Documentary Proof: University of North Carolina Generated COVID-19

Update:  VT has been tracking COVID stats and disinformation/censorship since day one.  Now, in light of the Beirut attack (Trump backs us up), we now view the release of a hybridized version of COVID 19 on the New York metropolitan area as a terror attack.

Stats on hospitalization and deaths there have been altered/censored which prove this was a biological attack.  Death rates were many times higher than elsewhere and even target specifically the Jewish population, something Israel has done before.

We have watched Google Corporation manipulation of the internet, we have tracked them and find clear and absolute evidence that ties those who executed the Beirut attack to those who released COVID 19 on the US and the world.

We have also watched Facebook, Google/YouTube and Twitter censored Beirut videos and coordinate with MSM to sell a fake narrative involving unexplodable fertilizer while evidence mounts of a massive not only attack by Israel but a brilliant set of feints also, drones, planes and even a missile.

Who knows, a nuke could have been loaded there with ease right off a truck and no one would notice.

Now with Beirut in shambles, the UAE joining Greater Israel and the Qanon monstrosity selling a police state to the rabble, the inexplicable becomes clear.

Below, we prove the creation of COVID, a CIA project done through a cover program at a private university using bioweapons experts.  Now we see it released, the target?  Looting the US economy, bringing America to civil war and allowing power to centralize under Kosher Nostra control without the subterfuge, now unnecessary.

This article contains hard proof that cannot be questioned or denied, which you may submit to any government agency or healthcare professional.

What is not yet proven but coming into focus is that the US biological weapons program at Fort Detrick, Maryland, equipment and certainly key staff, certainly migrated to secret labs at large state universities in order to “hide in plain sight.”

Follow the careers, all links are included, of those who worked on the Wuhan-COVID project in 2017.

Also, note that the exact same personnel and equipment is used for fake “prevention” research and testing as weaponization and actual production.

Since this article was written, we have begun to look at worldwide operations of US nuclear/bio/chem contractor, Kushner-Trump favorite, Battelle, and their secret labs around the world.

When we began, our people started to be threatened.  That was a serious mistake.

Submit this paper to any physician, or other qualified bio-sciences specialist.  See what they say.

https://www.veteranstoday.com/wp-content/uploads/2020/03/ScreenHunter-437-320x213.png 320w, https://www.veteranstoday.com/wp-content/uploads/2020/03/ScreenHunt... 640w, https://www.veteranstoday.com/wp-content/uploads/2020/03/ScreenHunt... 768w" sizes="(max-width: 864px) 100vw, 864px" />

TO SHARE THIS ARTICLE ON FACEBOOK, PLEASE COPY and PASTE this link:  https://www.veteranstodaynetwork.com/2020/04/29/documentary-proof-u...

Introduction

Documents below will show that research to create COVID 19 began in the United States in 2006 and culminated in a successful bio-weapon in 2015, with work done at the University of North Carolina and at Harvard and at the Food and Drug Administration’s lab in Arkansas.

Their work was titled:

A SARS-like cluster of circulating bat coronaviruses shows potential for human emergence

They did this and more, so much more as you will read below.

As Trump said, over and over and over, the Chinese were involved.

Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, China supplied the Wuhan Bat Virus which was used in the American study.  Their name was included for that reason only.

COVID 19 was a US Army bio-weapons project to manufacture a pneumonia-causing disease that would be nearly impossible to vaccinate for in patients over 40 years old.

The proof is here, simply scroll down.  The study was run by the University of North Carolina and funded by USAID/CIA.  It chose a Chinese bat virus and chose to include a medical facility in Wuhan as well.

Now we know why, a smokescreen of the blame for a program China had little or nothing to do with, something satanically evil and purely American.

In November 2015, a study was published outlining the capability of producing the virus we are dealing with now.  Among the many involved was a lab in Wuhan, China.  It was listed from the beginning as one of the dozens, mostly American, working on this project.

