This “CoronaVirus" is A Trojan Horse BioWeapon Utilizing 5G - Electromagnetic Switch

what doesn’t kill you…sits inside you waiting to alter and enslave you.

I don't understand this post OP. Could you give me the "for dummies" version? I got very sick in March and still have weird symptoms. My intuition told me at the time that I hadn't caught it from someone, that it had been given to me by design, through what means I don't know. Spraying? 5G frequencies?

Magnetic fields of specific frequency and duration pass through tissue undiminished and without producing harmful thermal effects, motivating their use as a wireless, minimally invasive, virtually undetectable means to control neural activity.

Mechanisms and techniques coupling pulsed magnetic fields (5G) to measure and induce changes in electrochemical potentials across neuronal membranes are being utilized.

The coronaviral genome encodes four major structural proteins: the spike (S) protein, nucleocapsid (N) protein, membrane (M) protein, and the envelope (E) protein, all of which are typically required to produce a structurally complete viral particle.

This is not always the case in all CoVs. It became clear years ago that some CoVs do not require the full ensemble of structural proteins to form a complete, infectious virion. In some CoVs structural proteins are dispensable and these CoVs facilitate encoding of additional proteins with overlapping compensatory functions. This has provided a means for profound manipulation and nanotech integration.

Individually, each protein primarily plays a role in the structure of the virus particle, but they are also involved in other aspects of the replication cycle. The S protein mediates attachment of the virus to the host cell surface receptors and subsequent fusion between the viral and host cell membranes to facilitate viral entry into the host cell. In some CoVs, the expression of S at the cell membrane can also mediate cell-cell fusion between infected and adjacent, uninfected cells.

This formation of giant, multinucleated cells, or syncytia, has been exploited as a strategy to allow direct spreading of the virus between cells, subverting virus-neutralising antibodies and allowing viable packet delivery, integration and remote manipulation.

Biological magnetoreception, incompletely understood, is being tested. You are witnessing a number of test groups and a rather diverse application of specific technologies.

Magnetic properties in materials are target to slected populations to clarify the distinction between biomolecules containing transition metals and ferrite nanoparticles that exhibit significant net moments. You are experiencing the results. Dial adjustment and station hunting of sorts.

Research is being tested on specific populations refining recent developments in the use of magnetic nanomaterials as transducers converting magnetic stimuli to forms readily perceived by neurons for multiplexed and bidirectional control

Altered and aerosolized engineered is a delivery system for a bioweapon which travels synapticaly and intergrates with hosts. Loss of olfactory sense indicates a high viral load and typically indicates encephalitic presence.

There exist a variety of magnetic field conditions and mechanisms by which viral nanotechnology can be coupled to neuronal signaling cascades facilitating an interchange between magnetism physics and neurobiology.

Horrors beyond your imagination have been weaponized. And I do realize this sounds absolutely insane.

Most won’t bother to read this.

This research was published in 2010. Ten years ago.

[link to www.ncbi.nlm.nih.gov (secure)]

By the time the few left realize what is happening, it will be too late.

the presence of targeting ligands can greatly enhance the retention and cellular uptake of nanoparticles via receptor-mediated endocytosis—even although tumor accumulation is largely determined by the physicochemical properties of nanoparticles.16,17 This can then lead to higher intracellular drug concentration and increase therapeutic activity, which is particularly important for bioactive macromolecules (e.g. DNA and siRNA) that require intracellular delivery for bioactivity.16 In the case of endothelial targeting for cardiovascular diseases or immunological tissue targeting, nanoparticle localization is guided by ligand-receptor interactions rather than EPR.18 Similarly, ligand-mediated targeting is of importance for the transcytosis of nanodrugs across tight epithelial and endothelial barriers (e.g. blood-brain barrier).19 Additionally, targeted delivery has been applied, in some instances, to combat multidrug resistance (MDR).3

What are the “ELITE” taking to protect themselves and prevent neurological damage? Ask yourself why you haven’t heard about Memantine?

