Was the Covid-19 virus created in the laboratory?-Remains a mystery

 How did the cleavage site of furin in the covid-19 virus S-protein come about?

(Disclaimer: -

The following preliminary scientific reports have not been extensively reviewed and, therefore, should not be considered conclusive or behavioral guidance or established information related to medical practice/health.)

Called by SARS-CoV-2 (2019-nCoV and HCoV-191), this new novel virus belongs to the rapid spread, of the genus of B betacoronavirus (CoV). It has now caused a global outbreak of coronavirus disease (COVID-19).

It is speculated that a unique furin cleavage site (FCS) in S- (spike) protein that is not present in other hereditary B βCOVs such as SARS-CoV, may be responsible for its high infectivity and proliferation. Is this site natural? Or artificial?

A coronavirus (CoV) infects the target cell through cytoplasmic or endosomal membrane fusion. Whichever path it chooses, the final step in virus entry involves releasing RNA into the cytoplasm for replication. Therefore, the fusion capacity of CoV-S is a leading indicator of the infectious potential of the Covid-19 related virus.

S (Spike) - The protein consists of the S1 receptor-binding subunit and the S2 fusion subunit. CoV-S must be primed by cleavage at the S1 / S2 site and S2 ′ site, in order for it to open the cell by inducing the furin protease enzyme in the human cell.

There is no report yet to prove this hypothesis experimentally.

Corona virus-2 (SARS-CoV-2), which causes the acute respiratory syndrome of the current coronavirus infection 2019 (COVID-19), contains a mysterious new addition of four amino acids (PRRA) unique across the S1 / S2 border. FCS is a genetic mutation that does not normally occur between spike protein (S) in any SARS-CoV and other related coronaviruses.

That is the FCS genetic interpolation of the furin cleavage site. It is not present between the spike protein (S) in any normal SARS-CoV and other related coronaviruses.

Before getting into these issues first let us know some basics in some basic molecular biology.

What is Protease?: -

Our body is made up of many cells. Many devices are located within those cells. They are essential for the growth of cells. Notable among these are protease-type enzymes.

Of these, the furin protease enzyme is the most important. This is the cell key. Nutrients from the blood use these keys to open the cells and go inside the cell and help in cell growth. Some viruses also use this key to infiltrate cells and destroy them.

They must have a system called Furin Cleavage Site (FCS) in their spike (S) protein to use this key stealthily. It is not present in natural coronaviruses. But how this new system got into this novel coronavirus-2, is a mystery.

In nature, there are four types of corona: alpha, beta, gamma, and delta (∝,β,γ,d). NCoV-SARS-2 is a novel coronavirus that is a mutant or strain of the beta type.

This site does not cite its precursors such as the NCoV-SARS mutant which caused the deadly SARS-1 disease in China. So that disease did not spread fast everywhere. Stopped with China. But how it got into the NCoV-2 strain that could have made this Covid-19 remains a mystery.

This research led to the discovery that furin protease may play a key role in facilitating the entry of SARS-CoV-2 into human cells.

Pathogenesis of the virus caused by furin

The role of furin in the dysfunction of pathogens was first identified by biochemical tests of anthrax toxin antigen (PA) and avian influenza virus hemagglutinin (HA).

This means that the furin cleavage site (FCS) can only be found for fast-spreading deadly viruses. But how it got into the Covid-19 virus alone remains a mystery when it does not exist among other natural coronaviruses, which cause a mild form of normal infection.

Following the anthrax infection, for example, the furuncle inside the cell is responsible for the cleavage of this toxin, which allows the toxin to penetrate into the cells, and the FCS in the virus, the furuncle site of FCS itself, is an important device that allows holes to form in the target cell membranes and eventually penetrate into the host (human) cells.

The cleavage of these glycoproteins, which are caused by furin, allows mature and fusogenic cells to form glycoproteins. Ebola Zire and Ivory Coast virus strains are found to have a consensual furin base in their cell envelope glycoprotein, which is similarly related to some cytotoxic activity of the highly dangerous Ebola virus.

Furin and coronaviruses

The structure of the SARS-CoV-2 virus is surrounded by trimeric (three-step) intramembrane spike (S) proteins, which have been shown to be important in the mechanism by which the virus penetrates human cells.

Within S protein there are two functional domains, one of which is the receptor-binding domain and the second is the power domain, which enables the second domain to ignite the receptor-binding domain (part) to attach to the phospholipid membrane of the viral host (human) cells.

A specific type of protease enzyme is usually involved in the fusion of viruses and cell membranes; however, the specific properties of this protease may differ between coronaviruses. For example, the S protein surrounding the Middle East Respiratory Syndrome (MERS) -Cov virus contains the cleavage site of furin, which promotes the virus' entry into cells.

