UPDATE 09. October 2020: NYT tries to maintain the 'virus narrative' with computer-gaming scientists: The Coronavirus Unveiled?

UPDATE 14. July 2020:  Medical Empire Beats Back: 'People have died from the coronavirus, contrary to article claiming to report pathologist’s “revelations” on COVID-19.'

ICYMI: Viral Realities Revealed: Dr John Lee, Pathology Professor + 12 COVID-19 Autopsy Cases Reveal the TRUTH How COVID-19 Patients Dying - Doctor Explains

PROLOGUE: There is so far still NO proof even for the existence of SARS-CoV-2 Virus ❗️

“No one has died from the coronavirus”

Important revelations shared by Dr Stoian Alexov, President of the Bulgarian Pathology Association

Artistic view of what is called corona virus

By Rosemary Frei and Patrick Corbett - 02. July 2020

A high-profile European pathologist is reporting that he and his colleagues across Europe have not found any evidence of any deaths from the novel coronavirus on that continent.

Dr. Stoian Alexov called the World Health Organization (WHO) a “criminal medical organization” for creating worldwide fear and chaos without providing objectively verifiable proof of a pandemic.

Another stunning revelation from Bulgarian Pathology Association (BPA) president Dr. Alexov is that he believes it’s currently “impossible” to create a vaccine against the virus.

He also revealed that European pathologists haven’t identified any antibodies that are specific for SARS-CoV-2.

These stunning statements raise major questions, including about officials’ and scientists’ claims regarding the many vaccines they’re rushing into clinical trials around the world.

They also raise doubt about the veracity of claims of discovery of anti-novel-coronavirus antibodies (which are beginning to be used to treat patients).

Novel-coronavirus-specific antibodies are supposedly the basis for the expensive serology test kits being used in many countries (some of which have been found to be unacceptably inaccurate).

And they’re purportedly key to the immunity certificates coveted by Bill Gates that are about to go into widespread use — in the form of the COVI-PASS — in 15 countries including the UK, US, and Canada.

Dr. Alexov made his jaw-dropping observations in a video interview summarizing the consensus of participants in a May 8, 2020, European Society of Pathology (ESP) webinar on COVID-19.

The May 13 video interview of Dr. Alexov was conducted by Dr. Stoycho Katsarov, chair of the Center for Protection of Citizens’ Rights in Sofia and a former Bulgarian deputy minister of health. The video is on the BPA’s website, which also highlights some of Dr. Alexov’s main points.

We asked a native Bulgarian speaker with a science background to orally translate the video interview into English. We then transcribed her translation. The video is here and our English transcript is here.

Among the major bombshells Dr. Alexov dropped is that the leaders of the May 8 ESP webinar said no novel-coronavirus-specific antibodies have been found.

The body forms antibodies specific to pathogens it encounters. These specific antibodies are known as monoclonal antibodies and are a key tool in pathology. This is done via immunohistochemistry, which involves tagging antibodies with colours and then coating the biopsy- or autopsy-tissue slides with them. After giving the antibodies time to bind to the pathogens they’re specific for, the pathologists can look at the slides under a microscope and see the specific places where the coloured antibodies — and therefore the pathogens they’re bound to – are located.

Therefore, in the absence of monoclonal antibodies to the novel coronavirus, pathologists cannot verify whether SARS-CoV-2 is present in the body, or whether the diseases and deaths attributed to it indeed were caused by the virus rather than by something else.

It would be easy to dismiss Dr. Alexov as just another crank ‘conspiracy theorist.’ After all many people believe they’re everywhere these days, spreading dangerous misinformation about COVID-19 and other issues.

In addition, little of what Dr. Alexov alleges was the consensus from the May 8 webinar is in the publicly viewable parts of the proceedings.

But keep in mind that whistleblowers often stand alone because the vast majority of people are afraid to speak out publicly.

Also, Dr. Alexov has an unimpugnable record and reputation. He’s been a physician for 30 years. He’s president of the BPA, a member of the ESP’s Advisory Board and head of the histopathology department at the Oncology Hospital in the Bulgarian capital of Sofia.

On top of that, there’s other support for what Dr. Alexov is saying.

For example, the director of the Institute of Forensic Medicine at the University Medical Center Hamburg-Eppendorf in Germany said in media interviews that there’s a striking dearth of solid evidence for COVID-19’s lethality.

