The corona virus is a toxic mix of four different flu families that magically came together to form a virus that had never existed before.
David Spring M. Ed.
There is a debate about whether we are allowed to describe the corona virus as simply another version of the flu or whether the corona virus is completely different from the flu. On a technical level, the corona virus is slightly different from the seasonal flu. But on a practical level, there are only a few important differences between these two viruses. In this chapter, we will look at the differences and similarities between the corona virus and the seasonal flu virus that most of us are already very familiar with.
Why Some Corona Virus Cases are Worse than Others… Corona Virus Spikes and ACE 2 Receptors
The above drawings are just artistic renditions of the seasonal flu and Corona virus. We will look at actual electron microscope images in a moment. The above drawings show the major structural difference which is that the seasonal flu has rounded spikes on the outside of the virus shell. These rounded spikes of the seasonal flu virus are not very good at attaching to human cells and makes it easier for our immune system to fight off the seasonal flu.
By contrast, the Corona virus has club like spikes on the outside of the virus shell. These club like spikes make it easier for the Corona viruses to attach themselves to ACE-2 receptors which are on the surface of many human cells. But the good news is that the corona virus can only attach to “weakened” cells.
As the dead human cells build up, they can gather in our lungs. If enough of these dead cells build up, they fill up our lungs and make it difficult to breathe. This is known as viral pneumonia.
A few victims eventually suffocate to death – even when the victims are in hospitals with respirators! Thankfully, things only get this bad with extremely old patients who also suffer from cardiovascular disease and/or other risk factors. Even then, only a small percent are affected. In victims without cardiovascular disease, the chance of death is much less than one percent – and may be even lower than the seasonal flu (about one in one thousand). The reason we are highly likely to survive a corona virus infection is our remarkable immune system is able to find a way to identify and kill off all the Corona viruses before they can kill us off.
Given that the seasonal flu, the SARS virus and the MERS virus or any other virus in thousands of years is not as good as the Corona virus in attaching themselves to ACE 2 receptors, an important question we need to examine is:
What exactly are ACE 2 receptors and why are they weaker and less able to stop the corona virus in older people?
ACE 2 receptors have many functions. One of those functions is to respond to cardiovascular disease (CVD) – which is the underlying cause of most of the leading causes of death – including heart attacks, strokes and high blood pressure. ACE stands for Angiotensin Converting Enzyme. The 2 at the end means that this enzyme counter-acts the effect of an enzyme which is simply called ACE. As with many other systems in the human body, our immune system is extremely complex and involves all kinds of complex molecules that balance each other out. In fact, there are nearly an infinite number of possible organic chemical reactions.
The bottom line is that people with Cardio Vascular Disease have cells with weakened ACE 2 receptors. If we are to reduce the number of fatalities from the Corona virus, the best way to do this to reduce cardiovascular disease which in turn will strengthen our immune system and help ACE 2 receptors fight off corona viruses. Therefore, the key to understanding how to protect in the long run against the Corona virus is to have a better understanding of how to reduce Cardio Vascular Disease. We will explain how to reduce cardiovascular disease later in our section on Prevention. But what increases the risk of Cardio vascular Disease and therefore death from the Corona virus is sitting on the couch all day getting stressed out listening to the talking heads on TV explaining why you can not leave your house! In short, the “Stay Home” order being promoted on TV is certain to increase fatalities rather than reduce them!
Now that we better understand the interaction between the corona virus, ACE 2 receptors and our immune system, we need to ask: How did the Corona Virus develop this remarkable ability to attack human ACE 2 receptors?
First, it must be noted that the closest cousin to the Corona Virus, the 2002 SARS virus was pretty well designed for attacking the ACE 2 receptor. But just not as good as this new 2019 version. We have already noted that the flu virus and corona virus mutate rapidly – with 100 mutations per year. So some might argue that this new and better version of SARS was bound to happen someday. But the rapid rate of mutation raises more questions than it answers. The main question is that if this ability to attack ACE 2 receptors this well was really a possible mutation of the virus in nature, then why did this particular mutation not show up until 2019? Why didn’t it show up a thousand years ago? We have new flu virus outbreaks every 10 years and have new serious flu outbreaks every 100 years.