In comparison, the S protein of the acute respiratory syndrome (SARS) -Cov virus molecule does not divide after attachment to a human cell, thus indicating that its division occurs after the virus has already entered the cell.

Furin and SARS-CoV-2

The binding of the S protein to the angiotensin-converting enzyme 2 (ACE2) has been confirmed as an important mechanism for the penetration of SARS-CoV-2 into human cells.

Studies on the S protein of SARS-CoV-2 have identified four unwanted furin cleavage sites in that.

Interestingly, furin protease enzymes are found in large quantities throughout the human respiratory tract, leading researchers to question whether SARS-CoV-S protein S can use its cleavage sites to rapidly divide epithelial cells in the human respiratory tract and cause more infection and pathogenesis.

The discovery of the furin cleavage sites also provides researchers with information on why SARS-CoV-2 is highly contagious in humans and how the virus was first transmitted from bats to humans.

A recent study developed a strain of SARS-CoV-2 that does not have the cleavage site of conventional furin. From their series of tests, they found that the strain was less contagious and could provide some further protection against the original SARS-CoV-2.

Finally, findings suggest that the cleavage site of furin in SARS-CoV-2 may play a key role in SARS-CoV-2 infection.

FURIN CLEAVAGE SITE-FCS: -

By this strain, the old SARS-1 virus spike glycoprotein has a furin cleavage site (FCS) attached with a new look. Furin is a serine protein that is widely expressed in human cells, splitting the SARS-CoV-2 spike at the interface of its two subunits. It is encoded in a gene on chromosome 15 in the nucleus of human cells.

Furin acts on substrates containing single or paired base residues when proteins are added to cells. The cleavage site of polybasic furosemide, which opens cells with the protease key of furin, is not commonly found in various proteins of many viruses, including beta coronavirus, Embecovirus, and Merbecovirus.

However, it is doubtful whether this site was uniquely, innovatively, or artificially inserted into the SARS-CoV-2 strain or strain of the Sarbecovirus lineage beta coronavirus.

The study was conducted using genetic data available at the National Center for Biotechnological Information (NCBI) databases to identify the origin of the furin split site.

What is Furin?

First identified in 1990, furin is a cellular cell enzyme. It is the key to the entry of many pro-protein molecules into the cell, from pathogens to growth factors, receptors, and matrix proteins that must enter the cell from the inside.

Like other endoproteases, the mechanism of action of furin is the hydrolysis of specific internal peptide bonds, peptides, and protein substrates called enzymatic hydrolysis (ENZYMATIC HYDROLYSIS).

The actions of furin play important roles in every stage of life, starting with the activation of pro-B-neuro growth factor (NGF) and allowing neurodevelopment during development and continuing into late life during amyloid dementia.

The ancestor of the same virus

At the genetic level, they identified three coronaviruses that are very similar to SARS-CoV-2. These are Pangolin-CoVs (2017, 2019), Bat-SARS-like (CoVZC45, CoVZXC21), and Bat RaTG13.

Three gene fingerprints were used to identify these matches, including the fingerprint 1, nsp2, and nsp3 genes in the orf1a RNA polymerase gene; The fingerprint 2, at the beginning of the S gene, contains the N-terminal domain and the receptor-binding domain (RBD), which mediates binding to the host cell receptor, the angiotensin-converting enzyme 2 (ACE2); And fingerprint 3, the orf8 gene.

These fingerprints differ only in the RNA level of the three closely related coronaviruses, but in the amino acids in the translated proteins, the sequences are similar to those of other surface viruses.

The division of these gene sequences indicates their common lineage, supported by other short sequence features, one deletion, and three insertions. All three strains show the same removal-insertion pattern at the same four different locations in the spike gene.

Spike genetic remodeling in a common ancestor

Analysis of the phylogeny of these three strains showed that the first difference was the pangolin coronavirus, with which the RatG13 virus was most closely related. However, when analyzing spike alone, there is a strong resemblance between pangolin CoV, RaTG13, and SARS-CoV-2.

This may indicate the occurrence of recombination events between Pangolin-CoV (2017) and RatG13 ancestors. Following this pangolin CoV was transferred to pangolin hosts.

Unique codons that encrypt arginine at the furin cleavage site

The furin cleavage site consists of four amino acids PRRA, which are encoded by 12 inserted nucleotides in the S gene. A characteristic feature of this site is an Arginine Doublet.

This insertion may have occurred by random insertion mutation, reconstruction, or laboratory insertion. The researchers say that the possibility of random insertion is very small to explain the origin of this nucleus.

