Friday, December 4, 2020

Part 2: The Contagion Myth....From AID's to Covid...Testing Scam...Exosomes

The Contagion Myth

why viruses including

"Coronavirus" are not

the cause of disease

by  Sally Fallon Morell &

Thomas S. Cowan, MD



To understand the story of coronavirus, it’s instructive to go back to 1971. That was the year that President Nixon declared the War on Cancer. The theory of the day was that viruses caused cancer, and the medical establishment vowed they would find a cure by 1975. Hundreds of millions of dollars “flowed into a completely one-sided cancer research focused on wonder-drug production.”1 

Of course, the war was a complete failure, and by the early 1980s, NIH scientists were scrambling to obtain continued funding and the CDC “needed a major epidemic to justify its existence.”2 

Enter AIDS (Acquired Immune Deficiency Syndrome), said to be caused by HIV (Human Immunodeficiency Virus), a deadly virus that “made the jump from other primates to humans in west-central Africa in the early-to-mid [twentieth] century.”3 Some predicted that as an STD, AIDS would eventually spread through the whole population and kill us all. Between 1981 and 2006, almost two hundred billion dollars was invested in AIDS research, focused on the virus hypothesis and development of toxic antiviral drugs like AZT.

Many books 4 have carefully documented the case against the claim that a virus called HIV causes the disease called AIDS. Unfortunately, these careful arguments seem to make no difference to the man on the street—nor to scientists, for that matter. In essence, no matter what the evidence, 99 percent of the population, including most of the alternative medical community, still believe in this myth. 

Let’s look at the facts. AIDS was not a disease new to the 1970s and early 1980s. In fact, it is the same disease as the condition caused by immune-suppressive drugs used to prevent people from rejecting organs such as a heart or kidney after a transplant. The only thing new about the disease was the appearance of a new type of cancer called Kaposi’s sarcoma. AIDS is not a specific disease at all. It simply means a collapse of the cell-mediated immune system, known, even in the 1970s, to have many diverse causes. With the collapse of the immune system, you see conditions like frequent infections, TB, mononucleosis, peripheral neuropathy, and Guillain-Barré syndrome—all of which often come under the rubric of AIDS. 

The new part of the disease, Kaposi’s sarcoma, has been definitively linked to the use of “poppers” (alkyl nitrite drugs), which are immune suppressive. This drug was used to relax the anal sphincter and facilitate anal intercourse. The vast majority of people who got Kaposi’s sarcoma were gay men who used poppers (never people who “acquired the virus” from any other source). Once the use of poppers stopped in the gay community, so did Kaposi’s sarcoma. 

In spite of forty years of research, no one has isolated an HIV virus from any bodily fluid of a person suffering from AIDS. Not once. This is shocking for most people to hear, but cash awards are available for anyone who can show with an electron microscope purified HIV virus isolated from anyone with AIDS. Up to this point, no one has collected these cash awards. 

No one has ever documented transmission of any purified HIV virus from one person or one animal to another with any resultant sickness. Not once. In fact, the biggest study on AIDS ever carried out 5 clearly showed that HIV is not transmissible through sexual contact. 

And, finally, as we will discuss in chapter 5, the test used to make a “diagnosis” of AIDS can never determine causation. It is simply a test looking for genetic material of unknown origin. Since we have no proof that any virus or bacteria has ever caused any disease, the test is simply irrelevant for determining causation.

When the test for AIDS—called the PCR test—finds a higher level of genetic particles in the blood, it simply means that the person’s condition is causing a lot of genetic deterioration—from toxins, EMF poisoning, malnutrition, or stress. The test can never determine the cause of the illness. If one first isolated, purified, and characterized the entire genome of the virus in question, then one could determine whether the snippet of genetic material you are looking for is unique to that virus in question. Absent doing a purification, isolation, and characterization step, there is simply no way to say that the snippet you are looking at is either unique to that virus or even originated in that virus. 73s

If you poison an organism with any type of toxin that degrades your cells (which most poisons do, including EMF poisons 6 ), then more genetic material will be found in your blood and the PCR test will pick this up. This means you are sick. This also applies to antibodies: the more poisoned you are, the more antibodies you tend to produce to protect yourself. This simple fact explains why all PCR and antibody tests, including those for HIV and the coronavirus, tend to show higher “viral loads” (which are not viruses but genetic material) and to be more positive in sicker people. It doesn’t mean they have a viral infection; it means they are sick. This is why the package insert for PCR and antibody tests for both HIV and coronavirus say that you may get a false positive if the person has one of about forty conditions. These include strep throat, “viral infections,” autoimmune disease, cancer, pregnancy, or nursing. In other words, any stress on the body provokes us to make more antibodies and have more degraded genetic material in our blood and other fluids— no surprise there. There is nothing in these tests that either proves viral causation or, absent purification, proves that the PCR snippet even came from the virus in question—nothing. It is simply a house of cards. (For more on on testing, see chapter 5.) 

Since these facts are obvious and easily proven, how can they have escaped the scrutiny of the “brilliant” men and women who run our healthcare system and populate the ranks of virologists? 

Once our health authorities declared that the multifactorial condition called “AIDS” was caused by a virus, they needed to come up with a way to treat it. The pharmaceutical companies (in particular, BurroughsWellcome), dusted off an old and very toxic drug called azidothymidine (AZT) and remarketed it for use with AIDS patients. 

AZT is a nucleoside analogue drug; it interferes with the production of DNA from the RNA supposedly contained in the HIV virus. The theory is that without the ability of the HIV virus to make copies of DNA, it can’t grow, replicate, and cause infection and disease. In practice, not only did AZT show much of the toxicity associated with cancer chemotherapy drugs (many of which also interfere with some aspect of DNA replication), it was shown to be worse than worthless in preventing the progression from asymptomatic to full-blown AIDS. 

In the first trial of AZT on asymptomatic HIV-positive people, AZT was given to 877 people, while 872 received a placebo. As soon as a patient developed any AIDS symptoms, he or she (15 percent were women) would be offered “open label” AZT. The mortality rates were shocking; over the three years of the trial, there were seventy-nine AIDS related deaths in the AZT group, but only 67 patients in the placebo group. So not only were you more likely to develop symptomatic AIDS if you took AZT compared to doing nothing, you were also subjected to all the usual toxicity of taking a chemotherapy drug.7 

Adverse effects of AZT include nausea, vomiting, acid reflux (heartburn), headache, sleep problems, and loss of appetite. Long-term adverse effects include anemia, neutropenia (low white blood cells), hepatotoxicity (liver toxicity), cardiomyopathy (problems with the heart muscle), and myopathy (muscle weakness). 