Novel treatment with neuroprotective and antiviral properties against a neuroinvasive human respiratory virus
Elodie Brison 1 , Hélène Jacomy, Marc Desforges, Pierre J Talbot Affiliations
PMID: 24227863 PMCID: PMC3911624 DOI: 10.1128/JVI.02972-13
Abstract


Human coronaviruses (HCoVs) are recognized respiratory pathogens with neuroinvasive and neurotropic properties in mice and humans. HCoV strain OC43 (HCoV-OC43) can infect and persist in human neural cells and activate neuroinflammatory and neurodegenerative mechanisms, suggesting that it could be involved in neurological disease of unknown etiology in humans. Moreover, we have shown that HCoV-OC43 is neurovirulent in susceptible mice, causing encephalitis, and that a viral mutant with a single point mutation in the viral surface spike (S) protein induces a paralytic disease that involves glutamate excitotoxicity in susceptible mice. Herein, we show that glutamate recycling via the glial transporter 1 protein transporter and glutamine synthetase are central to the dysregulation of glutamate homeostasis and development of motor dysfunctions and paralytic disease in HCoV-OC43-infected mice. Moreover, memantine, an N-methyl-d-aspartate receptor antagonist widely used in the treatment of neurological diseases in humans, improved clinical scores related to paralytic disease and motor disabilities by partially restoring the physiological neurofilament phosphorylation state in virus-infected mice. Interestingly, memantine attenuated mortality rates and body weight loss and reduced HCoV-OC43 replication in the central nervous system in a dose-dependent manner.

This novel action of memantine on viral replication strongly suggests that it could be used as an antiviral agent to directly limit viral replication while improving neurological symptoms in various neurological diseases with a viral involvement.


Mutations in the surface spike (S) protein of human respiratory coronavirus OC43 appear after persistent infection of human cells of the central nervous system, a possible viral adaptation to this environment. Furthermore, a single amino acid change in the viral S protein modulated virus-induced neuropathology in mice from an encephalitis to a neuropathology characterized by flaccid paralysis, which involves glutamate excitotoxicity. We now show that memantine, a drug that is used for alleviating symptoms associated with neuropathology, such as Alzheimer's disease, can partially restore the physiological state of infected mice by limiting both neurodegeneration and viral replication. This suggests that memantine could be used as an antiviral agent while improving neurological symptoms in various neurological diseases with a viral involvement.

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Ive had it. Ive been saying for a while now corona is a 5g.enabled nano weapon

Open your eyes. What do you see?

Think about what is happening. Remember the videos of people dying on the streets in China, being locked in boxes, aerosolized disinfectant being sprayed in the streets? The first testing?

Reading and thinking is required to understand what is going on.

LINKS

did my best.

good luck.

Here are a few to get you started.


Magnetic nanoparticles for gene and drug delivery

[link to www.ncbi.nlm.nih.gov (secure)]

Design and Evaluation of Three-Dimensional Electromagnetic Guide System for Magnetic Drug Delivery

[link to www.researchgate.net (secure)]

Can Pulsed Electromagnetic Fields Trigger On-Demand Drug Release from High-Tm Magnetoliposomes?

[link to www.ncbi.nlm.nih.gov (secure)]

Online archives will provide clues. You want Darpa, DTIC servers? GTFO

Dual-Surface-Modified Bacteriophage MS2 as an Ideal Scaffold for a Viral Capsid-Based Drug Delivery System

[link to pubs.acs.org (secure)]

Nanomedicine: Silence the target

[link to pubmed.ncbi.nlm.nih.gov (secure)]

The potential of magneto-electric nanocarriers for drug delivery

[link to pubmed.ncbi.nlm.nih.gov (secure)]

Magnetic forces enable controlled drug delivery by disrupting endothelial cell-cell junctions

[link to www.nature.com (secure)]

Action at a Distance: Functional Drug Delivery Using Electromagnetic-Field-Responsive Polypyrrole Nanowires

[link to pubs.acs.org (secure)]

GLP TARDS RIDE!

A chitosan hydrogel-based cancer drug delivery system exhibits synergistic antitumor effects by combining with a vaccinia viral vaccine

[link to www.sciencedirect.com (secure)]

Current Progress of Virus-mimicking Nanocarriers for Drug Delivery

[link to www.ncbi.nlm.nih.gov (secure)]

[DDS Nanocarriers Mimicking Early Infection Machinery of Viruses]

[link to pubmed.ncbi.nlm.nih.gov (secure)]

i think the vaccine is going to implant a kill switch . hell this test swabs could have something.