“COVID-19 is a fatal disease only in exceptional cases, but in most cases it is a predominantly harmless viral infection,” Dr. Klaus Püschel told a German paper in April. Adding in another interview:

In quite a few cases, we have also found that the current corona infection has nothing whatsoever to do with the fatal outcome because other causes of death are present, for example, a brain hemorrhage or a heart attack […] [COVID-19 is] not particularly dangerous viral disease […] All speculation about individual deaths that have not been expertly examined only fuel anxiety.”

Also, one of us (Rosemary) and another journalist, Amory Devereux, documented in a June 9 Off-Guardian article that the novel coronavirus has not fulfilled Koch’s postulates.

These postulates are scientific steps used to prove whether a virus exists and has a one-to-one relationship with a specific disease. We showed that to date no one has proven SARS-CoV-2 causes a discrete illness matching the characteristics of all the people who ostensibly died from COVID-19. Nor has the virus has been isolated, reproduced and then shown to cause this discrete illness.

In addition, in a June 27 Off-Guardian article two more journalists, Torsten Engelbrecht and Konstantin Demeter, added to the evidence that “the existence of SARS-CoV-2 RNA is based on faith, not fact.”

The pair also confirmed “there is no scientific proof that those RNA sequences [deemed to match that of the novel coronavirus] are the causative agent of what is called COVID-19.”

Dr. Alexov stated in the May 13 interview that:

the main conclusion [of those of us who participated in the May 8 webinar] was that the autopsies that were conducted in Germany, Italy, Spain, France and Sweden do not show that the virus is deadly.”

He added that:

What all of the pathologists said is that there’s no one who has died from the coronavirus. I will repeat that: no one has died from the coronavirus.”

Dr. Alexov also observed there is no proof from autopsies that anyone deemed to have been infected with the novel coronavirus died only from an inflammatory reaction sparked by the virus (presenting as interstitial pneumonia) rather than from other potentially fatal diseases.

Another revelation of his is that:

“We need to see exactly how the law will deal with immunization and that vaccine that we’re all talking about, because I’m certain it’s [currently] not possible to create a vaccine against COVID. I’m not sure what exactly Bill Gates is doing with his laboratories – is it really a vaccine he’s producing, or something else?”

As pointed to above, the inability to identify monoclonal antibodies for the virus suggests there is no basis for the vaccines, serological testing and immunity certificates being rolled out around the globe at unprecedented speed and cost. In fact, there is no solid evidence the virus exists.

Dr. Alexov made still more important points. For example, he noted that, in contrast to the seasonal influenza, SARS-CoV-2 hasn’t been proven to kill youth:

[With the flu] we can find one virus which can cause a young person to die with no other illness present […] In other words, the coronavirus infection is an infection that does not lead to death. And the flu can lead to death.”

(There have been reports of severe maladies such as Kawasaki-like disease and stroke in young people who were deemed to have a novel-coronavirus infection. However, the majority of published papers on these cases are very short and include only one or only a small handful of patients. Moreover, commenters on the papers note it’s impossible to determine the role of the virus because the papers’ authors did not control sufficiently, if at all, for confounding factors. It’s most likely that children’s deaths attributed to COVID-19 in fact are from multiple organ failure resulting from the combination of the drug cocktail and ventilation that these children are subjected to.)

Dr. Alexov therefore asserted that:

the WHO is creating worldwide chaos, with no real facts behind what they’re saying.”

Among the myriad ways the WHO is creating that chaos is by prohibiting almost all autopsies of people deemed to have died from COVID-19. As a result, reported Dr. Alexov, by May 13 only three such autopsies had been conducted in Bulgaria.

Also, the WHO is dictating that everyone said to be infected with the novel coronavirus who subsequently dies must have their deaths attributed to COVID-19.

“That’s quite stressful for us, and for me in particular, because we have protocols and procedures which we need to use,” he told Dr. Katsarov. “…And another pathologist 100 years from now is going to say, ‘Hey, those pathologists didn’t know what they were doing [when they said the cause of death was COVID-19]!’ So we need to be really strict with our diagnoses, because they could be proven [or disproven], and they could be checked again later.”