There are many parallels with today’s situation in which “antiviral” drugs actually increase the likelihood of having a bad outcome from this imaginary viral disease called coronavirus. 

In the wake of AIDS followed other “viral” diseases, including hepatitis C, SARS (Severe Acute Respiratory Syndrome), MERS (Middle East Respiratory Syndrome), bird flu, swine flu, Ebola, and Zika. Great sums were dedicated to finding viral causes and one-drug-fits-all cures, all following a familiar playbook: 

inventing the risk of a disastrous epidemic, incriminating an elusive pathogen, ignoring alternative toxic causes, manipulating epidemiology with non-verifiable numbers to maximize the false perception of an imminent catastrophe, and promising salvation with vaccines. This guarantees large financial returns. But how is it possible to achieve all of this? Simply by relying on the most powerful activator of human decision-making process—FEAR!8 

Needless to say, researchers have yet to prove that a virus causes any of these conditions. 

Fast-forward to November 2019, when authorities in China noticed that a group of people were getting sick in a new way. They noticed that many of the people who contracted this illness reported visiting a particular fish market in Wuhan, China. The symptoms were respiratory in nature, including dry cough. Of course, these symptoms are not altogether new, as people throughout history have suffered from a variety of respiratory diseases such as bronchitis, pneumonia, and asthma. Still, as the number of cases increased, authorities looked into the situation. There was a suspicion that a new disease had appeared, which naturally triggered a search for the cause. 

Because the symptoms of the sick people resembled pneumonia, some of the original patients received antibiotics. This was done because one of the recent “postulates” proving causation of an infectious disease states that if antibiotics fail to resolve the symptoms, this constitutes “presumptive” evidence (rather than “direct” evidence) that the pneumonia is caused by a virus (which obviously doesn’t respond to antibiotic therapy). Since the patients didn’t improve with antibiotic therapy, this triggered the hypothesis that the new type of pneumonia must be caused by a new or modified virus. 

Let’s consider our original ping-pong ball example given in chapter 1. The whole issue at this point revolves around whether the viral causation of this new set of symptoms can be proven. We want and should demand proof of causation, not a ping-pong ball in a bucket of stones and ice cubes, a computer simulation, an analysis of the virus, or the testimony of experts. We are betting our lives, our children, the world economy, and much more on the weight of the evidence. We need rock-solid proof; we need to follow the Koch’s or Rivers’ postulates, which entail a simple line of reasoning that any rational human being can recognize as the way to prove infectious causation. In other words, here is what should have happened in early 2020. 

As soon as the Chinese medical authorities suspected an outbreak of a new and dangerous disease, they should have collected about five hundred people with identical, or at least nearly identical, symptoms. Then they should have identified another group of equal size as matched controls— that is, people of a similar age, lifestyle and background, also from Wuhan, who had no symptoms. Given the possible slow development of this illness, it would have been prudent to follow the five hundred control people over at least a few months to make sure that none developed these new symptoms. 

The next step would be to do a thorough microbiological examination of a variety of fluids taken from these one thousand subjects. At a minimum, this should have included blood, sputum, urine, and nasal swabs. The examination should have included conventional light microscopy to look for bacteria and electron microscopy to look for viruses. 

Once a novel bacteria or virus was found in all the sick people and none of the well people, the bacteria or virus should have been meticulously isolated, purified, and cultured in a neutral medium (which is actually not possible for viruses, since they “grow” only in other living cells). Once this purification step was accomplished, the purified microbe should have been introduced into a test animal in the normal way that one suspected the microbe might be spreading—by airborne droplets— not injected directly into the brain of the animal as scientists like Pasteur did to “prove” the contagious etiology of rabies, TB, or polio. 

Finally, a control group of test animals should have been subjected to the same attempts at contamination. In other words, if you are going to spray purified virus into the animals’ nostrils to see whether they get sick, you need to spray pure saline into the nostrils of a control group of animals to make sure the animals are not getting sick just because you are spraying stuff up their noses. 

Any sane and logical person would agree that this is what should have happened. Finally, if for some reason the medical authorities in China were unable to carry out such an investigation, they should have enlisted the help of the CDC and the equivalent organizations in Europe and Russia, or the World Health Organization (WHO), to make sure the investigations were done carefully, properly, and thoroughly. 

The amazing part of this story is that not only do we lack this kind of evidence for a viral cause of Covid-19, we also lack this kind of evidence for the many “viral” epidemics we have faced during the last century, including polio, AIDS, SARS, Ebola, Zika, and hepatitis C. In fact, not a single part of this clear and simple proof has been attempted. 

Let’s look then at what was done to prove that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was the cause of this new set of symptoms. Four papers published in China are cited as proof that the new and novel coronavirus is the probable cause of this new disease.9 

For an in-depth analysis of these papers, please refer to a presentation by Andrew Kaufman MD,10 in which he dissects in great detail the methods and conclusions of these seminal studies. 

To review these four studies, let’s look again at Rivers’ postulates for determining whether a particular virus causes a disease. 

1.The virus can be isolated from diseased hosts. 

2.The virus can be cultivated in host cells. 

3.Proof of filterability—the virus can be filtered from a medium that also contained bacteria. 

4.The filtered virus will produce a comparable disease when the cultivated virus is used to infect experimental animals. 

5.The virus can be re-isolated from the infected experimental animal. 

6.A specific immune response to the virus can be detected. 

None of these four studies met all six postulates. Of the four studies said to prove that a coronavirus causes this disease, not one of them satisfied the first three postulates, and none of them even addressed postulates four and five. One paper claimed to find an immune response (postulate six) by looking at antibody levels from the patient. 

The first two papers are honest enough to claim only an association of coronavirus and the disease; the third paper claims that the coronavirus is “identified as the causative agent.” The fourth paper, from McMaster University, falsely claims that the coronavirus is the causative agent of the disease and that the virus “set in motion the pandemic,” with no evidence to back up these statements.

These papers never show that all the people with Covid-19 had the same set of symptoms; they never purify any virus from the sick people; they never demonstrate the absence of the virus from well people; and they never show that the transmission of purified virus could make well people become sick. This is scientific fraud of the first order. 

It’s interesting to look more closely at how virologists work to “prove” something like causation by coronavirus. One example is a paper published in 2003 in Nature, titled “Koch’s Postulates Fulfilled for SARS Virus.”11 Researchers claimed that Severe Acute Respiratory Syndrome is caused by a coronavirus. The title itself is misleading, if not dishonest, because the researchers satisfied neither Koch’s nor Rivers’ postulates. 