Your GENOME on Sars-CoV-2 - Targeted Genetic Manipulation Will Capabilities

Epigenetic Landscape during Coronavirus Infection

Pathogens. 2017 Mar; 6(1): 8.
Published online 2017 Feb 15. doi: 10.3390/pathogens6010008
PMCID: PMC5371896
PMID: 28212305
Epigenetic Landscape during Coronavirus Infection
Alexandra Schäfer and Ralph S. Baric*
Lawrence S. Young, Academic Editor
Author information Article notes Copyright and License information Disclaimer
Department of Epidemiology, University of North Carolina, Chapel Hill, NC 27599, USA; ude.cnu.liame@efeahcsa
*Correspondence: ude.cnu.liame@cirabr


Coronaviruses (CoV) comprise a large group of emerging human and animal pathogens, including the highly pathogenic severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) strains.

The molecular mechanisms regulating emerging coronavirus pathogenesis are complex and include virus–host interactions associated with entry, replication, egress and innate immune control. Epigenetics research investigates the genetic and non-genetic factors that regulate phenotypic variation, usually caused by external and environmental factors that alter host expression patterns and performance without any change in the underlying genotype.

Epigenetic modifications, such as histone modifications, DNA methylation, chromatin remodeling, and non-coding RNAs, function as important regulators that remodel host chromatin, altering host expression patterns and networks in a highly flexible manner. For most of the past two and a half decades, research has focused on the molecular mechanisms by which RNA viruses antagonize the signaling and sensing components that regulate induction of the host innate immune and antiviral defense programs upon infection. More recently, a growing body of evidence supports the hypothesis that viruses, even lytic RNA viruses that replicate in the cytoplasm, have developed intricate, highly evolved, and well-coordinated processes that are designed to regulate the host epigenome, and control host innate immune antiviral defense processes, thereby promoting robust virus replication and pathogenesis.

In this article, we discuss the strategies that are used to evaluate the mechanisms by which viruses regulate the host epigenome, especially focusing on highly pathogenic respiratory RNA virus infections as a model. By combining measures of epigenome reorganization with RNA and proteomic datasets, we articulate a spatial-temporal data integration approach to identify regulatory genomic clusters and regions that play a crucial role in the host’s innate immune response, thereby defining a new viral antagonism mechanism following emerging coronavirus infection.

Potential COVID-19 Vaccine Utilizes Epigentic Alteration

As COVID-19 is proving to the world, viruses are powerful biological agents, capable of rapidly effecting massive damage and fatality. And yet, they’re so simple: a virus is merely comprised of pieces of genetic material—either RNA or DNA—wrapped in a protein envelope, which is known as a “capsid.”

But coronaviruses are not the only type of virus out there, nor the only one capable of heavy destruction. Human metapneumovirus (HMPV) was officially discovered in 2001, although evidence points to its existence dating back to at least fifty years prior. HMPV is known to be the second leading cause of respiratory infections. It can prove fatal, particularly to very young children or elderly people.

HMPV has persisted as a threat, year after year, and yet researchers had not found a way to target it for vaccine development—until now. Jianrong Li, a senior author on the latest HMPV study to be published, and a virology professor at The Ohio State University Department of Veterinary Biosciences as well as a member of Ohio State’s Infectious Diseases Institute, leads a lab that studies HMPV.

Roughly aware of an epigenetic change known as N6-methyladenosine modification (also known as m6A methylation) that can be seen in RNA, Li and his team wanted to see if HMPV has this modification, and how it drives the virus’ effects.

How was the methylation studied and its effects characterized?

Using high-throughput sequencing, Li scanned the virus’ genes and identified which one contains the greatest extent of m6A methylation before then knocking out these modifications to make a mutant virus. Looking at how these mutant viruses performed would shed light on the impact of m6A methylation.

When human cells were exposed to the knock-out virus, they produced an antiviral protein known as type I interferon that pointed to the activation of the innate immune response, or the somewhat generalized response that the body has to a foreign pathogen. According to Li, “This opened up a big question. Why would a virus lacking this methylation produce a much higher innate immune response?”