He disclosed that pathologists in several countries in Europe, as well as in China, Australia and Canada are strongly resisting the pressure on them to attribute deaths to COVID-19 alone:

I’m really sad that we need to follow the [WHO’s] instructions without even thinking about them. But in Germany, France, Italy and England they’re starting to think that we shouldn’t follow the WHO so strictly, and [instead] when we’re writing the cause of death we should have some pathology [results to back that up] and we should follow the protocol. [That’s because] when we say something we need to be able to prove it.”

(He added that autopsies could have helped confirm or disprove the theory that many of the people deemed to have died of COVID-19 in Italy had previously received the H1N1 flu vaccine. Because, as he noted, the vaccine suppresses adults’ immune systems and therefore may have been a significant contributor to their deaths by making them much more susceptible to infection.)

Drs. Alexov and Katsarov agreed that yet another aspect of the WHO-caused chaos and its fatal consequences is many people are likely to die soon from diseases such as cancer because the lockdowns, combined with the emptying of hospitals (ostensibly to make room for COVID-19 patients), halted all but the most pressing procedures and treatments.

They also observed these diseases are being exacerbated by the fear and chaos surrounding COVID-19.

We know that stress significantly suppresses the immune system, so I can really claim 200% that all the chronic diseases will be more severe and more acute per se. Specifically in situ carcinoma – over 50% of these are going to become more invasive […] So I will say that this epidemic isn’t so much an epidemic of the virus, it’s an epidemic of giving people a lot of fear and stress.”

In addition, posited Dr. Alexov, as another direct and dire result of the pandemic panic many people are losing faith in physicians.

Because in my opinion the coronavirus isn’t that dangerous, and how are people going to have trust in me doing cancer pathology, much of which is related to viruses as well? But nobody is talking about that.”

We emailed Dr. Alexov several questions, including asking why he believes it’s impossible to create a vaccine against COVID-19.

He didn’t answer the questions directly. Dr. Alexov instead responded:


We also emailed five of Dr. Alexov’s colleagues in the European Pathology Society asking them to confirm Dr. Alexov’s revelations. We followed up by telephone with two of them. None responded.

Why didn’t Dr. Alexov or his five colleagues answer our questions?

We doubt it’s due to lack of English proficiency.

It’s more likely because of the pressure on pathologists to follow the WHO’s directives and not speak out publicly. (And, on top of that, pathology departments depend on governments for their funding.)

Nonetheless, pathologists like Drs. Alexov and Püschel appear to be willing to step out and say that no one has died from a novel-coronavirus infection.

Perhaps that’s because pathologists’ records and reputations are based on hard physical evidence rather than on subjective interpretation of tests, signs and symptoms. And there is no hard physical evidence that COVID-19 is deadly.

Rosemary Frei has an MSc in molecular biology from the Faculty of Medicine at the University of Calgary, was a freelance medical writer and journalist for 22 years and now is an independent investigative journalist. You can watch her June 15 interview on The Corbett Report, read her other Off-Guardian articles and follow her on Twitter.
Patrick Corbett is a retired writer, producer, director and editor who’s worked for every major network in Canada and the US except for Fox. His journalistic credits include Dateline NBC, CTV’s W-5 and the CTV documentary unit where he wrote and directed ‘Children’s Hospital’, the first Canadian production to be nominated for an International Emmy. You can follow Patrick on Twitter.


There is NO proof even for the existence of SARS-CoV-2 Virus ❗️

Dr. Andrew Kaufman: The Postulates of Koch; basic proof for the "Plandemie"?

•April 20, 2020 - Evidence that Viruses Cause Disease or The Rooster in the River of Rats (improved audio) (already once deleted from https://www.youtube.com/embed/fvcEIarencM)

Andrew Kaufman

Please visit my website for consultation, interviews, research contributions, questions, and slide reprints: andrewkaufmanmd.com



NYT tries to maintain the 'virus narrative' with computer-gaming scientists: 

The Coronavirus Unveiled

By Carl Zimmer - 09. October 2020

In February, as the new coronavirus swept across China and shut down entire cities, a scientist named Sai Li set out to paint its portrait.

An atom-by-atom model of the coronavirus.Lorenzo Casalino, Amaro Lab, U.C. San Diego

At the time, the best pictures anyone had managed to take were low-resolution images, in which the virus looked like a barely discernible smudge.