Here’s what they did: first they took respiratory secretions from some sick people; in other words, they took sputum from people with a cough. They centrifuged the sputum, which separates the cellular part (where presumably the virus is residing in the cells) from the liquid part. They discarded the liquid part. This is what they referred to as “purification.” Then they took this centrifuged, unpurified sediment from sick people, containing God-only-knows-what, and inoculated that into vero (monkey kidney) cells. Here we have to understand that if virologists want to get enough “virus” to use experimentally, they must grow it in a biological medium such as an animal or at least cells from an animal. Unlike bacteria, which can be grown in petri dishes, viruses are not alive, and they can “grow” only in other living cells. For convenience and because cancer cell lines are “immortal,” they generally grow their “viruses” in cancer cells; however, in this case they used kidney cells. This practice is fraught with obvious problems for proving it is the virus and not the kidney or cancer cells that are causing disease when these viruses then get injected into the test animals. Also, it is well known now that as part of their “detoxification” strategy, cells, especially cancer cells produce particles called exosomes, which are identical to “viruses.” (More on this in chapter 6.) 

Again, the researchers took unpurified sediment from the nasal mucus of sick people and grew that in vero cells until they got a sufficient quantity of cellular material to work with. Then they centrifuged this mess again, not even attempting to purify any virus from the mixture. Finally, they took this witch’s brew of snot sediment, kidney cells, and who knows-what-else and injected that into two monkeys. They didn’t do a control group by injecting saline into other monkeys or injecting vero cells into monkeys, or even injecting the liquid supernatant from the centrifuged material into monkeys. They just injected this cellular- debris laden goop. One monkey developed pneumonia and the other appeared to have respiratory symptoms possibly related to a lower respiratory disease. That, claim the researchers, is the proof that a “coronavirus” can cause disease. 

To be fair, in a related study,12 researchers did the exact same procedure, except to make it more reflective of how the new “virus” actually spreads, they took unpurified, lung-cancer-grown, centrifuged snot and (again, without any controls) squirted it down the throats and into the lungs of hamsters. (Where is PETA when you need them?) Some, but not all, of the hamsters got pneumonia, and some died. We have no idea what would have happened if they had squirted plain lung cancer cells into the lungs of these hamsters, but probably not anything good. And even more perplexing, some of the hamsters didn’t even get sick at all, which certainly doesn’t square with the deadly, contagious virus theory. 

In short, no study has proven that coronavirus, or indeed any virus is contagious, nor has any study proven anything except that virologists are a dangerous, misguided group of people and that hamster- and monkey rights people are not doing their jobs! 

This story is analogous to “proving” that the ping-pong ball can knock down walls by throwing a bucket of rocks and ice cubes containing a single ball at a small wall and showing that this does knock down the wall. These “proofs” make no sense and prove nothing, and yet the whole edifice of corona “virus” causation rests on these bogus studies. In chapter 5, we will deconstruct the equally bogus “testing” now used to provide what passes for supportive evidence of a viral causation. Stay with us, the ride gets more interesting as we go.



In a series of recent articles published in local and national news media, as well as in various scientific papers, some of the world’s leading medical doctors and immunologists have made surprisingly honest—and shocking —statements about coronavirus testing. The test used is called a PCR test —PCR means polymerase chain reaction. Here are some samples of these statements: 

“We did not perform tests for detecting infectious virus in the blood.”1 This statement came from a paper in which the authors allege they had discovered the novel coronavirus in patients suffering from Covid-19. 

“There is no way to tell whether the RNA being used in the new coronavirus PCR test is found in these particles seen under the electron microscope. There is no connection between the test and the particles, and no proof that the particles are viral.”2 Ironically, this statement does not come from a paper attempting to debunk the coronavirus causation of Covid-19. It comes from a paper that adamantly espouses this connection, but which claims that more research is needed to understand the interesting intricacies of this new virus. 

Or this, from the head of the Marin County Public Health Department, charged with making public health policy for Marin County, California: “The PCR tests means you either are infected with the novel coronavirus or you are not infected with the virus.”3 Such a statement is akin to going to the refrigerator store to purchase a new refrigerator and asking the salesman about a new model in the showroom. He says to you, “It’s a new and interesting model; it will either keep the food cool or it won’t.” Most people would not choose to elevate this person to head of refrigeration for Marin County. 

An NBC news feed reported on certain puzzling results: sailors who test positive, then negative, then positive for Covid-19 using the PCR test. This should not happen if the test is any good. A CDC representative stated, “Detection of viral RNA does not necessarily mean that infectious virus is present.”4 

According to one infectious disease expert at Vanderbilt University Medical Center in Nashville, “It’s possible that people could shed remnants of the virus for some period of time. That doesn’t mean anything is wrong with them or that they are contagious.”5 

These statements are all referring to the test used to claim that a person is infected and can spread the disease! When asked about these statements, the head of a lab that specializes in testing for infectious disease told us: “A positive PCR test means you have active disease or you are a carrier and don’t have active disease.” When we asked how to distinguish between those who have active disease and those who are carriers, she confidently replied: “Those with active disease are sick, the carriers are well.” 

Then we asked how one knows whether sickness is caused by the virus, since the test can be positive whether or not you are sick. She replied, “You can do a PCR test and find out whether the sick person has the virus.” Welcome to the Alice-in-Wonderland world of virology! 

Finally, the most revealing quote of all, this one from the chief of infectious diseases at Wake Forest Baptist Health in Winston-Salem, North Carolina: “We just don’t have enough details yet to make confident statements about immunology.”6 This quote is by an immunologist, and immunologists are the ones deciding public policy. They have put the world under house arrest. It would be nice if they could at least confidently say they knew something about immunology. 

How did this shocking situation concerning tests for viral diseases come about? Let’s return to the story of Stefan Lanka, PhD, a virologist from Germany, whom we discussed in chapter 3. Lanka’s work has helped cut through the veils behind which the field of virology is shrouded. As a young graduate student in Germany, Lanka made the chance discovery of the first virus in seawater. Using electron microscopy in his studies of sea algae, he noticed that the algae contained “particles.” To find out what these particles were, and knowing that no one had described viruses living within healthy algae before, he proceeded as follows: He ground up the algae in a sort of blender, essentially to break apart the walls of the algae. Then he purified this mixture using an extremely fine filter to separate out particles the size of viruses from everything else. In this way, he obtained a pure solution of water and viruses and anything else that is the size of a virus or smaller. Then he put this mixture into a density-gradient centrifuge, which spins the solution and allows the particles to separate out into bands. The final step uses a micropipette to suck out the band that contains only the virus.7 This simple procedure is the gold standard for the purification and isolation of a virus from any tissue or solution. It’s not an easy process, but it is not unduly difficult either. 

He could then study this purified virus under an electron microscope, elucidate its shape and structure, analyze the genome, and ascertain which proteins it contained. With this work, he could confidently state he had discovered a new virus and was sure of its makeup. For this discovery, he received his doctorate and was about to embark on a promising career as a virologist. 