Surprisingly, the CGGCGG codons that encode the two arginines of the twin in SARS-CoV-2 are not found in any of the furin sites in other viral proteins that are exposed by the virus.

Even in SARS-CoV-2, arginine is encoded by six codons, but only a minority of arginine residues are encoded by the CGG codon. Again, only two of the 42 arginines in the SARS-CoV-2 spike are encoded by this codon - which is the PRRA core.

For the restoration to occur, there must be a donor from another furin site and another virus. In the absence of a known virus containing this arginine duplicate coded by CGGCGG codons, researchers dismiss the reconstruction theory as the underlying mechanism for the emergence of PRRA in SARS-CoV-2.

Acquisition time

The second question is when this change occurred. It should be noted that the RaTG13 virus was isolated and isolated in the laboratory in 2013, after which the site was acquired, which may have paved the way for the current SARS-CoV-2 strain.

The first scenario is demonstrated by the detection of identical RBD mutations in bats and human viruses, obtained from two of the three O-linked glycans around the furin base. The two viruses show completely identical scenes around this site.

However, to add strength to this hypothesis, there is no significant evidence. RaTG13 sequences obtained in 2021 should be analyzed to determine if the furin site is derived from this virus, as well as the source of SARS-CoV-2 in the bat.

Conclusion

Researchers briefly describe this mysterious site as "a Furin site that changed the world":

These sources and analyses only show that the acquisition of the Polyphasic Furin Cleavage-site by SARS-CoV-2 is a "missing link" in our understanding of its evolutionary history, which can only be resolved by the discovery of new viruses.

POST COVID-19 CONSEQUENCES-1. BLACK FUNGUS

 Black fungus -Description

Covid-19 disease, along with its confusing corticosteroid, and antimicrobial therapies such as chloroquine and azithromycin, has led to the development of fungal infections today.

The patients too no longer have peace.

Also, there is no peace for those who too have recovered from their illness. There is no peace for anyone in the community.

How do such situations develop? The medical world does not have the answer. 

Did this agony suddenly arise or was created with a purpose at the final stage of this twentieth century? 

But don’t just say created. It is a crime.

Still the medical experts do not explain clearly how it came to be. Because it is still in the alphabetical stage of the study says the medical expertise.

There is no need for further proof that the upper ruling class is filled with immoral science and by that, they reign all over the world. The end of the world is near. 

What is  Black Fungus or MUCORMYCETES?

In general, the fungus, bacteria, and viruses are the most vulnerable and weakest creations among all the creatures. These cannot surpass the natural immunity that the Lord has given to our bodies. These overwhelm us only when our immune system is weakened.

The same is true of black fungus.

This black fungus is present in rotten fruits, dirty soil, manure, leaf litter, and animal wastes and in other dirty environments. So it will be ubiquitously related to our body. The body of everyone who can be healthy will develop its immunity accordingly. This resistance is greater for those who live on the sidewalk and in the garbage that can live in the dirt.

But black fungus or mucormycosis, is a rare but dangerous infectious disease that is caused by the loss of immunity in people with diseases such as diabetes mellitus, AIDS, or COVID-19 patients and those recovering from it.

 The disease often affects the skin, lungs, and brain.

The causative agent of this disease is the fungus Mucormycetes.

Disease Types: -

1. Respiratory fungal infections:-

-Cough

-Fever

-Headache

-chest pain

-Nasal or sinus congestion and pain

-wheezing

All of the above symptoms are associated with fungal pneumonia. This is the most dangerous pneumonia.

2. Fungal symptoms related to the skin:-

-Dark skin tissue

-Reddening, swelling, tenderness

-Blisters

-bruises

What happens if a person is affected?: -

Warning symptoms include pain and redness around the eyes or nose, fever, headache, cough, shortness of breath, bloody vomiting and mood swings.

If you have the following symptoms

Black fungal infections should be suspected: -

* Sinusitis - nasal congestion or, heartburn, nasal discharge (black blood);

* Localized pain in the cheekbone, one-sided facial pain, numbness or swelling;

* Black discoloration on bridge of nose / palate;

* Tooth decay, jaw injury;

* With blurred or double vision pain;

* Thrombosis, necrosis, skin ulcer;

* Chest pain, pleural effusion, worsening of respiratory symptoms.

Experts advise that all cases of nasal congestion should not be considered as normal bacterial or viral sinusitis, especially in patients with immunodeficiency due to Covid-19.

Do not hesitate to carry out aggressive tests to detect fungal infections, they advise.