This has been going on for thousands of years. So one wonders why this scary mutation shows up now and not earlier. Just consider the math. 100 mutations every year is 10,000 mutations every hundred years and 100,000 mutations every century. Now suddenly, after hundreds of thousands of mutations, the virus finally figures out how to attack one of the human immune system’s most important functions? It seems hard to believe we can be that unlucky - or put the other way, that the corona virus could be that lucky.
There are many other strange and unique aspects of the 2019 Corona virus that are equally hard to understand. One is the rate of people who get the corona virus without symptoms. It is almost certainly at least 50% and may be as high as 90%. Below are some links and quotes:
March 2020 Clinical characteristics of 24 asymptomatic infections with COVID-19 screened among close contacts in Nanjing, China. https://www.ncbi.nlm.nih.gov/pubmed?term=32146694
“None of the 24 asymptomatic cases presented any obvious symptoms while screening. 7 (29.2%) cases showed normal CT chest images and had no symptoms during hospitalization. The median communicable period, defined as the interval from the first day of positive tests to the first day of continuous negative tests, was 9.5 days (up to 21 days among the 24 asymptomatic cases).
“In a COVID-19 outbreak on a cruise ship where nearly all passengers and staff were screened for SARS-CoV-2, approximately 17 percent of the population on board tested positive; about half of the 619 confirmed COVID-19 cases were asymptomatic at the time of diagnosis. A total 318 (51%) of all confirmed cases were asymptomatic.”
Study from China: “By our most conservative estimate, at least 59% of the infected individuals were out and about, without being tested and potentially infecting others,” says Wu Tangchun, a public-health expert at Huazhong University in Wuhan, who led the study. “This may explain why the virus spread so quickly in Hubei and is now circulating around the world.”
By contrast, the seasonal flu has about 20 percent of asymptomatic cases: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4586318/
Even with people who have symptoms, the symptoms often do not show up for several days. These two problems greatly increase the ability of the virus to travel undetected from victim to victim. By contrast, the seasonal flu is most contagious in the three to four days after symptoms begin. https://www.cdc.gov/flu/about/disease/spread.htm
The 5% who require hospitalization is also much more than the seasonal flu (which is only 1 to 2 percent). Also, these severe cases stay in hospital twice as long (11 to 14 days versus 5 to 6 days).
Finally, the percent of people to get the corona virus is estimated to be more than the flu. Each year 15% to 20% of people get the flu, but estimates of people getting the corona virus this year range from 24% to 50%. However, there was no evidence given to support such a high infection percentage other than the Princess Cruise ship infection rate. https://www.nature.com/articles/s41591-020-0822-7
So how can a virus evolve or mutate to have these hidden infection characteristics – when for thousands of years, it has had much different characteristics?
What about the bat virus?
The primary narrative in the corporate media is that the corona virus resulted from someone in China eating a bat. I have read the research on the genetic correlation and I find this difficult to believe. How can a virus evolve in a bat to be able to so precisely target the human immune system? Here is one study of ACE2 receptors in Bats https://www.ncbi.nlm.nih.gov/pubmed/20567988
While there was some minor activation, the SARS virus did not do very well with these bats. Another 2013 study stated: “To date, no SL-CoVs have been isolated from bats, and no wild-type SL-CoV of bat origin has been shown to use ACE2.”
The study then found some bat SARS viruses that had a 95% match to the human SARS virus. This Bat SARS virus was able to invade human ACE 2 cells but did not replicate very efficiently once inside. Also, a 95% match means that a lot of mutation would be needed to go from the Bat SARS to the 2019 Corona virus. I am therefore skeptical of the Bat to human theory -as are many other people.
Part of the problem in determining the original of the Corona virus is the complexity of viruses in general. It is not like there are just a few common viruses. Instead, due to massive mutation over time, there are millions of different types of viruses. Because they are so small, it is very difficult to study these viruses. This next study used a short-cut method trying to determine the human ACE2 activity of hundreds of related SARS viruses. https://www.biorxiv.org/content/10.1101/2020.01.22.915660v1.full
The 2019 Corona virus and the 2002 SARS virus are part of a family of viruses called Beta Corona Viruses. The Beta Co-V family is further divided into four lineages. We as humans are mainly interested in studying lineage B, which includes the 2002 SARS virus and the 2019 Corona Virus. But lineage B also has 200 other family members. We are also interested in lineage C, which includes the 2012 MERS virus. Lineage C has over 500 family members. So the 2019 Corona virus lives in a family with 200 closely related brothers and sisters - and it also has 500 other “close cousins” and all of them are mutating at a rate of 100 mutations per year. And these mutations have been going on for thousands of years.