The only part of Lanka’s experiment that surprised him was that in studying the interaction of algae with this new virus, he was forced to come to the conclusion that algae containing the virus were thriving and were much healthier than the algae without the virus, which were barely surviving. He may have been the first to come to the conclusion that real viruses in the bodies of other species are not pathogens (as was thought at the time) but rather are integral to the healthy functioning of the host. In essence, he was one of the first to propose that in addition to having a microbiome inside us, we also have a virome; and without this virome, we cannot be healthy. This was a radical concept in the 1980s, as no one else had proposed such a theory. 

If we compare the simple, logical, straightforward way in which Lanka isolated, purified, and characterized his virus, with the description of how modern virologists propagate viruses now, one begins to see the problem and confusion around testing for viral diseases. When Lanka realized that workers in the field of modern virology were never isolating, purifying, or properly characterizing “viruses” but instead confusing what they were finding with artifacts made by their propagation techniques, he naturally questioned whether the viruses that supposedly were causing disease even existed. His question was not so much about whether viruses are infectious entities, but something even more fundamental—whether these viruses even exist at all. 

Compare Lanka’s careful work with how current virologists find and characterize viruses, including the “novel coronavirus.” They start with sputum from a sick person, having no idea how this person got sick. They centrifuge but do not filter the sputum. This is not a purification process, as they readily admit in all of the papers written about the “coronavirus.” 

Here’s what the authors of the original papers that found and linked the “novel” coronavirus (SARS-CoV-2) to the disease now called “Covid-19” have to say. The following quotations come from the brilliant paper “Covid-19 PCR Tests are Scientifically Meaningless,” by Torsten Englebrecht and Konstantin Demeter.

Referring to a published image in a paper claiming to have isolated a new virus, they say, “The image is the virus budding from an infected cell. It is not purified virus.” 

If it’s not purified virus, how do the authors know whether or not it is even a virus, what it is, or where it came from?9 

In the paper “Identification of Coronavirus Isolated from a Patient in Korea with Covid-19,” the authors stated: “We could not estimate the degree of purification because we do not purify and concentrate the virus cultured in cells.” In other words, they did not isolate the virus, even though they claim to do so in the title.10 

In the article “Virus Isolated from the First Patient with SARSCoV-2 in Korea,” the authors admitted, “We did not obtain an electron micrograph showing the degree of purification.”11 In other words, the authors have no idea whether or not the sample is purified, as an electron micrograph is the only way to determine that. They then claim to have characterized the genetic material of something they never purified, having no idea what they were looking at. This was an important study, as it describes the first case of “Covid-19” in Korea. 

Finally, the article “A Novel Coronavirus from Patients with Pneumonia in China,” states: “We show an image of sedimented virus particles, not purified ones.”12 The researchers took nasal mucus (“snot”) from sick people, centrifuged it (which is not a purification step) and then showed a fuzzy picture of what they found. Then they carried out a “genetic analysis” of this sediment in order to characterize the “novel” coronavirus. This piece of fraud was published in the esteemed New England Journal of Medicine. 

What is in the centrifuged material that these papers describe? The centrifuged material contains bacteria and perhaps viruses, fungi, human cells, cell debris, and anything else found in the lungs or sinus passages of a sick person. Researchers then inoculate this unpurified mess onto “living tissue” to make it “grow.” Sometimes this tissue is lung cancer tissue, sometimes aborted fetal tissue, and sometimes tissue from monkey kidneys. In any case, it is a complex mixture of many components, known and unknown. And then because this “virulent, infectious virus” won’t infect and kill this living tissue unless you starve and poison the tissue first, you deprive the tissue of nutrients and add oxidizing agents to “weaken” the tissue. Then you add antibiotics to make sure it’s not bacteria that is killing the tissue. 

The tissue from this treatment naturally disintegrates into thousands of components. Then you centrifuge this mess again to find your “virus.” At that point, you start the PCR testing to determine the genetic and protein makeup of this “virus.” The problem is that (unlike the clear situation that Lanka encountered) in this slapdash way, you never have the isolated intact “virus” as a reference to allow you to know which genetic parts of your unpurified mess actually belong to the “virus” you are trying to characterize. 

As mentioned in chapter 3, after studying the way in which virologists said they had found the measles virus—without isolating and purifying it, and actually deciding on the genetic makeup by consensus—Lanka offered a prize of one hundred thousand Euros to anyone who could demonstrate its existence. In the first court to hear the proceedings, the claimant for the prize won the case, the judge concluding that proof of the measles virus did indeed exist. However, the German Supreme Court, with its more stringent rules of evidence and the appointment of a science master to oversee the case, ruled that the claimant, in fact, did not prove the existence of the measles virus. Lanka did not have to pay the claim. 

How is Lanka’s work relevant to the current test used to detect the presence of viruses, specifically for the coronavirus? Clearly, if one can’t prove that the coronavirus even exists and that the testing for this imaginary virus is bogus, then the world has been led wildly astray. If the test for the coronavirus is inaccurate and misleading, as is the case, then there are no grounds for believing the reports about the number of Covid19 cases, the number of Covid-19 deaths, or any other statistics coming from the orthodox medical institutions. If the testing is bogus, then the coronavirus emperor has no clothes. 

Let’s contrast Lanka’s elegant experiments with the testing procedures used to determine the alleged presence of coronavirus (SARSCoV-2) “infection.” 

The first thing we need to understand about a PCR (polymerase chain reaction) test is that it is a surrogate test—it does not find a virus; rather, it finds something else said to indicate the presence of the virus. A surrogate test is one that is generally easier and less expensive to perform and can stand in for the gold-standard test (of actually finding the virus) and thereby make the clinical practice of medicine easier, safer, and cheaper. 

For example, pulmonary emboli result from blood clots that travel to the lungs. Symptoms include chest pain and shortness of breath. Pulmonary emboli can be fatal. It is important to diagnose the condition early, as it can be treated with blood thinners. It is also important to diagnose accurately, as pulmonary emboli share many symptoms with heart attacks and pneumonia, which call for different kinds of treatment. 

Fortunately, there is a test that is 100 percent reliable for finding pulmonary emboli when performed properly. The procedure, called an angiogram, involves inserting a catheter into the arteries of the lungs. Then the radiologist injects dye into the artery; the dye contains heavy metals that one can see on an X-ray. If a clot is present, the angiogram reliably and accurately demonstrates its presence to the radiologist on the real-time X-ray. With this test, referred to as the “gold standard,” one can confidently say whether or not the patient has an embolus. 