Dr. Li, a structural biologist at Tsinghua University in Beijing, joined forces with virologists who were rearing the virus in a biosafety lab in the city of Hangzhou. Those researchers doused the viruses with chemicals to render them harmless and then sent them to Dr. Li.

Dr. Li and his colleagues then concentrated the virus-laden fluid from a quart down to a single drop. He could only hope that they had done everything just right, so that the weeks of work to produce that drop would not have been a waste.

“At the time, you don’t know what’s inside,” Dr. Li said. “It’s just liquid, right?”

Glimpsing the Structure

Dr. Li carefully froze the drop in a fraction of a second. If he made the slightest mistake, ice crystals could spear the viruses, tearing them apart.

Hoping for the best, Dr. Li placed the smidgen of ice into a cryo-electron microscope. The device fired beams of electrons at the sample. As they bounced off the atoms inside, Dr. Li’s computer reconstructed what the microscope had seen. When the picture formed, he was taken aback.

“I saw a screen full of viruses,” Dr. Li recalled.

A cryo-electron tomography image of SARS-CoV-2 viruses, in gray, with a computer reconstruction of one virus.Sai Li, Tsinghua University School of Life Sciences

He could see thousands of coronaviruses packed in the ice like jellybeans in a jar. They were beautifully intact, allowing him to inspect details on the viruses that measured less than a millionth of an inch.

“I thought, I was the first guy in the world to see the virus in such good resolution,” Dr. Li recalled.

Over the following weeks, Dr. Li and his colleagues pored over the viruses. They inspected the proteins that studded its surface and they dove into its core, where the virus’s strand of genes was coiled up with proteins. The pictures reminded Dr. Li of eggs in a nest.

A computer reconstruction overlaid on an image of several SARS-CoV-2 viruses.Sai Li, Tsinghua University School of Life Sciences

Thanks to the work of scientists like Dr. Li, the new coronavirus, known as SARS-CoV-2, is no longer a cipher. They have come to know it in intimate, atomic detail. They’ve discovered how it uses some of its proteins to slip into cells and how its intimately twisted genes commandeer our biochemistry. They’ve observed how some viral proteins throw wrenches into our cellular factories, while others build nurseries for making new viruses. And some researchers are using supercomputers to create complete, virtual viruses that they hope to use to understand how the real viruses have spread with such devastating ease.

“This time is unlike anything any of us has experienced, just in terms of the bombardment of data,” said Rommie Amaro, a computational biologist at the University of California at San Diego.

Probing the Spike

Earlier this year, Dr. Amaro and other researchers directed much of their attention to the proteins, called spikes, that stud the virus’s surface. Spike proteins have an essential job to play: They latch onto cells in our airway so the virus can slip inside. But it soon became clear that the name is a misnomer. The spike protein is not sharp, narrow or rigid.

Each spike protein snaps together with two others, forming a structure that has a tulip-like shape. A long stem anchors the proteins to the virus, and their top looks like a three-part flower.

Gerhard Hummer, a computational biophysicist at the Max Planck Institute of Biophysics, and his colleagues used the frozen microscopy method to take pictures of spike proteins embedded in the virus membrane. Then they calculated how the atoms in the proteins pushed and pulled on each other. The result was a molecular dance: The spike proteins swivel around on three hinges.

“You can see these flowers waving with all kinds of bending angles,” Dr. Hummer said. “It’s quite surprising to have such a long, slender stalk with so much flexibility.”

A Sugar Shield

Dr. Hummer speculated that the flexibility of the spike was important to the virus’s success. By sweeping around, the spike increases its odds of encountering the protein on the surface of our cells it uses to attach.

As they sweep around, however, the spikes can be attacked by antibodies, the powerful soldiers of our immune system. To hide, they create a shield out of sugar. Sugar molecules, in navy below, swirl around the proteins and hide them from antibodies.

A spike protein, at left, and a protective coating of sugars, at right.Lorenzo Casalino, Amaro Lab, U.C. San Diego.

A little hook at the end of the spike protein, in light blue below, sometimes flips up above the sugar shield. If it encounters a particular protein on the surface of our cells, it sets off a series of reactions that allows the virus to fuse to a cell membrane and inject its genes.

Latching on to an ACE2 receptor, in yellow, allows the coronavirus to enter human cells.Lorenzo Casalino, Amaro Lab, U.C. San Diego.