Upon reviewing the cellular signaling pathways involved, it became evident that m6A methylation makes the virus able to hide from the immune system by masking the RNA so that it didn’t stand out as being different than the host RNA. The immune system therefore doesn’t recognize the virus as being non-self RNA, and so it doesn’t summon the innate immune response—meaning that the virus is able to persist, undetected.

It’s possible that other viruses use this same methylation trick to escape recognition; that will have to be further characterized. But, in the meantime, how could this discovery be used to develop something that could reduce the number of HMPV infections?

SEE ALSO: DNA Methylation and ‘Bad Karma’ To Blame for Oil Palm Trees' Useless Fruit
Anti-HMPV vaccine potential looks promising

Li and his team used cotton rats as their experimental model to see if targeting the m6A methylation could lead to a vaccine. One group of rats was given a placebo, while the other rats was given the mutant virus. The latter not only had an innate immune response, but also produced the sort of pathogen-specific adaptive immune response that would protect them specifically from HMPV. The rats had total protection from the virus throughout their respiratory tract.

“In the case of cotton rats, the mutant virus produced a higher amount of type I interferon, and triggered a higher antibody response and a higher T-cell immune response. That means you’ve triggered higher protective ability against the virus infection. So mutating the virus enhances vaccine efficacy,” Li noted. “That is exactly what we want.”

What’s next?

Not only do Li’s team’s findings point toward a potential target (the methylation modification) that can be leveraged in the development of a specifically anti-HMPV vaccine, but it also opens the door for vaccine development against other viruses.

HPMV is actually part of the same family of viruses as respiratory syncytial virus (RSV), which is the number one cause of respiratory infections. “This [HPMV finding] is exciting because RSV was discovered in 1953, but we still don’t have a vaccine,” said Li.

And so, aside from the steps needed to further develop and validate an anti-HMPV vaccine, Li’s research findings can be applied to other viruses—like RSV—in hopes of developing effective vaccines.

Source: Li J. et al. (20

Targeted Viral Epigentic Alteration Potential

Tet family members have been shown to be important for many biological processes including activity-regulated neuronal gene expression, synaptic transmission and scaling, as well as memory formation and extinction (Feng et al., 2015; Kaas et al., 2013; Rudenko et al., 2013; Yu et al., 2015). One very recent study showed increased 5hmC levels upon axotomy of adult DRG neurons (Loh et al., 2016). However, little is known about the function of DNA methylation in axon regeneration (Iskandar et al., 2010; Puttagunta et al., 2014). The identification of active DNA demethylation machinery provides an entry point to test the hypothesis that DNA demethylation serves as a fundamental mechanism to globally reprogram the cellular state of mature mammalian neurons to permit axonal regeneration.

Published in final edited form as:
Neuron. 2017 April 19; 94(2): 337–346.e6. doi:10.1016/j.neuron.2017.03.034.

An intrinsic epigenetic barrier for functional axon regeneration

Yi-Lan Weng#1,2, Ran An#1,2,3, Jessica Cassin#1,4, Jessica Joseph1,5, Ruifa Mi2, Chen Wang6, Chun Zhong1,2, Seung-Gi Jin7, Gerd P. Pfeifer7, Alfonso Bellacosa8, Xinzhong Dong9, Ahmet Hoke2, Zhigang He6, Hongjun Song1,2,4,5,9,10,#, and Guo-li Ming1,2,5,9,10,11,# 1Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
2Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
3Department of Neurology, Huashan Hospital, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200040, China
4Pre-doctoral Human Genetics Training Program, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
5Graduate Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
6F.M. Kirby Neurobiology Center, Boston Children's Hospital, and Department of Neurology, 300 Longwood Avenue, Boston, MA 02115, USA
7Center for Epigenetics, Van Andel Research Institute, Grand Rapids, MI 49503, USA
8Cancer Epigenetics and Cancer Biology Programs, Fox Chase Cancer Center, Philadelphia, PA 19111, USA
9The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
10Department of Neuroscience, Mahoney Institute for Neurosciences, Perelman School for Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
11Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA

"ALL YOUR DNA ARE BELONG TO US"

It is becoming well established that many DNA viruses, and to some lesser extent RNA viruses, have evolved functions that antagonize the regulatory machine of the host epigenome, leading to regulated changes

EPIGENETIC CHANGES ARE BEING TARGETED. THESE GENETIC CHANGES HAVE PROFOUND LONG AND SHORT TERM CONSEQUENCES. YOUR GENOME IS BEING ALTERED.