Angiography, however, is technically challenging. It is difficult to find the artery with the catheter. It is costly, due to the time and equipment needed. It is dangerous, as the artery may tear during insertion of the catheter. Another problem with angiography is that it requires injecting heavy metals into the artery and subjecting the patient to a lot of radiation. 

Consequently, medicine has looked for a surrogate test that can more easily and safely detect pulmonary emboli. The V/Q scan looks at the blood flow into and through the lungs and compares this with the air movement into and through the lungs. When all is well with the lungs, these two parameters match up. When an embolus is present, they usually don’t match up because blood flow is compromised. This allows the diagnostician to surmise that even though they have not actually seen a clot, it is likely to be present. 

A surrogate test is one that does not look for what you need to find but rather for something likely to be there if the condition is present. The surrogate test allows doctors to make an educated guess. To validate a surrogate test, one must first do a careful study in which the surrogate test is compared to the gold standard test. This gives you exact information as to how accurate you can expect the surrogate testing to be. These validating studies are usually carried out at a large medical center or a group of medical centers. The researchers begin by finding a large number of patients—say two thousand—with symptoms typical of pulmonary emboli. For simplicity’s sake, let’s say that one thousand do have an embolus as demonstrated with an angiogram, the gold standard test, whereas the other one thousand do not. Now, we have a group of people who either have or don’t have the condition we are testing for. Then we do a V/Q scan on each of these two thousand patients. In the group that we know has an embolus, if nine hundred are positive on the V/Q scan, then we know that the surrogate test picks up the diagnosis 90 percent of the time. In the other 10 percent, for whatever reason, the surrogate test fails to demonstrate the emboli even though we know it’s there. We now know that the false negative rate is 10 percent. This allows the clinician to forgo the more difficult angiogram because they know how likely the V/Q scan will be to pick up the embolus if it is there. They also know that in the event that the test is negative they still have a 10 percent chance the test missed it. In that case, they may want to move to the angiogram if the level of suspicion is high that the patient does, in fact, have an embolus in spite of the negative V/Q scan. This is basically the art of modern medicine.

Likewise, the researchers can then take the one thousand people who test negative on the angiogram, do a V/Q scan on all of them, and determine the false positive rate. If one hundred subjects test positive on the V/Q scan even though you know for sure they have no clot, then you can accurately and confidently say that for whatever reason 10 percent of the time the V/Q scan is saying you have a clot when you don’t. Again, this helps the clinician who may be confronted with a patient whom he is pretty sure doesn’t have a clot (for example, they may have evidence of pneumonia or a heart attack) but orders a V/Q scan anyway. If the V/Q scan is positive they may want to confirm this by moving on to an angiogram because they know that in 10 percent of the cases the V/Q scan is falsely positive. Clearly the lower the number of false positives and false negatives, the better and more reliable is the test. 

The point is, without having a gold standard test with which to compare your surrogate test, and without this comparison having been performed in the clearest and most meticulous way possible, there is no possibility of having an accurate surrogate test. To be even clearer, without this comparison, the surrogate test is completely useless and misleading . . . completely—yet officials are using surrogate Covid-19 tests to send people into nursing homes, remove children from their families,13 and even separate newborn babies from their mothers if the mom tests positive!14 

PCR tests, antibody tests, and every other test for a “coronavirus” are surrogate tests, which have never been compared to any gold standard; therefore, they are completely and utterly useless and misleading. They are propaganda, not science. 

The gold standard test for a viral infection is the isolation, purification, and characterization of the virus (as outlined in the description of Lanka’s experiment) and the proving of contagion. Lanka didn’t prove that the virus he found was contagious simply because it isn’t, and no virus is contagious. This is the only possible gold standard there can be. 

The PCR test examines the pieces of genetic material taken from a swab from the back of the sinus cavity (a very unpleasant procedure). No research has shown that this genetic material is unique to that of coronavirus or even that it comes from a coronavirus. 

Furthermore, in order to examine this genetic material, the test “amplifies” it. An amplification cycle means they start with a probe that matches the snippet of DNA or RNA they are looking for. Then, because this is too small to detect, they repeatedly double the snippets. If the sample changes the color of a solution, the test is considered positive. If you do too few amplification cycles, you never find the snippet, resulting in a false negative. If you do too many amplification cycles, you find the snippet too often because the test also amplifies the background genetic snippets (“noise”). These are false positives. 

One can therefore manipulate the amplification cycles to get whatever result one wants. Too few cycles and everyone tests negative; too many cycles and most test positive. 

John Magufuli, president of Tanzania, may be the wisest world ruler alive today. A chemist by training, Magufuli submitted samples to the World Health Organization (WHO) for testing. Said Magufuli, “We took samples from goats; we sent samples from sheeps; we took samples from pawpaws; we sent samples from car oil; and we took samples from other different things; and we took the samples to the laboratory without them knowing.” His officials named the sample of car oil Jabil Hamza, thirty years old, male. The results came back negative. They named a sample of jackfruit Sarah Samuel, age forty-five, female. The results came back inconclusive. Pawpaw got sent in as Elizabeth Ane, twenty-six years old, female. The poor pawpaw came back positive. Samples from a bird called kware and from a goat also tested positive; rabbit was indeterminate; sheep was negative.15 President Magufuli is not wasting any government money on testing for his people, but in the West, governments have spent millions for the PCR test kits. 

Since no PCR test has ever undergone comparison to any gold standard, the results are meaningless. This is not a situation where we just need better or more accurate testing. As Kary Mullis, the inventor of the PCR technology, has insisted, time and again, PCR tests do not prove causation and cannot diagnose illness.16 

The CDC and the FDA concede that the PCR test cannot be used for diagnosis. A file from March 30, 2020, stated: “Detection of viral RNA may not indicate the presence of infectious virus or that 2019-nCoV is the causative agent for clinical symptoms” and “This test cannot rule out diseases caused by other bacterial or viral pathogens.”17 

Furthermore, the FDA admits that “positive results … do not rule out bacterial infection or co-infection with other viruses. The agent detected may not be the definite cause of disease.”18 

According to a product announcement for the LightMix® Modular SARS-CoV Assays, “These assays are not intended for use as an aid in the diagnosis of coronavirus infection.”19 

One can only wonder what exactly the test is supposed to do if not diagnose a coronavirus infection? 

The same methodological problems are found with the new antibody tests for assessing immunity to “coronavirus.” Antibody testing is another type of surrogate testing that does not diagnose illness or ascertain its cause. A brilliant paper by David Crowe 20 explains in detail the fact that the theoretical underpinnings of antibody testing have not been demonstrated in any experiment. This is why the Wake Forest immunologist had to admit, “we don’t know enough about immunology to make any conclusions.” 