However, one key participant was left out, USAID.  It is suspected, deeply so, that USAID is a front for American bio-warfare research such as that done in Tbilisi, Georgia, and elsewhere, much documented.  This is the citation that adds USAID to the research funding group.

Change history

Similarly, when Forbes Magazine and others stated they could prove COVID 19 was made naturally, and of course they had the same access we have, we suspect that they are part of a disinformation effort tied to USAID and bio-warfare.

Suspicion is not proof.  The proof is proof and there is proof enough to drown in.  Our thanks to the American medical professionals who pimped themselves out to the US Army and CIA and who helped bring us where we are now, a nation broken to pieces.

Pravda.Ru: Such material appeared in 2015 on the website of the scientific journal Natura in 2015. Then the authors claimed that after the advent of the SARS virus (2002-2003) and the Middle East respiratory syndrome (MERS), scientists were aware of the risk of interspecific transmission that would lead to an epidemic among people.

Successful lab experiment

Among other things, the research team studied bats, which are the largest incubators of coronaviruses. Nevertheless, bats could not transmit the coronavirus to humans because they could not interact with human cells with ACE2 receptors.

The material also stated that horseshoe bats carry a strain of SARS coronavirus that can be transmitted to humans. It has been named the SHC014-CoV virus.

To better study this virus, scientists copied the coronavirus and infected it with laboratory mice. The results showed that the virus is really able to bind to human cells with ACE2 receptors and multiply in the cells of the respiratory system.

In the research work, it is noted that laboratory materials, samples and equipment that were used in the research were obtained from the Army Medical Research Institute of Infectious Diseases. Although it is not yet possible to say for sure that the virus that was tested in laboratory mice is the same as the SARS-Cove-2 coronavirus.

NATO policy

However, interesting things can be found in earlier documents. 

For example:

• The 2019 Alliance’s activity report says that in 2019, the Alliance’s first place in research and development was occupied by the topic of radiochemical and biological protection (29%), shifting the seemingly most pressing problem of Europe – counterterrorism (it turned out to be 4- m priority).
• A year earlier, in 2018, the situation was exactly the opposite: terrorism, as it should be, was in the first place (28%), and radiochemical and biological protection in the fourth (13%).

As the Brussels snitch writes in the telegram channel, “given the absence of visible reasons for such a sharp change in scientific interests, there are two options and both are unpleasant:

• or NATO now wags the fifth point, falsifying the data to show “and we always prepared for viruses, we are modern”,
• or even in 2019 in the alliance, God forgive me, they knew where the trouble would come from.

Yes, the first option is much more real, but, you see, the facts are surprising.

Source:  Pravda

https://www.veteranstoday.com/wp-content/uploads/2020/01/coronavirus2-320x180.jpg 320w, https://www.veteranstoday.com/wp-content/uploads/2020/01/coronaviru... 640w, https://www.veteranstoday.com/wp-content/uploads/2020/01/coronaviru... 768w" sizes="(max-width: 1200px) 100vw, 1200px" />Original 2015 Research Unedited and Complete

Published: 09 November 2015A SARS-like cluster of circulating bat coronaviruses shows potentia... by Vineet D Menachery, Boyd L Yount Jr, Kari Debbink, Sudhakar Agnihothram, Lisa E Gralinski, Jessica A Plante, Rachel L Graham, Trevor Scobey, Xing-Yi Ge, Eric F Donaldson, Scott H Randell, Antonio Lanzavecchia, Wayne A Marasco, Zhengli-Li Shi, Ralph S Baric

Nature Medicine volume 21, pages1508–1513 (2015)

A Corrigendum to this article was published on 06 April 2016

This article has been updated

Abstract

The emergence of severe acute respiratory syndrome coronavirus (SARS-CoV) and the 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 approach 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.

Main

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 impact^3,4. 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 threat^1,6.

However, sequence data alone provides minimal insights to identify and prepare for future pre-pandemic 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 binding^7,8, 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). Similar 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.

Figure 1: 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 the 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.

Full size image

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.