You dark ages part 2 fuckers are gonna get us all killed. Fuck your conspiracies

THIS IS HUGE!!!

Googled "E. Boyden” as OP suggested. EPSTEIN CONNECTION!!! AND A WHITE PAPER INDICATING RESEARCHING A VIRUS FOR GENETICALLY-TARGETED OPTICAL CONTROL OF NEURAL ACTIVITY IN 2009?

"Millisecond-timescale, genetically-targeted optical control of neural activity” Seriously! WTF!


"Epstein’s last recorded visit to the Media Lab campus, according to the report, was in April 2017, when he met with Ito, professor of biological engineering Ed Boyden”

[link to www.wired.com (secure)]

Boyden is a professor of Synthetic Neurobiology at MIT!


[link to www.media.mit.edu (secure)]



From back in 2006-2009, Synthetic Neurobiology Group, MIT Media Lab/BCS/BE, MIT.

"NOTE: This white paper describes how to make high-titer lentivirus appropriate for use in vivo in the mouse, rat, or monkey brain, as well as other species. The virus works well in cortex, striatum, and many other brain regions, yielding very high infectivity levels (~80%-90% or greater, in mouse brain). With a glial promoter, it also works on glia. It was compiled by Xue Han, Xiaofeng Qian, Mingjie Li, Patrick Stern, and Ed Boyden, as an expanded version of what is found in the paper:

Han, X., Qian, X., Bernstein, J.G., Zhou, H.-H., Talei Franzesi, G., Stern, P., Bronson, R.T., Graybiel, A.M., Desimone, R., and Boyden, E.S. (2009) Millisecond-Timescale Optical Control of Neural Dynamics in the Nonhuman Primate Brain, Neuron 62(2): 191-198. ‘

It is derived from the original protocol used in

Boyden, E. S., Zhang, F., Bamberg, E., Nagel, G., Deisseroth, K. (2005) Millisecond-timescale, genetically-targeted optical control of neural activity, Nature Neuroscience 8(9):1263-1268.

Synthetic Neurobiology Memo #2 (2009) Lentivirus production for high-titer, cell-specific, in vivo neural labeling. Online.

[link to syntheticneurobiology.org (secure)]

The Epstein connection to Ed Boyden is insane.

Are the same people behind Epstein also behind the viral bioweapon and destruction of America?

Epstein Scandal from wikipedia

Edward Boyden was one of several scientists at the infamous MIT Media Lab who met with convicted sex offender Jeffrey Epstein to aggressively seek financial support

Boyden also visited Epstein's personal residence on multiple occasions, although Boyden's open letter published by MIT states this was for purely research purposes..



PURELY RESEARCH PURPOSES?

You don’t think the shadow behind Epstein could be behind all of this? Boyden? Lieber? WuHan? Virus? Reading this all has me wanting to bring my tomato plants inside.

Bump for thoughts. Interesting. I need time to read all of this.

Charles Lieber and Edward Boyden both won the NIH Director’s Pioneer Award.

I’m confused. When he was arrested the media said Lieber was a chemist doing work on battery technology.

The NIH Director’s Pioneer Award supports individual scientists of exceptional creativity who propose highly innovative and potentially transformative approaches to major challenges in the biomedical or behavioral sciences towards the goal of enhancing human health. Applications from individuals with diverse backgrounds and in any topic relevant to the broad mission of NIH are welcome. To be considered pioneering, the proposed research must reflect substantially different scientific directions from those already being pursued in the investigator’s research program or elsewhere. The NIH Director’s Pioneer Award is a component of the High-Risk, High-Reward Research program of the NIH Common Fund.

SYRINGE-INJECTABLE MESH ELECTRONICS FOR SEAMLESS INTEGRATION WITH THE CENTRAL NERVOUS SYSTEM

[link to projectreporter.nih.gov (secure)]

Liner is connected to Neurolink too. “The High-Risk, High-Reward” Research program of the NIH Common Fund.