Scientists believe that antibodies have a predictable and exact course as they track a viral infection. Antibodies are proteins made by our immune system to either fight off an illness or “remember” that we have encountered an infectious organism like a virus—at least, this is what we’ve been told. The theory is that before we encounter a virus or get sick from a virus, we have no antibodies to it. After getting sick, the PCR test should detect the virus (or, more accurately, the genetic pieces we think could have come only from that virus). Then after one week (because viruses and our immune system seem to understand the concept of one week), we begin to make an antibody called IgM, which is not specific to this coronavirus but is made by our immune system to fight off any virus. Then on day fourteen, as the virus is cleared from your body, the PCR test goes back to negative, the IgM levels go down, and we see the appearance of the more targeted IgG antibody. Then at day twenty-one (because viruses understand that this happens in weekly intervals), the IgM is gone, the antibody test is reliably negative, and the IgG has peaked. At day twenty-eight (because your immune system also understands weeks), the IgG level drops to a level it can sustain for the long term. Once the test manufacturer or virologist sees a stable IgG level, they supposedly know you are immune for life from the effects of the virus . . . or maybe not. 

This theoretical and imaginary construct has many holes big enough that you could drive a truck through them. Consider the following: it turns out that a small percentage actually have IgM, IgG, or both antibodies months before having the “infection.” 21 How this is possible, since this is a novel virus that humans have never seen before, is not explained. 

Finally, studies show that IgG sometimes appears before and sometimes appears after IgM; sometimes there is no IgM; sometimes there is no IgG.22 In either case, it may mean you either had the virus or you didn’t. And as with AIDS, there is no proof that a particular level of IgG confers immunity. 

Ah, but virologists have an explanation for this: these new wily viruses somehow know how to escape detection and neutralization even if the person has a robust antibody response! That, of course, is nonsense. 

Then we’re told that a positive PCR test means you are either sick or not sick, infectious or not infectious, and that sometimes the test is positive, then negative, then positive, then negative. It’s enough to make even the Mad Hatter go silent with disbelief!



After reading the last two chapters you may be shaking your head in disbelief; you may have so many questions swirling in your mind that you feel disoriented. The main question for us all is how the entire world of medicine, virology, and immunology, along with our political leaders, could have made such an obvious mistake? How could generations of doctors and researchers have become convinced that many of our common diseases are viral in origin? [let me think...greed,being a coward,and the main problem at least here in America is that at this time is it appears that for the first time in over 50 years, we actually have someone who wants to lead, the problem is all the politicians who are desperate to get rid of him DC]  

Let’s first provide the scientific basis for challenging the notion of contagion. As we have said, an in-depth look at the scientific literature reveals no proof of the contagion theory, but the alternate explanations for so-called “bacterial” or “viral” illness do have research behind them. Only Western medicine invokes the concept of contagion—person-to-person transmission of harmful bacteria or viruses. Neither traditional Chinese medicine (TCM) nor Ayurveda (a system of medicine with historical roots in the Indian subcontinent) entertains the concept of contagion. These ancient healing systems look at imbalances, diet and toxins as the causes of disease. 

So how did the theory of viral causation come about? During the late 1800s, with the popularity of Pasteur and the increasing materialistic thinking of the age, the germ theory gained popularity. The germ theory explained common observations, such as why drinking sewage water made people sick and why people who share a workspace or household seem to get sick in a similar way at the same time. With the advent and widespread use of the light microscope, scientists and doctors could clearly identify bacteria associated with particular illnesses. 

In the nineteenth century, scientists and physicians assumed that the teeming forms they saw in their microscopes caused disease and were hostile to life. In writing On the Origin of Species (published in 1859), Charles Darwin (a contemporary of Pasteur) proposed a theory of evolution in which only the plants and animals best adapted to their environment survive to reproduce. He painted a picture of life in which the various organisms were in constant struggle against each other. Darwin borrowed popular concepts (such as “survival of the fittest”) from sociologist Herbert Spencer and “struggle for existence” from economist Thomas Malthus. The notion of hostility and competition in all of nature fit with attempts to justify the social inequalities, poverty, and sufferings that characterized the dawning Industrial Age. Social Darwinism actually preceded biological Darwinism! 

For all the known “infectious” bacterial illnesses, the science points to other accurate explanations—namely starvation and poisoning. However, the microscope gave scientists the ability to find germs at the site of disease. Their observations revolutionized the practice of medicine and our thinking. The microscope allowed medicine to enter a “scientific” age and provide a ready and easy explanation for illness—one that circumvented the more difficult and less profitable work of cleaning up the cities, improving diets, mitigating poverty, and reducing pollution. 

However, bacteria are found at the site of disease for the same reason that firemen are found at the site of fires. Bacteria are the cleanup crew tasked with digesting and getting rid of dead and diseased tissues. Claiming that bacteria cause a certain disease is no more reasonable than claiming that firemen cause fires, especially as experimental evidence shows this to be false. Likewise, maggots on a dead dog are there to clean up dead tissue—no one would accuse the maggots of killing the dog. In fact, one therapy for necrotic tissue is maggot therapy (applying maggots to the wound). The maggots kill only the dead tissue; when there is only live tissue left to eat, they die off. 

But scientists could not always find an offending bacterium for a specific disease. Louis Pasteur could not find a bacterial agent for rabies, and he speculated about a pathogen too small to be detected using a microscope.1 The same held true for polio—hard as they tried, scientists could find no bacteria at the site of the illness.2 Following Pasteur, and completely wedded to germ theory, they postulated a tiny enemy, something that our technology could not yet visualize. The search was on to find this disease-causing organism. 

The eureka moment came with the invention of the electron microscope; scientists finally saw tiny “particles” at the site of disease. These particles had “stuff” inside them, suggesting they were “alive.” They were more abundant in diseased tissue than in healthy tissue (although this is not what Lanka found in algae). There were variations between types of particles, suggesting that one type of particle caused one disease and another particle type caused a different disease. Immediately assuming that these particles were bad for us, scientists named them viruses, after the Latin word for “toxin.” 

Further research revealed that these particles often emerged from within the cell; this led to the conclusion that these viruses were not just bad for the cell in which they resided, but they could invade other cells. Scientists surmised that viruses co-opted the “machinery” of the cell like parasites, turning the cells into “slaves,” meaning the cell would do the bidding of its new master, the infecting particle. Like alien invaders in science fiction movies, the particle would come from the outside, inject itself into the cell, take over the genetic machinery of the cell, reproduce itself by the thousands, and then emerge from the cell to continue on its evolutionary path, spreading to take over the world. 

The wily virus theory was born—except that what scientists had really discovered with their electron microscopes was not viruses but exosomes. The only thing infectious in this scenario was the noxious belief that these small particles, dubbed viruses, caused disease. This false theory was the part that spread all over the world and is now threatening to kill us all. 