Tangled Loops

The genes of the new coronavirus are arrayed on a molecular strand called RNA. On Jan. 10, Chinese researchers published its sequence of 30,000 letters. That genetic text stores the information required for a cell to make the virus’s proteins.

But the genome is more than a cookbook. The strand folds into a devilishly complex tangle. And that tangle is crucial for the virus’s exploitation of our cells. “You have a lot more information stored in how it’s shaped,” said Sylvi Rouskin, a structural biologist at the Whitehead Institute.

Dr. Rouskin led a team of scientists who mapped that shape. In a high-security lab at Boston University, her colleagues infected human cells with the viruses and gave them time to make thousands of new RNA strands. Tagging the genetic letters on the strands with chemicals, Dr. Rouskin and her colleagues could determine how the strand folded in on itself.

A small portion of the coronavirus genome, showing how it folds into loops.Tammy C. T. Lan et al., bioRxiv

In some places it only formed short side-loops. In other places, hundreds of RNA letters ballooned out into big hoops, with loops coming off, and more loops coming off of them. By comparing millions of viral genomes, Dr. Rouskin and her colleagues discovered places where the virus slips from one shape to another.

A number of researchers are now closely examining some of these regions to figure out what they’re doing. Their studies suggest that these knots allow the virus to control our ribosomes, the tiny cellular factories that pump out proteins.

After the virus enters a human cell, our ribosomes attach to its RNA strands and glide down them like a roller coaster car running along a track. As the ribosomes pass over the genetic letters, they build proteins with corresponding structures. Scientists suspect that the loops of RNA may throw the roller coaster car off its track and then guide it to a spot thousands of positions away.

Other loops force the ribosome to back up a bit and then move forward again. This little hiccup can cause the virus to make entirely different proteins from the same stretch of RNA.

Jamming the Machinery

The viral proteins that spew out of our ribosomes fan out across the cell to carry out different tasks. One of them, called Nsp1, helps seize control of our molecule machinery.

Joseph Puglisi, a structural biologist at Stanford, and his colleagues mixed Nsp1 proteins and ribosomes together in test tubes. They found that the proteins, in pink below, slipped neatly into the channels inside the ribosomes where RNA would normally fit.

A ribosome with RNA, in blue, and with Nsp1, in pink.Christopher Lapointe, Stanford University School of Medicine. Ribosome models by Angelita Simonetti et al., Cell Reports and Matthias Thoms et al., Science

Dr. Puglisi suspects that Nsp1 stops our cells from making proteins of their own — especially the antiviral proteins that could destroy the virus. But that raises the question of how the virus gets its own proteins made.

One possibility is that “somehow the virus is just amped up in its ability to produce protein,” Dr. Puglisi said. From time to time, Nsp1 falls out of ribosomes, and somehow the virus does a better job of taking advantage of those brief opportunities. “We hoped it was going to be something simple,” he said. “But, as usual in science, it wasn’t.”

Blobs and Droplets

While Nsp1 is manipulating ribosomes, other viral proteins are busy making new viruses. A half-dozen different proteins come together to make new copies of the virus’s RNA. But something remarkable happens along the way: Together, the proteins and RNA spontaneously turn into a droplet, akin to a blob in a lava lamp.

Physicists have long known that molecules in a liquid spontaneously form droplets if the conditions are right. “This is just making salad dressing,” said Amy Gladfelter, a cell biologist at the University of North Carolina.

But only in recent years have biologists discovered that our cells regularly make droplets for their own purposes. They can bring together certain molecules in high concentrations to carry out special reactions, shutting out other molecules that can’t enter the droplets.

Richard Young, a biologist at the Whitehead Institute, and his colleagues have mixed together SARS-CoV-2 proteins that build new RNA along with RNA molecules. When the molecules assemble, they spontaneously form droplets. The virus likely gets the same benefits as the cell does from this strategy.

A microscopy image of droplets formed by SARS-CoV-2 proteins and RNA.Eliot Coffey and Richard Young, Whitehead Institute for Biomedical Research

Given the sophistication of the coronavirus in so many other regards, Dr. Young wasn’t surprised by his discovery. “Why wouldn’t viruses exploit a property of matter?” he said.

