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The Protein Sequence of Covid-19 Prevents Vaccinations

The Protein Sequence of Covid-19 Prevents Vaccinations

by Eugene Passofaro -
Number of replies: 2

The article below was originally published on May 1 2020, but it points out the power of mutation in the Covid-19 virus so we have republished it.


Below is an excerpt from a scientific lab report, you can read the entire article here.  At the bottom is underlined text where it is clearly stated that 'any variation' in the RNA" will render a treatment ineffective, plus the virus creates mutation paths of replicating proteins each of which has to be treated, but the problem being, the virus creates 'parallel routes' and testing shows more than one mechanism of their creation.  This makes any specific vaccine to be extremely difficult to synthesise accurately given the internal robust capacity for bio mutations and in effectiveness one would have to say it must be relatively small.   

1.5. Human protein targets for design of therapeutics against COVID-19

The immune system by its nature can make its own adjustments to recognize pathogens and vaccines, but designing some kind of therapeutic antagonist against virus binding to the lung cells requires rather more consideration about what human protein the spike protein is binding. Bioinformatics as the study of biosequences is a powerful tool, but it is well known that having the detailed three dimensional structure of the human protein target for a potential new pharmaceutical agent, or to which a virus attaches, is a great benefit to rational computer-aided design. Studies specifically investigating human protein binding and activation of previously known SARS viruses have for some years been carried out by several groups (e.g. Refs. [[54][55][56][57]]). It seems reasonably well agreed that angiotensin converting enzyme type 2 (ACE2) is responsible for binding the SARS associated with the 2002 outbreak, combined with a proteolytic cleavage to activate the spike protein, for which type II transmembrane serine protease (TMPRSS2) is the current popular candidate [3]. Several three dimensional structures are known for ACE2 complexed with SARS spike protein e.g. protein data bank (PDB) entry (6ACG) and of variants of the latter (e.g. TMPRSS2 protein data bank entry 2OQ5).

However, the full story involving human cell surface proteins (with which SARS-CoV-2 interacts in order to infect and replicate) is possibly not quite as firmly established at the time of this present study as some summaries would suggest. The origin of the general problem for a more detailed conformational chemistry approach is that diversity of genome and means of infecting cells are readily generated in nature in the case of different virus hosts, virus strains, and species jumps, and it is long established that the binding shows variation in the receptors used that correspond to viral groups. There have been alternative proposed candidates for initial binding receptors, e.g. carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), and various dipeptidyl peptidases. Highly virulent coronaviruses that form syncytia between cells can even spread in a receptor-independent fashion. Even when an initial binding receptor such as ACE2 is identified for a coronavirus, initial uncertainty or enduring complexity for the rest of the entry process may be the norm. Many other human proteases present in the lung seem capable of cleaving various sites on the spike protein and which could cause its activation. For example, a variety of proteases such as trypsin, tryptase Clara, mini-plasmin, human airway trypsin-like protease (HAT), and TMPRSS2 (transmembrane protease, serine 2) are known to cleave the glycoprotein hemagglutinin (HA) of influenza A viruses as prerequisite for the fusion between viral and host cell membranes and viral cell entry. Human airway trypsin like protease (HAT), TMPRSS3, TMPRSS4, TMPRSS6 have also all been considered by SARS researchers at various stages. Other human proteins that might have similar involvement to the above in the SARS-CoV-2 case, and that are also affected by the same antagonists against the SARS-Cov-2 targets in the preceding paragraph, have also attracted the attention of researchers. The trypsin-like serine protease hepsin which has a fairly broad action and which is significantly inhibited by a diverse set of ligands, a particular example of one such binding is represented by protein data bank entry 5ce1. Even intracellular proteases could be released on cell damage resulting from the first wave of lung infection or from other disease or tissue trauma. Some variants and strains may use other, as yet unknown, proteins, or sugars, to assist entry. It is also plausible the spike protein might be activated by other proteases on exit from the epithelial lung cells, so allowing it efficiently to infect other cells. The spike glycoprotein of SARS-CoV-2 also has the so-called furin cleavage sequence (PRRARS or PRRARS), which is an extension to the so-called PIGAG motif of ref [3]. Consistent with the present author's preferred choice of KRSFIEDLLFNKV motif, coronaviruses with high sequence homology (such as that isolated from a bat in Yunnan in 2013), lack the furin cleavage sequence. Nonetheless, because furin proteases are abundant in the respiratory tract, SARS-CoV-2 spike glycoprotein might be cleaved on exit from cells.

Even if the means of binding, activation and entry is well established for a viral strain, recall that a single RNA base difference resulting in a single amino acid residue difference could alter all that, and there also appear to be several other possibilities that the virus can exploit in parallel. Indeed, somewhat similarly, potential inhibitors of SARS entry and/or activation proposed by researchers  may work by several routes in parallel, and significantly at least three mechanisms were reported in one relevant study .


