile purposes or in armed conflict. Article II
Each State Party to this Convention undertakes to destroy, or to divert to peaceful purposes, as soon as possible but not later than nine months after the entry into force of the Convention, all agents, toxins, weapons, equipment and means of delivery specified in Article I of the Convention, which are in its possession or under its jurisdiction or control. In implementing the provisions of this Article all necessary safety precautions shall be observed to protect populations and the environment. Article III
Each State Party to this Convention undertakes not to transfer to any recipient whatsoever, directly or indirectly, and not in any way to assist, encourage, or induce any State, group of States or international organizations to manufacture or otherwise acquire any of the agents, toxins, weapons, equipment or means of delivery specified in Article I of the Convention. Article IV
Each State Party to this Convention shall, in accordance with its constitutional processes, take any necessary measures to prohibit and prevent the development, production, stockpiling, acquisition or retention of the agents, toxins, weapons, equipment and means of delivery specified in Article I of the Convention, within the territory of such State, under its jurisdiction or under its control anywhere. Article V
The States Parties to this Convention undertake to consult one another and to co-operate in solving any problems which may arise in relation to the objective of, or in the application of the provisions of, the Convention. Consultation and co-operation pursuant to this Article may also be undertaken through appropriate international procedures within the framework of the United Nations and in accordance with its Charter. Article VI
(1) Any State Party to this Convention which finds that any other State Party is acting in breach of obligations deriving from the provisions of the Convention may lodge a complaint with the Security Council of the United Nations. Such a complaint should include all possible evidence confirming its validity, as well as a request for its consideration by the Security Council.
(2) Each State Party to this Convention undertakes to co-operate in carrying out any investigation which the Security Council may initiate, in accordance with the provisions of the Charter of the United Nations, on the basis of the complaint received by the Council. The Security Council shall inform the States Parties to the Convention of the results of the investigation. Article VII
Each State Party to this Convention undertakes to provide or support assistance, in accordance with the United Nations Charter, to any Party to the Convention which so requests, if the Security Council decides that such Party has been exposed to danger as a result of violation of the Convention. Article VIII
Nothing in this Convention shall be interpreted as in any way limiting or detracting from the obligations assumed by any State under the Protocol for the Prohibition of the Use in War of Asphyxiating, Poisonous or Other Gases, and of Bacteriological Methods of Warfare, signed at Geneva on 17 June 1925. Article IX
Each State Party to this Convention affirms the recognized objective of effective prohibition of chemical weapons and, to this end, undertakes to continue negotiations in good faith with a view to reaching early agreement on effective measures for the prohibition of their development, production and stockpiling and for their destruction, and on appropriate measures concerning equipment and means of delivery specifically designed for the production or use of chemical agents for weapons purposes. Article X
(1) The States Parties to this Convention undertake to facilitate, and have the right to participate in, the fullest possible exchange of equipment, materials and scientific and technological information for the use of bacteriological (biological) agents and toxins for peaceful purposes. Parties to the Convention in a position to do so shall also co-operate in contributing individually or together with other States or international organisations to the further development and application of scientific discoveries in the field of bacteriology (biology) for the prevention of disease, or for other peaceful purposes.
(2) This Convention shall be implemented in a manner designed to avoid hampering the economic or technological development of States Parties to the Convention or international co-operation in the field of peaceful bacteriological (biological) activities, including the international exchange of bacteriological (biological) agents and toxins and equipment for the processing, use or production of bacteriological (biological) agents and toxins for peaceful purposes in accordance with the provisions of the Convention. Article XI
Any State Party may propose amendments to this Convention. Amendments shall enter into force for each State Party accepting the amendments upon their acceptance by a majority of the States Parties to the Convention and thereafter for each remaining State Party on the date of acceptance by it. Article XII
Five years after the entry into force of this Convention, or earlier if it is requested by a majority of Parties to the Convention by submitting a proposal to this effect to the Depository Governments, a conference of States Parties to the Convention shall be held at Geneva, Switzerland, to review the operation of the Convention, with a view to assuring that the purposes of the preamble and the provisions of the Convention, including the provisions concerning negotiations on chemical weapons, are being realized. Such review shall take into account any new scientific and technological developments relevant to the Convention. Article XIII
(1) This Convention shall be of unlimited duration.
(2) Each State Party to this Convention shall in exercising its national sovereignty have the right to withdraw from the Convention if it decides that extraordinary events, related to the subject matter of the Convention, have jeopardized the supreme interests of its country. It shall give notice of such withdrawal to all other States Parties to the Convention and to the United Nations Security Council three months in advance. Such notice shall include a statement of the extraordinary events it regards as having jeopardized its supreme interests. Article XIV
(1) This Convention shall be open to all States for signature. Any State which does not sign the Convention before its entry into force in accordance with paragraph 3 of this Article may accede to it at any time.
(2) This Convention shall be subject to ratification by signatory States. Instruments of ratification and instruments of accession shall be deposited with the Governments of the United Kingdom of Great Britain and Northern Ireland, the Union of Soviet Socialist Republics and the United States of America, which are hereby designated the Depositary Governments.
(3) This Convention shall enter into force after the deposit of instruments of ratification by twenty-two Governments, including the Governments designated as Depositories of the Convention.
(4) For States whose instruments of ratification or accession are deposited subsequent to the entry into force of this Convention, it shall enter into force on the date of the deposit of their instruments of ratification or accession.
(5) The Depository Governments shall promptly inform all signatory and acceding States of the date of each signature, the date of deposit of each instrument of ratification or of accession and the date of the entry into force of this Convention, and of the receipt of other notices.