Pores and Tunnels

Coronaviruses can coax human cells to form new chambers to house their genetic material. But when Montserrat Bárcena, a microscopist at the Leiden University Medical Center in the Netherlands, inspected those chambers, she was baffled: There seemed to be no holes in the membranes, allowing no path for the RNA to get in or out.

Recently, Dr. Bárcena and her colleagues took a closer look and discovered a way through. One of the coronavirus’s proteins, called Nsp3, folds into a tunnel, which then plugs itself into the membranes.

“It’s a coronavirus escape route,” Dr. Bárcena said. “We had this riddle, and now we have an answer.”

Assembling New Viruses

In a matter of hours, an infected cell can make thousands of new virus genomes. The cell’s ribosomes read their genes, spewing out even more viral proteins. Eventually, some of those proteins and the new genomes assemble themselves to make new viruses.

This is no easy task, because the coronavirus’s strand of genes is a hundred times longer than the virus itself.

Recent experiments suggest that, once again, SARS-CoV-2 uses lava-lamp physics to its advantage. Proteins called nucleocapsids glue themselves to spots along the length of the RNA strand. Together, the molecules quickly collapse into droplets.

Dr. Gladfelter speculated that this strategy prevented two strands of genes from becoming tangled with each other. As a result, each new virus winds up with just one set of genes.

These droplets are swallowed up inside viral membranes and spike proteins, and the new viruses are ready to escape the cell. To simulate these viruses down to every atom, Dr. Amaro is gathering the emerging pictures of SARS-CoV-2 proteins and RNA. She and her colleagues then construct virtual viruses on supercomputers, each consisting of a half-billion atoms. These machines can then use the laws of physics to simulate the dancing of the viruses every femtosecond: in other words, a millionth of a billionth of a second.

Dr. Amaro and her colleagues hope to use her simulated viruses to tackle one of the most contentious questions about Covid-19: how the virus spreads from person to person.

When infected people exhale, talk or cough, they release tiny drops of water laden with viruses. It’s not clear how long SARS-CoV-2 can survive in these drops. Dr. Amaro is planning to build these drops, down to their individual water molecules, on her computer. Then she’ll add viruses and watch what happens to them.

“I’m pretty confident that probably within a year, we would be able to have the whole virus, including all the bits on the inside,” she said.

Drugs and Vaccines

Already, however, the new pictures of SARS-CoV-2 have become essential for the fight against the pandemic. Vaccine developers study the virus’s structure to ensure that the antibodies made by vaccines grip tightly to the virus. Drug developers are concocting molecules that disrupt the virus by slipping into nooks and crannies of proteins and jamming their machinery.

A drug molecule, in blue, blocks the tip of the coronavirus spike.Ian Haydon, Institute for Protein Design

The virus’s genome may offer other targets. Drugs may be able to lock onto loops and tangles to prevent the virus from controlling our ribosomes. “It’s very important that you know what the shape is, so you can develop the right chemistry to bind to that shape,” Dr. Rouskin said.

Dr. Gladfelter, meanwhile, wants to see if the physics of viral droplets may offer a new line of attack against SARS-CoV-2.

“You could get a compound that would make them stickier, make them more jelly,” she said. “There are probably a lot of Achilles’ heels.”

Future Research

While the past few months have delivered a flood of data about the virus, some studies have made it clear that it will take years to make sense of SARS-CoV-2.

Noam Stern-Ginossar and her colleagues at the Weizmann Institute in Israel, for example, have found evidence that the virus makes proteins that scientists have yet to find.

Dr. Stern-Ginossar and her colleagues surveyed the RNA of the virus in infected cells, tallying up all the ribosomes that were reading it. Some ribosomes clustered along known genes. But others were reading genes that had never been found before.

Ribosomes sometimes read just a section of the spike protein gene, for example. Presumably they make a mini-spike, which may very well carry out some essential job for the virus. A drug that disables it might cure Covid-19.

But scientists can’t even begin to guess at these possibilities, because no one has yet spotted the mini-spike in the wild. And the same will be true for the other new genes, Dr. Stern-Ginossar’s team has found.

“Each one will require additional work to figure out what they’re doing,” she said. “Biology takes time.”

Produced by Jonathan Corum. For the fully interactive content go to SOURCE

NYT Correction: An earlier version of this story misspelled the first name of a scientist. She is Montserrat Bárcena, not Monsterrat. (Comment: LOL - some of these 'scientists' really appear as Monster-Rats.)