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Re: The Protein Sequence of Covid-19 Prevents Vaccinations

by Eugene Passofaro -
But you can see the problem is ........which one?

whichever one the vaccine blocks has to account for - a mutation (up to 50 so far tested) - or a parallel protein chain (so far three have been discovered) - a mechanism that can make three more protein chains from each residue of protein (dust or ash). Now one can ask as the researchers are asking; whoever did this, were they actually caught in the middle of making it? Why? Because the researchers have noted some chains are now becoming active.

What does this mean? Some researchers believe the experiments were in the middle stages, i.e. it not finished, as it is mutating and mutating as if it needed the organisms to work in i.e. the whole of humanity. And if that is true, one can ask:  Where will it stop? and What is true?  If it is not finished then, is it justin its beginning stages?  And how far will it go?

And there maybe someone who knows the answers, the one who made the virus!  The Nobel Prize Winning HIV researcher just announced that it was man-made just a few days ago to the French Officials. The virus sequence 19 is a modified HIV sequence material and also identifies a chain of researchers and scientists that must have worked on the protein chain sequences and obtained top secret research documents.  And it can rework it once it has reached a peak level and project it into an even greater threat than the 1st.

That is the potential which perhaps some officials now are aware and fear, just as we discover it here is why?  And what about stopping it? They thought for a time about a vaccine, but that will not work in this next phase of this virus! And why? Because it will no longer be a virus! The protein chain sequence called covid-19, the fear is, it will mutate! And the biggest fear is that it will mutate into a mass of living material i.e to become a bacteria as deadly as e-coli which is far more deadly than the Corona Flu virus it was thought to be.  It seems everyone is getting caught in the game of cover-ups!  Read more, for the truth is coming clearer as the head of this beast begins to appear. You can ask now why Italy and why New York?

The symptoms of the sick do not show a person with flu virus. They reveal that the virus is changing through the molecular protein makeup of the internal materials of the human being it is within. That means the persons infected are not showing symptoms of a virus infection, or a flu, but something that is changing and mutating, and resembling other diseases. Maybe it is other diseases, and even unknown as yet?

And now the true question is what have the scientists done? Have they been good scientists?  Their labs have been hidden everywhere and money and intrigue has followed them as a shadow follows a ghost.  Have they created a network of disgusting spies and espionage all around the globe full of the dramas of nightmares of formulas and threats of powerful and unheard of, until now, knowledge? And a huge and dark mess more ugly than the people who thought it is emerging! As a huge dark hole now bursts open and now sputters like a volcano ready to spit out a huge chunk of molten mountain! A dragon is crawling up from the depths of molten hot seas of chains of liquid proteins that they mutated with corpses of aborted children and infected blood sent through monkey brains, and endocrine glands to arrive at secret formulas that we have been taking about and understand in our lectures here at our school. These are the secret ingredients of the formulas of the vaccines the governments have been forcing on people! And who will wash their hands now? Who? And you may ask of the land of Italy that fired all of their Vaccine Happy Health Officials two days ago! These were the doings of men who thought of inflicting punishments on Religious People with blind cause, but the darkest evil behind them. 

More to come .....

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Re: The Protein Sequence of Covid-19 Prevents Vaccinations

by Eugene Passofaro -
From the report"Highly virulent coronaviruses that form syncytia between cells can even spread in a receptor-independent fashion. Even when an initial binding receptor such as ACE2 is identified for a coronavirus, initial uncertainty or enduring complexity for the rest of the entry process may be the norm. Many other human proteases present in the lung seem capable of cleaving various sites on the spike protein and which could cause its activation. For example, a variety of proteases such as trypsin, tryptase Clara, mini-plasmin, human airway trypsin-like protease (HAT), and TMPRSS2 (transmembrane protease, serine 2) are known to cleave the glycoprotein hemagglutinin (HA) of influenza A viruses as prerequisite for the fusion between viral and host cell membranes and viral cell entry." 

Which means the host is making the protein chains and testing shows the virus has been shown to mutate as much as 50 times in a sequence chain, and that three sequencing chains have been tested to form in parallel from each strand of RNA. Even residue changes the sequences. So, good luck trying to make a vaccine for it. The theory is this, someone spliced the human protein into the animal sequences of the protein. That is, someone who knew what they were doing. If that is true, then this one will mutate and that is when the vaccine will weaken the persons instead of strengthening them. why? because the body needs to adjust to each vaccine, which are stimulants to make protein chains. But you can see the problem - which protein chain does one stimulate the cell to produce,  through the agency of the protein sequences in the vaccine?

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