Menachery et al. shows us (in a 2015 paper) COVID virus was developed in the US, let me say again, NIH & NIAID, UNC Chapel Hill etc., in US; pay attention to University of North Carolina Chapel Hill

by Paul Alexander

See this paper: "SARS-like WIV1-CoV poised for human emergence" by Menachery et al. and published March 2016; this paper with the 2015 publication tells us that these malfeasants created this; why?

Why? Like for the mRNA technology gene injection, why develop this, these chimera deadly coronaviruses?

Was this developed in a lab? Yes. US lab, likely. This one paper, and their 2015 ‘NATURE’ paper, shows clearly that COVID virus was developed in collaboration between U.S. and Chinese researchers (main funding by US) and this collaboration played a key role in creating SARS-CoV-2.

In the NATURE paper below Menachery et al. describe exactly how they created the chimeric deadly COVID like virus.

‘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.

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.’


Fauci, Francis Collins central? Yes.

Was it a leak or release? I say release. Intentional or accidental? Well, that is the key issue and I say either, yet still saying accidental but also I would say that if it is shown deliberate, then we would be saying someone deliberately released this from a lab.

Deliberate? Yes, potentially yes.

Why? To damage the US and Trump. This was used to remove a sitting POTUS.

This article is critical and Dr. Martin and I discuss it here and I praise him. Dr. David Martin deserves huge praise for his scholarship and relentless work and teeing us up.

Title: SARS-like WIV1-CoV poised for human emergence

Pay attention to the title. It was received for journal peer review in 2015, then it is very likely this research was going on in 2014 and maybe, even earlier.

This sentence is important:

‘The results indicate that viruses using WIV (Wuhan Institute of Virology) 1-CoV spike are poised to emerge in human populations due to efficient replication in primary human airway epithelial cell cultures.’

These sentences are also important:

‘Using the SARS-CoV infectious clone as a template (7), we (Chapel Hill, NIH etc.) designed and synthesized a full-length infectious clone of WIV1-CoV consisting of six plasmids that could be enzymatically cut, ligated together, and electroporated into cells to rescue replication competent progeny virions’

Do you understand the implications of this above sentence?

So is this sentence:

‘In addition to the full-length clone, we also produced WIV1-CoV chimeric virus that replaced the SARS spike with the WIV1spike within the mouse-adapted backbone’

These last 2 sentences show us, tells us that they created the very same coronavirus that killed us. Yes, they did this. Key is this is the US e.g. NIH, NIAID, Chapel Hill etc. You may not want to hear it but yes, it is very likely based on this, that this was done in a lab (100%), released (leans to either accident or intent yet more intent) and US led. It was built and configured within America.

Now read this paragraph in the paper:

‘Next, we wanted to determine WIV-CoV replication potential in models of the hu-man lung. Previous examination of WIV1-CoV recovered from bat samples demonstrated poor replication in A549 cells (5); however, replication of epidemic SARS-CoV is also poor in this cell type, potentially due to ACE2 expression levels (9).Therefore, well-differentiated primary human airway epithelial cell (HAE) air–liquid interface cultures were infected with WIV1-MA15, WIV1-CoV, SARS-CoV Urbani, or SARS-CoV MA15. At24 and 48 h post infection, both WIV1-MA15 and WIV1-CoVproduce robust infection in HAE cultures equivalent to the epi-demic strain and mouse-adapted strains’

Now see this sentence:

‘To extend analysis to pathogenesis, we next evaluated in vivo infection following WIV1-MA15 and WIV1-CoV challenge. Initial studies compared WIV1-MA15 to mouse-adapted SARS-CoV (MA15) to determine spike-dependent pathogenesis.’

See these 2 paragraphs and declarations:

‘Biosafety and Biosecurity.

Reported studies were initiated after the Universityof North Carolina Institutional Biosafety Committee approved the experi-mental protocol: project title: Generating infectious clones of Bat SARS-likeCoVs; lab safety plan ID: 20145741; schedule G ID: 12279. These studies wereinitiated before the US Government Deliberative Process Research FundingPause on Selected Gain of Function Research Involving Influenza, MERS, andSARS Viruses (,and the current paper has been reviewed by the funding agency, the Na-tional Institutes of Health (NIH). Continuation of these studies has been requested and approved by the NIH.


We thank Dr. Zhengli-Li Shi of the Wuhan Institute of Virology for access to bat CoV sequences and plasmid of WIV1-CoV spike protein. Research was supported by the National Institute of Allergy and Infectious Disease and the National Institute of Aging of the NIH under Awards U19AI109761 and U19AI107810 (to R.S.B.), AI1085524 (to W.A.M.),and F32AI102561 and K99AG049092 (to V.D.M.). Human airway epithelial cell cultures were supported by the National Institute of Diabetes and Digestive and Kidney Disease under Award NIH DK065988 (to S.H.R.). Support for the generation of the mice expressing human ACE2 was provided by NIH Grants AI076159 and AI079521 (to A.C.S.).’

This as Dr. Martin says, is a public admission. Public admission, of crimes.


‘Outbreaks from zoonotic sources represent a threat to both human disease as well as the global economy. Despite a wealth of metagenomics studies, methods to leverage these datasets to identify future threats are underdeveloped. In this study, we describe an approach that combines existing metagenomics data with reverse genetics to engineer reagents to evaluate emergence and pathogenic potential of circulating zoonotic viruses. Focusing on the severe acute respiratory syndrome (SARS)-like viruses, the results indicate that the WIV1-coronavirus (CoV) cluster has the ability to directly infect and may undergo limited transmission in human populations. However, in vivo attenuation suggests additional adaptation is required for epidemic disease. Importantly, available SARS monoclonal antibodies offered success in limiting viral infection absent from available vaccine approaches. Together, the data highlight the utility of a platform to identify and prioritize pre-pandemic strains harbored in animal reservoirs and document the threat posed by WIV1-CoV for emergence in human populations.’

See where the authors are attached to:

a Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; b Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; c Division of Microbiology, National Center for Toxicological Research, Food and Drug Administration, Jefferson, AR 72079; d Department of Cell Biology and Physiology and Marsico Lung Institute/Cystic Fibrosis Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599; e Institute for Research in Biomedicine, Bellinzona, Switzerland; f Institute of Microbiology, Eidgenössische Technische Hochschule Zurich, Zurich, Switzerland; g Humabs BioMed SA, Bellinzona, Switzerland; and h Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute–Department of Medicine, Harvard Medical School, Boston MA 02215