All 700 of these related viruses have receptor binding domains (RBD) that potentially play a crucial role in binding to human ACE2 receptors.
What is a Receptor Binding Domain (RBD)?
A Receptor Binding Domain is a specific protein molecule at the end of a virus spike. This Receptor Binding Protein works as a key to open the lock into the target cell as is shown on the following figure:
The following studies look at how the corona virus RBD was mutated to give it the ability to unlock human ACE2 receptors.
This study found that the 2019-Corona virus RBD was capable of entering cells expressing human ACE2, but not any of the other receptors of other animals tested. In plain English, the Corona virus comes with a key made to unlock human and only human ACE2 cells – it seemed to be designed for the human ACE 2 cells.
Even more interesting, their study showed that the 200 lineage B virus families could be divided into three distinct clades or clans.
Note: Clades are a biological family term similar to the human “clan” family term. It means a group of closely related viruses.
The 2002 SARS 1 virus was definitely and exclusively in Clan 1. Clan 1 viruses and only Clan 1 viruses with Clan 1 RBD were capable of entering ACE2 cells. But surprisingly, just having the RBD from Clan 1 was not sufficient to facilitate entry into the ACE 2 cells.
Instead, the study found that “Corona virus entry is a multi-step process involving multiple, distinct domains in spike that mediate virus attachment to the cell surface, receptor engagement, protease processing and membrane fusion.” In short, there are several factors needed to make the 2019 Corona virus work.
“Our results show that, despite all (700 types of Beta Corona viruses) being classified as the same virus species, most lineage viruses do not use currently known corona virus receptors.”
“The RBD for 2019-nCoV has residues and motifs found in all 3 clades but forms a distinct clade, so we tested it for receptor usage and observed entry only with human ACE2 - but not other known corona virus receptors.”
“Interestingly, the 2019-Corona virus RBD forms a clade that is distinct from the other 3 clades. However, the 2019- Corona virus RBD contains most of the contact points with human ACE2 that are found in clade 1 as well as some amino acid variations that are unique to clade 2 and 3. Taken together with our receptor assay results, it may be possible that 2019-Corona virus arose from recombination between clade 1 and the other clades. “
Please read the previous two sentences slowly three times. Then think to yourself: How could that even be possible? How can a clan 1 virus recombine itself with precise sections of clan 2 and clan 3 such that the resulting RBD is a perfect match for human ACE 2 receptors – and have all of this mutation occurring inside of bats???
Their study showed beyond any reasonable doubt that the Corona virus is not only perfectly designed for the ACE2 receptors, including all of the essential features of the 2002 SARS virus (Clan 1).
But in addition, it has some of the features of the Clan 2 family (aka the 2012 MERS virus) and it has some of the features of the Clan 3 viruses – which are not well covered in the literature because they are not considered relevant to humans.
“2019- Corona virus RBD contains most of the contact points with human ACE2 that are found in clade 1 as well as some amino acid variations that are unique to clade 2 and 3.”
How is this possible? Let’s look at another study to see if we can find some more clues that might have been left at the scene of the crime. Here is a study published on February 16 2020: http://virological.org/t/the-proximal-origin-of-sars-cov-2/398
The Proximal Origin of SARS-CoV-2
“SARS-CoV-2 appears to be optimized for binding to the human ACE2 receptor… The receptor binding domain (RBD) in the spike protein of SARS-CoV and SARS-related corona viruses is the most variable part of the virus genome…. Five of these six residues are mutated in SARS-CoV-2 compared to its most closely related virus, RaTG13… Thus the SARS-CoV-2 spike appears to be the result of selection on human or human-like ACE2.”
The author then notes that the 2019 Corona virus has a poly-base cleavage site. This description is followed by this quote:
“A polybasic cleavage site has not previously been observed in related lineage B beta corona viruses and is a unique feature of the 2019 Corona virus.” Later the author explains that this function enhances cell fusion. Put in plain English, the 2019 Corona virus is breaking new ground in several structural areas.