(6) This Convention shall be registered by the Depository Governments pursuant to Article 102 of the Charter of the United Nations. Article XV This Convention, the English, Russian, French, Spanish and Chinese texts of which are equally authentic, shall be deposited in the archives of the Depositary Governments. Duly certified copies of the Convention shall be transmitted by the Depositary Governments to the Governments of the signatory and acceding States.
Edits. This page was last edited on 15 February 2021, at 20:26. THE AFOREMENTIONED DOCUMENTS ARE STRONG CLUES THAT THE AMERICAN ADMINISTRATION AND BIDENS IN PARTICULAR MAY HAVE VIOLATED THE INTERNATIONAL CONVENTION ON BIOLOGICAL WEAPONS BY COVERT FUNDING OF PATHOGENS CAPABLE OF CAUSING A PANDEMIC AND SHOULD BE REFERRED TO INTERPOL AND THE ICC AND UN SECRETARIAT ON BIOLOGICAL WEAPONS FOR CRIMINAL INVESTIGATION.
I am really excited to be the 2020 CBC Massey Lecturer. It was a great honour to be invited and be among the great authors and thinkers who have inspired me over the years, including MargaretAtwood, Ursula Franklin, Jane Jacobs, Charles Taylor, and so many others.
I had two principal aims in writing RESET: the first was to summarize what I see as an emerging consensus about the many pathologies of social media and the organization of our entire communications ecosystem; the second was to lay out a principled framework for what to do about them.
RESET is published in the United States and Canada with House of Anansi Press, and in the United Kingdom by September Publishing. Thanks to Misha Glenny, Ziya Tong, Marietje Schaake, Cory Doctorow, and Edward Snowden for the very generous reviews!
“No one has done more than Ron Deibert and his lab to expose the enemies of the internet — shadowy companies whose sole business is to make it unsafe for all of us. No one is better placed to explain the intersection of law and technology that makes these abuses possible — and how we can put an end to them. Reset is the definitive narrative of where we went wrong and a last chance to make things right.” — Edward Snowden
“Tech is at a crossroads between oppression and liberation, and Ronald J. Deibert is our leading expert on the forces steering it in either direction. Reset is a road map revealing the secret alleys and byways that brought us to this juncture, and the ways ahead that we could navigate to a better future.” — Cory Doctorow, bestselling author of Radicalized and Walkaway
“One thing is for sure: your phone knows a lot more about you than you know about it. Ronald J. Deibert expertly cracks open our gadgets and electronics to reveal the who, what, and why behind our communications infrastructure. From digital espionage to big-data policing, Reset is a timely and critical look at how cutting-edge surveillance technologies are being weaponized against civil society. With the rise of authoritarianism around the world, Deibert’s book is a must-read for all who want to ensure that dark power stays in check.” — Ziya Tong, science broadcaster and author of The Reality Bubble
“Ronald J. Deibert is a rare hybrid who combines an advanced understanding of computer technology with a rich background in political science. He is also already a legend in security and tech circles because of his work as the founder and director of Citizen Lab . . . In Reset, Deibert outlines with tremendous economy and verve the major threats that face us as a consequence of our rapidly growing dependency on internet technologies, AI, robotics, and, further down the line, machine-to-machine learning and quantum computing. The clarity of his writing enables Deibert to categorize each aspect of the threat on a profound level that will nonetheless be accessible to any reader . . . Covid-19 has made it clear that our globalized world faces fundamental challenges to the survival of our species, along with most others. If we listen to Ron Deibert, we are still in position to head off another of those threats.” — Misha Glenny, bestselling author of McMafia and DarkMarket
“A reset is needed in the relation between privately run technologies and the public interest. Ron Deibert sketches what meaningful change looks like. Ron has been at the heart of analyzing the harms of technology to human rights, and increasingly to the human condition, for decades. His deep research and clear moral compass make his plea for a ‘reset’ an urgent one. To technology experts this book shines a clear light forward beyond current headline-grabbing incidents. To readers new to the depth of effects of the online information ecosystem, it is essential reading to gain clarity on where our values are at stake, and how we may preserve them.” — Marietje Schaake, International Policy Director of the Cyber Policy Center, Stanford University, and President of the CyberPeace Institute
“Reset is a shocking call to action and a persuasively argued book. It is the sort of text one hopes will be read widely … After all, a reset of the basic infrastructure of life will only come through a profound political reckoning — and like the foment of 1968, it may just be a reconceptualization of what we want and why we want it that finally drives change.” — Quill & Quire
Who exactly is Trudeau working for?
He took a Handshake from Klaus Schwab to lead the Great Reset. Did he mention this double role to the House of Parliament and how he proposed to integrate it into Canadian law and policy? I not that he has kept political prisoners in jail for hundreds of days with no charge. Is this part of the Great Reset?
Democracy would be Utopia but for the liars, crooks, bullies, con artists, druggies, plagiar’rs, slanderers, lazy asses, cold hearted lovers, barking dogs and the extinctions and disease they cause by pollution. Then there are the violators of the human rights and charter rights people, in Canada the notwithstanding clause in the constitution and then there is Israel, selling spyware to the worlds despots. Then there is the problem of the majority getting its way all the time pissing on the minority. Yes it could be such a wonderful thing. The trouble with Utopia is us dumb fucks (Zuckerberg-referring to Facebook Users).
Personal Page of Jorma Jyrkkanen, Composer, Author, Researcher 