Exosomes are simple, well-characterized features in the cells of all creatures, and conventional scientists have carefully elucidated their functions.3 When a living organism is threatened in almost any way— through starvation, chemical poisoning, or electromagnetic effects—the cells and tissues have a mechanism for “packaging,” “propagating” and releasing these poisons. Modern researchers have shown that exosomes have exactly the same attributes as “viruses.” They are the same size, contain the same components, and act on the same receptors.

HIV researcher James Hildreth, president and CEO of Meharry Medical College and former professor at Johns Hopkins, put it this way: “The virus is fully an exosome in every sense of the word.”5 Exosomes are completely indistinguishable from what the virologists have been calling “viruses.” 

Here’s how exosomes work: let’s say you have a poorly nourished organism, then you expose it to a common environmental toxin. The tissues and cells that are affected begin to produce, package, and secrete these poisons in the form of exosomes. This is a way of ridding the cells and tissues of substances that would do it great harm. The greater the exposure to toxic assaults, the more exosomes will be produced. 

Studies have shown that if one somehow stops the cells from producing and excreting these exosomes, then the cells and tissues, in fact the organism, will have a worse outcome.6 This research demonstrates that the production and excretion of exosomes is a crucial detoxification function of all cells and tissues. 

Another clearly demonstrated function of these exosomes is that they act as a kind of key that circulates in the blood and lymph of organisms, such as mammals and humans, until they find a distant cell with a lock into which this key fits.7 The exosome acts as a messenger, essentially warning the other cells and tissues that danger is afoot and that they need to prepare. 

Far from acting as hostile invading viruses, exosomes provide a brilliant system of communication within an organism to rid the cells and tissues of poisons and then communicate to the rest of the organism what has happened.8 Far from acting as a source of illness, these particles are an integral part of our detoxification system. They are the true firemen, obviously present in higher amounts in cases of disease, in which a higher burden of poisoning has occurred. 

In fact, these “viruses” are not invaders but toxin-gobbling messengers that our cells produce to help us adjust to environmental assaults, including electro-smog.9 After all, most people have adjusted to worldwide radio waves, electricity in our homes, and ubiquitous Wi-Fi— and the sparrow population rebounded after the Great Plague of 1738. It is exosomes that allow this to happen. These tiny messengers provide real time and rapid genetic adaptation to environmental changes. (Whether these exosomes can help us adapt to the extreme disruption of 5G is the question of the day.) 

If you do an Internet search, you will find that exosomes are the latest thing in medicine, used as a treatment for cancer, antiaging products, facial rejuvenation, hair regrowth, and even “exosome penis treatment.”10 

Finally, the research shows that toxic exposure, including exposure to fear and stress, increases exosome production.11 This should come as no surprise to any honest observer of sickness and health since many have noted that stressed, worried, fearful people get sick easier, so it makes sense that you would find increased detoxification “products” in their tissues. 

There is now clear experimental evidence that exosomes made by one organism can be picked up by other organisms (of the same or different species) and cause protective reactions in these new organisms.12 

One study showed that if mice are exposed to the liver toxin known as acetaminophen (Tylenol), the liver cells increase their production of protective exosomes. The researchers isolated and purified these exosomes and exposed other mice to them. The second group of mice did not get sick, as would be predicted by the virus theory; instead they developed protective responses in their livers and secreted more exosomes.13 

This is similar to what trees do when confronted with a beetle infestation. The originally affected tree produces chemicals that help the tree survive the beetle exposure. These same chemicals are secreted, with the help of the fungus or mycelium in the soil, through the root system of the tree. These chemicals then serve as messengers to the surrounding trees, telling them that beetles have taken hold and that protective measures may be needed. If the beetles go away, then these measures are not taken; if the beetles show up, the surrounding trees also produce a protective response. 

The real point here is that thanks to exosomes, nature is not raw in tooth and claw but a superb cooperative venture. The originally affected tree is not competing for survival with the other trees; the affected tree needs the other trees in order to survive and thrive. We need each other— members of our own species and other species—otherwise none of us will survive. 

The germ theory is wrong; the virus theory is wrong. Viruses are not here to kill us; in reality they are exosomes whose role is to provide the detoxification package and the communication system that allows us to live a full and healthy existence. A war on viruses is a war on life. 

It’s clear that the misidentification of exosomes as viruses was a tragic mistake, one that it’s about time we correct, once and for all. 

What we know about exosomes can help us solve the mystery of childhood diseases like chicken pox and measles, and also of STDs, which seem to require an explanation of “contagious.” This will be the subject of the next chapter.




Chapter 4 

1.Torsten Engelbrecht and Claus Kohnlein, Virus Mania, 21

2.Ibid, 90. 

3.PM Sharp and BH Hahn, “Origins of HIV and the AIDS pandemic,” Cold Spring Harbor Perspectives in Medicine 1, no. 1 (September 2011), a006841. doi:10.1101/cshperspect.a006841. PMC 3234451. PMID 22229120. 3.

4.The three best are books on this subject are Virus Mania by Torsten Engelbrecht and Claus Kohnlein; The Silent Revolution in AIDS and Cancer by Heinrich Kremmer; and AIDS, Opium, Diamonds and Empire by Nancy Banks.

5.NS Padian et al, “Heterosexual Transmission of Human Immunodeficiency Virus (HIV) in Northern California: Results From a Ten-Year Study,” Am J Epidemiol 146, no. 4 (August 15, 1997): 350-7. doi: 10.1093/oxfordjournals.aje.a009276.

6.M Fioranelli et al, “5G Technology and induction of coronavirus in skin cells,” Journal of Biological Regulators & Homeostatic Agents 54, no. 4 (June 9, 2020). 

7.Simon Garfield, “The rise and fall of AZT: It was the drug that had to work. It brought hope to people with HIV and AIDS, and millions for the company that developed it. It had to work. There was nothing else. But for many who used AZT - it didn’t,” The Independent, May 2, 1993, and-fall-of-azt-it-was-the-drug-that-had-to-work-it-brought-hope-to-people-with-hiv-and2320491.html.l 

8.Torsten Engelbrecht and Claus Kohnlein, Virus Mania, 11

9. Peng Zhou et al, “Discovery of a novel coronavirus associated with the recent pneumonia outbreak in humans and its potential bat origin,” bioRxiv. doi:; Na Zhu et al, “A Novel Coronavirus from Patients with Pneumonia in China, 2019,” N Engl J Med 382 (February 20, 2020) 727- 733, DOI: 10.1056/NEJMoa2001017.; Jeong-Min Kim et al, “Identification of Coronavirus Isolated From a Patient in Korea With COVID-19,” Osong Public Health Res Perspect.11, no. 1 (February 2020): 3-7.doi: 10.24171/j. phrp.2020.11.1.02.; Karen Mossman, “I study viruses: How our team isolated the new coronavirus to fight the global pandemic,” McMaster University, March 25, 2020, 

10.“The Rooster in the River of Rats,” by Andrew Kaufman, MD,

11. R AM Fouchier et al, “Koch’s postulates fulfilled for SARS virus,” Nature 423 (2003): 240. 

12.JFW Chan et al, “Simulation of the Clinical and Pathological Manifestations of Coronavirus Disease 2019 (COVID-19) in Golden Syrian Hamster Model: Implications for Disease Pathogenesis and Transmissibility,” Clin Infect Dis. (March 26, 2020), ciaa325. doi: 10.1093/cid/ciaa325. 