#1: The corona virus spans clans and lineages: It is not only a mixture of at least three different Beta clans. It also has characteristics previously reserved for Lineage A viruses that aids them in fusing to the victim cell.
#2: The corona virus is the first and only virus of its kind to acquire polybasic cleavage. Here is another quote from the study: “Acquisition of a polybasic cleavage site converts low pathogenicity viruses into highly pathogenic forms” In plain English, this unusual feature adds to the deadliness of the virus. So how can that happen? How can a virus not only mutate out of its clan – but also mutate out of its lineage. It is basically a magic mix that managed to grab all of the advantages of lineage B and combine them with all the advantages from several other families. And throw everything into the same virus at the same time.
#3: The corona virus is ideally shaped to attack weakened human immune system ACE 2 receptors.
#4 The corona virus has a unique ability to hide inside of victims and transmit itself from victim to victim without the transmitting host showing any visible symptoms.
These four very unusual properties have led some to claim that the 2019 Corona virus was genetically engineered. I have been unable to find any information to positively confirm or refute this claim. We need more and better proof that this before we can reach a conclusion one way or the other. We will return to these unusual issues of the corona virus when we discuss vaccines.
Variation in the Seasonal Flu and Corona Virus Over Time
Variations of the seasonal flu virus have been around and interacting with the human immune system for at least three thousand years. Each winter, one of more variations of the flu virus cause massive numbers of fatalities. All flu viruses undergo frequent genetic variation through mutations in order to evade our body’s immune system antibody responses. Seasonal flu viruses mutate about 8 times per month or 100 times per year. This is because they are under pressure not only from our body’s natural immune system but also because each year a new flu vaccine is developed to deal with the previous year’s viral mutations. Each year becomes a game of cat and mouse to see which flu viruses will be able to survive the adjustments of our body’s immune system and the annual changes in flu vaccines. Rapid mutation of viruses are the primary reason that flu vaccines are only effective about 40% of the time – even less in people over the age of 65.
Here is a chart of the effectiveness of flu vaccines over the past four years:
The average is about 35% effective for all age groups but much less effective for those over age 65. This rate of effectiveness is not much different than the rate of effectiveness of our body’s own immune system. This is one of several reasons that holding out hope for a magic bullet “vaccine” that will end the corona virus problem in a year is so ridiculous. We have been trying to stop flu viruses for 50 years and have gotten no where. If anything it will be harder to create a vaccine for the corona virus than it has been for the seasonal flu.
Three Reasons all Viral Genes Mutate Extremely Rapidly
There are three main reasons all viruses change so rapidly – and in fact are capable of changing as much as is needed. First, the populations of viruses are extremely large – on the order of millions to billions in any given epidemic. Second, all viruses replicate extremely rapidly. There can be hundreds of generations of viruses in a single epidemic. Third, as we have already mentioned all viruses have extremely high mutation rates. Every mutation, which helps the virus to evade the host immune system, or helps the virus evade a vaccine, will be positively selected, passed on to the next generation, and distributed the mutation more widely. So the idea that some magic vaccine is going to permanently fool the corona virus is simply not very honest.
Once the human immune system starts to figure out how to fight back against the corona virus – a change that has already occurred in many people who now have immunity and will occur in many more people in the coming months – then the corona virus will have more of an incentive to evolve and it will likely adopt about the same rate of mutation as the seasonal flu.
It will then mutate even more rapidly once it faces the challenge of whatever billion dollar vaccine we throw up against it. There is almost no doubt that within a matter of days, it will mutate enough to evade the vaccine – and there goes a billion dollars – and once again we will be faced with mass isolation “to protect the ones we love.”
A better alternative is to strengthen our own immune system – as each person’s immune system may develop a slightly different way of fighting the corona virus. The immune system is a free bottom up solution to the corona virus problem whereas the vaccine method is an expensive and ineffective way of pretending to deal with the corona virus. But vaccines are really just supporting drug companies. This extremely rapid rate of mutation viruses is never mentioned in the corporate media because they do not want you to know that a reliable permanent vaccine is simply not possible. Even if a temporary vaccine could be found, the Corona virus would simply mutate into a different form and we would be back to square one.
Now that we have some understanding of the structural challenges of the corona virus, in the next section we will see how it is similar to and different from the seasonal flu.