Mucormycosis is not contagious to those with normal immunity, and most people who come in with the fungus cannot easily develop an infectious disease. However, people with a severely weakened immune system have a higher risk of developing mucormycosis. This includes the following patients:-

-Diabetes

-Cancer

-HIV

-Skin injury

-surgery

-COVID-19

General Warnings: -

The sinuses, or lungs, are affected after inhaling fungal spores from the air. In some states, physicians report an increase in the incidence of mucormycosis among those hospitalized for COVID-19 disease or those recovering from COVID-19, some requiring emergency surgery. In general, mucormycetes do not pose a major threat to those with a healthy immune system.

Covid-19 and Mucormycosis (black fungal disease): -

Covid-19 leads to a weakened immune system, preventing the body from effectively protecting itself from infection. As a result, individuals recovering from Covid-19 are at increased risk for mucormycosis.

Christopher Coleman, Assistant Professor of Infectious Diseases, University of Nottingham in the United Kingdom, told Medical News: -

"The virus, as part of its duplication cycle, suppresses the immune system, so the immune system cannot destroy other bacteria or fungi. The most famous example of this is HIV. However, other viruses do this in a very short period of time - that is, other viruses only slightly suppress the immune system for a few days or weeks. 

Steroid treatments for Covit-19 can also suppress the body's immune system. It may also be responsible for the now-increasing rates of mucormycosis infection.

"In this case, there is a suggestion that steroids play an important role," says Coleman. "They suppress the body's normal immune system, allowing a fungus to infiltrate and infect the body."- He further says.

Disadvantages of oxygen therapy:-

Oxygen therapy for severe COVID-19 has been shown to dry out the nasal cavity and increase the risk of fungal infections.

What is the next treatment?: -

There is still no proper treatment for this.

If the patient presents with early symptoms, some antifungal drugs can be given to save him. But in the advanced stage there is no other option but to surgically remove the affected organ or part.

It is difficult to determine the best course of action to treat these two infections simultaneously. Coleman raises some questions, and experts should move this forward:

"Can a patient infected with Covid-19 along with mucormycosis be treated with Covid-19 simultaneously with a fungicide for fungal infections?" And "Is it possible to reduce the dose of Covid-19 treatment and maintain sufficient immunity in the body so that the fungus cannot enter?"

Conclusion: -

The combined risks of Covid-19 and mucormycosis raise challenging issues and require careful coordination

OXYGEN AND COVID-19 --- Oxygen deficiency or hypoxia in the blood

(Disclaimer: - The information included on this site is for educational purposes only, not for medical treatment.) 

OXYGEN AND HEALTH-HAPPY HYPOXIA

Fig-1

One of the aims of this article is to make people get a general understanding of oxygen, even though it is given two types of headings above.

Oxygen is a Gas of Life. If there is no oxygen then there are no lives.

After drinking water like a camel, you can live for a few days without drinking any more water. 

After one time eating with a full stomach and further a few days without food you can live with starvation.

Albeit you breathe in a lot of oxygen once with full lungs if no oxygen is further available for the next breath you cannot survive for the next moment.

 Oxygen is essential for all living things in this world, not just for humans but for bacteria and fungi too. But the virus does not need oxygen. Because it is not a living system.

The amount of oxygen in the air is only one-fifth. The remaining three parts are nitrogen, and further, the remaining one part is of other gases, such as carbon dioxide, hydrogen, helium, argon, krypton, neon, and xenon.

This formula is the air formula designed by the Almighty God, the all-knowing biochemistry expert for our safety. (Figure-1)

In the verses of the Holy Quran (55: 7,8,9) God warns man not to disturb this equation.

OXYGEN IS A CHEMICAL:-

Oxygen can be described up as a physical and chemical substance.

Oxygen is a heavy gas. Its molecular weight (MW) is -32gm / mole

Molecular Formula of Oxygen (MF) -(Fig-2)

Fig-2
MF-Molecular Formula
MW-Molecular Weight

Oxygen in the air is a single molecule in which two oxygen atoms are connected by an electrovalent bond (Figure-2). This connection may be broken under some unusual circumstances. Then the oxygen will be ionized and the action will be understood. For example. When hydrogen is burned in oxygen, the oxygen reacts with it to form water (Figure-3A).

Fig-3A
H2O=Water

Oxygen will trigger the burning object but not burn itself. That means it is a supporter of combustion and not a combustible gas. That is why in the atmosphere the Lord holds one part oxygen and three parts nitrogen. If not, with our body temperature of 98.4 Fahrenheit we would all be burned to ashes in oxygen.

Because nitrogen is an inert gas, it limits potent oxygen.