Chapter 5 

1.C. Huang et al, “Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China,” The Lancet (January 24, 2020), 

2.David Crowe, Flaws in Coronavirus Pandemic Theory, 5, 

3.Peter Fimrite, “Studies show coronavirus antibodies may fade fast, raising questions about vaccines,” San Francisco Chronicle, July 17, 2020, 

4.“Clinical Questions about COVID-19: Questions and Answers,” Accessed July 26, 2020. 

5.Erika Edwards, Courtney Kube and Mark Schone, “Some have tested positive for COVID-19 after recovering. What does that mean?” NBC News, May 19, 2020, 


8.Torsten Engelbrecht and Konstantin Demeter, “COVID-19 PCR Tests Are Scientifically Meaningless,” OffGuardian, June 27, 2020, pcr-tests-are-scientifically-meaningless/?fbclid=IwAR0OFMLQoW85YSrDczm8rjLC1cCJmJ4lIIoW3_-PIYYJRypsmgh2CH8fJ4. 

9.L Leo et al, “Emergence of a novel human Coronavirus threatening human health,” Nature Medicine (March 2020).. 

10.Myung-guk Han et al, “Identification of Coronavirus Isolated from a Patient in Korea with COVID-19,” Song Public Health and Research Perspectives (February 2020). 

11.Wan Beom Park et al, “Virus Isolated from the First Patient with SARS-CoV-2 in Korea,” Journal of Korean Medical Science (February 24, 2020). 

12.Na Zhu et al, “A Novel Coronavirus from Patients with Pneumonia in China, 2019,” New England Journal of Medicine (February 20, 2020). 

13.Danielle Wallace, “Ventura County clarifies claims it would force people from homes into isolated coronavirus centers,” Fox News, May 7, 2020, 

14.Adrianna Rodriguez, “‘Heartbreaking’: Moms could be separated from their newborns under coronavirus guidelines,” USA Today, March 26, 2020, could-separated-babies-birth/2907751001/. 

15.Jessica Lee, “Did Tanzania’s President Expose Faulty COVID-19 Testing by Submitting Non-Human Samples?” Snopes, May 7, 2020, 

16.James Herer, “Coronavirus: The Truth about PCR Test Kit from the Inventor and Other Experts,” Weblyf,

17. “CDC 2019-Novel Coronavirus (2019-nCoV) Real-Time RT-PCR Diagnostic Panel,” Centers for Disease Control and Prevention, 

18.“Accelerated Emergency Use Authorization (Eua) Summary Covid-19 Rt-Pcr Test (Laboratory Corporation Of America),” 

19. documentID=1cca7ff9-388a-ea11-fa90- 005056a772fd&fileName=TP00886v2&extension=pdf&mimeType=application%2Fpdf& inline=False 

20.David Crowe, “Antibody Testing for COVID-19,” May 13, 2020, 

21.F Zhou et al, “Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study,” The Lancet (March 11, 2020), 22 1 2 3 4 5 6 7 8 9 11 10 

22. R. Prasad, “Meta-analysis does not support continued use of point-of-care serological tests for COVID-19,” The Hindu, July 4, 2020, 

Chapter 6 

1.G. Bordenave, “Louis Pasteur (1822–1895),” Microbes and Infection / Institut Pasteur 5, no. 6 (May 2003): 553–60, doi:10.1016/S1286-4579(03)00075-3. 

2.“Dr. Stefan Lanka Debunks Pictures of ‘Isolated Viruses,’” Vaccination Information Network, 

3.MD Keller et al, “Decoy exosomes provide protection against bacterial toxins,” Nature 579 (2020): 260–264 (2020); “Newfound Cell Defense System Features Toxin-Isolating ‘Sponges,’” Yahoo Finance, March 4, 2020, 

4.G Pironti et al, “Circulating Exosomes Induced by Cardiac Pressure Overload Contain Functional Angiotensin II Type 1 Receptors,” Circulation no. 131 (2015): 2120–2130, Originally published 20 May 2015, 

5.William A. Wells, “When is a virus an exosome?” Journal of Cell Biology 162, no. 6 (2003): 960, 

6.“Newfound Cell Defense System Features Toxin-Isolating ‘Sponges,’” Yahoo Finance, March 4, 2020, 

7.G Raposo and W Stoorvogel, “Extracellular vesicles: Exosomes, microvesicles, and friends,” J Cell Biol 200, no. 4 (February 18, 2013): 373–383, doi: 10.1083/jcb.201211138. 

8.C Frühbeis et al, “Extracellular vesicles as mediators of neuron-glia communication,” Front Cell Neurosci 7 (2013): 182. Published online 2013 Oct 30. doi: 10.3389/fncel.2013.00182. 

9.OD Mrowczynski et al, “Exosomes impact survival to radiation exposure in cell line models of nervous system cancer,” Oncotarget 9, no. 90 (November 16, 2018): 36083– 36101. Published online 2018 Nov 16, doi: 10.18632/oncotarget.26300. 


11.J Smythies J et al, “Molecular mechanisms for the inheritance of acquired characteristics —exosomes, microRNA shuttling, fear and stress: Lamarck resurrected?” Front Genet 5 (2014): 133. Published online 2014 May 15. Prepublished online April 16, 2014. doi: 10.3389/fgene.2014.00133; KeFang et al, “Differential serum exosome microRNA profile in a stress-induced depression rat model,” Journal of Affective Disorders 274 (September 1, 2020):144–158, 12 13 1 2 3 2 3 5 6 7 8 9 1 4 

12.YE Young-Eun Cho et al, “Exosomes: An emerging factor in stress-induced immunomodulation,” Seminars in Immunology 26, no. 5 (October 2014): 394–401. 

13.W Seo et al, “Exogenous exosomes from mice with acetaminophen-induced liver injury promote toxicity in the recipient hepatocytes and mice,” Scientific Reports 8, Article number: 16070 (2018), Published: October 30, 2018.

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