Understanding the Reaction of Oxygen with Nitrogen:

Fig-3B

Nitrogen and oxygen do not react at normal atmospheric temperature and pressure (ATP). But in extreme heat conditions caused by pollutant gases emitted from factories, especially from coal mines nitrogen reacts with oxygen rapidly to release more deadly nitrogen trioxide, which produces a photochemical smog. At the same time, if there is lightning and rain, there will be more acid rain.

However, in a hygienic climate where there are no factories, there will be harmless rain due to the small amount of nitric acid produced by lightning (Figure 3-B). It will also enrich the land.

How the body uses oxygen:

Before we know it, let's take a brief look at the hemoglobin in our blood and the red blood cells that enclose it.

Usually, the real form of blood is a yellow liquid called plasma. It contains soluble materials and non-soluble floating materials. One such floating substances are the red blood cells (RBCs).

It is these millions of red cells that float on the plasma and give color to the blood. It is through these RBCs that the body utilizes oxygen in various ways. It is through hemoglobin contained in RBC that the blood carries oxygen and transfers it to every cell of our body. (Figure-4)

Fig-4

Hemoglobin turns red after oxygenation. It leaves oxygen and turns blue after taking up carbon dioxide. So the color of the impure blood is blue.

Air contains 21% oxygen. The remaining 75% is nitrogen and the rest is gases.

We cannot breathe pure 100% oxygen. If we breathe like that it will burn our lungs' air sacs. Also, oxygen is a gas that suppresses respiration.

That is why medical oxygen is produced in multiple percentages. They are as follows:

1.Oxygen 99.5% + Carbon dioxide 300 ppm (0.03%)

2.Oxygen 95% + Carbon dioxide 5%

3.Oxygen 60%+ Nitrogen 40%+> 0.03% Carbon dioxide

None of the above medical oxygen contains 100% oxygen. But there is carbon dioxide in everything above. The reason is that carbon dioxide is a respiratory stimulant.

Carbon dioxide promotes the transfer of oxygen from the air to the lungs and from the blood to the tissues.

99.5%, and even 95% oxygen will be used very carefully. The reason is that these do not contain nitrogen as a diluent.

Inhaled oxygen is carried through the trachea to the lungs with inhaled air. Oxygen is absorbed due to partial pressure of air/blood in the air sacs.

The oxygen absorbed in the air sacs is carried by the capillary and the gas exchange is achieved by the same partial gas pressure difference with the carbon dioxide in the blood vessels. Thus oxygenated (OXYGENATED) pure-blood reaches the left ventricle of the heart through the pulmonary vein and from there through the aorta to the body tissues. (Figure-4)

HAPPY HYPOXIA or HAPPY HYPOXEMIA: -

This is one of the end-of-life symptoms of Covid-19 patients. Strange condition. Dangerous condition.

Normal blood oxygen levels can be as high as 95% -99%. If this level drops below 40% in some cases, the patient may faint. Vital organs such as the heart, lungs, kidneys, and brain can be affected and the patient may die. Shortness of breath may also occur.

But even with this amount of oxygen depletion in the blood, most patients do not experience any immediate symptoms, such as dizziness and shortness of breath. They shall show happiness. That is why it is so named like this.

Happy hypoxia does not trigger such obvious external symptoms. As a result, in the early stages

The COVID-19 patient, on the outside, seems to be right and "happy."

Why does oxygen level decrease in patients with coronavirus infection?

Small clottings and more widespread clots caused by clotting in the complex network of small blood vessels in the lungs are considered by many researchers and medical professionals to be the primary causes of happy hypoxia.

The underlying factor is the inflammatory reaction in the body, which is often triggered by SARS-CoV-2 infection and the subsequent onset of COVID-19. It stimulates cellular protein. Although this symptom disappears in the early stages, it is also a factor in the death of the patient in the later stages.

The list of COVID-19 symptoms is long. The most recent addition of these is ‘happy hypoxia’, which means the patient is happy without any symptoms despite having very low levels of oxygen in the blood. This has left medical professionals around the world confused.

This means that even those who have no symptoms from a covid-19 infection should know their oxygen level through an oximeter, according to a recent study. The reason may be happy hypoxia that does not show symptoms.

How to identify happy hypoxia in people who are asymptomatic or have only mild symptoms of COVID-19?: -

1.by the oximeter

2. Blue discoloration of the lips

3. Skin discoloration from the original color to red/purple appearance.

4. Persistent sweating even after not doing strenuous exercise or in hot environments

Finally paying attention to these warning signs of happy hypoxia ensures immediate treatment in a hospital setting, thereby restoring the lung capacity and normal breathing of the affected person and helping to recover from COVID-19.