Medical Empire Beats Back: 

People have died from the coronavirus, contrary to article claiming to report pathologist’s “revelations” on COVID-19

By Healthfeedback - 14. July 2020


“no one has died from the coronavirus”


SOURCE: , , , 2 Jul. 2020  


Inaccurate: Contrary to the article’s claims, people have died from COVID-19. This is evident from the excess mortality seen in 2020, in which a higher number of deaths are occurring relative to previous years before the pandemic. As reported by several published studies, antibodies specific for SARS-CoV-2 have also been discovered and the novel coronavirus has been shown to cause COVID-19.


People have died from COVID-19. This is evident from the excess mortality observed in 2020 compared to previous years before the pandemic occurred. Monoclonal antibodies that bind to SARS-CoV-2 have also been discovered and reported in published studies, and pathologists have been using such antibodies, as well as other techniques like in situ hybridization which do not require antibodies, to detect SARS-CoV-2 infection in human tissue.


FULL CLAIM: “no one has died from the coronavirus”; “no novel-coronavirus-specific antibodies have been found”; “the novel coronavirus has not fulfilled Koch’s postulates”; “the inability to identify monoclonal antibodies for the virus suggests there is no basis for the vaccines”; “the WHO is creating [worldwide] chaos is by prohibiting almost all autopsies of people deemed to have died from COVID-19”

Originally published by OffGuardian, this article makes numerous claims about the COVID-19 pandemic that have been republished in other outlets such as GlobalResearch.ca and Australian National Review, both of which have been described as conspiracy websites by Media Bias/Fact Check. The article purportedly discloses “important revelations” by Stoian Alexov, a Bulgarian pathologist and president of the Bulgarian Pathology Association, which he allegedly made during a webinar organized by the European Society of Pathology (ESP). The article has received more than 60,000 interactions on social media including Facebook and Twitter.

Health Feedback reached out to several scientists regarding the veracity of Alexov’s claims, including members of the ESP leadership, who responded with a joint clarification on behalf of the Society. You can read the ESP’s official clarification in full here.


Claim 1:

The article states that Alexov claims that “No one has died from the coronavirus” and that no antibodies specific to SARS-CoV-2 have been identified. It goes on to say that “Dr. Alexov made his jaw-dropping observations in a video interview summarizing the consensus of participants in a May 8, 2020, European Society of Pathology (ESP) webinar on COVID-19.

The webinar referenced in the article, titled “COVID-19: Unprecedented Daily Challenges in Pathology Laboratories across Europe” was indeed organized by the ESP. However, although Alexov is a member, he is not listed among the presenters. Therefore, the claim that Alexov made his remarks at a “consensus of participants” during the ESP webinar—with the implication that his comments were accepted as part of the scientific or medical consensus—is false. The complete proceedings were recorded and are publicly available on the ESP’s YouTube channel.

Claim 2:

no novel-coronavirus-specific antibodies have been found

This is false. Several published studies report the discovery of antibodies that bind specifically to SARS-CoV-2, the causative agent of COVID-19, as well as antibodies against SARS-CoV-2 in people who had been previously infected[1-4].

Claim 3:

The body forms antibodies specific to pathogens it encounters. These specific antibodies are known as monoclonal antibodies

This description of monoclonal antibodies is inaccurate and serves as the springboard for other inaccurate claims regarding pathological findings and COVID-19 vaccines that appear later in the article, as we will see below.

When the immune system encounters a pathogen, part of its response is to generate antibodies against the pathogen, a process that is carried out by B cells[5]. These antibodies can help other cells of the immune system recognize and destroy the pathogen. In the case of viral infections, antibodies can also bind to the virus to prevent the virus from infecting cells.

The term “monoclonal” indicates that the antibodies come from the same clone of a B cell. When a B cell divides, its daughter cells are described as clones. Antibodies produced by clones of the same B cell are described as monoclonal antibodies. Monoclonal antibodies bind to the same part of a protein (antigen-binding site).

On the other hand, polyclonal antibodies, which are produced by clones of different B cells, bind to different antigen-binding sites on the same pathogen. Both monoclonal and polyclonal antibodies are generated commercially for use in various laboratory techniques, such as the enzyme-linked immunoassay (ELISA), which is used to detect and measure the levels of certain proteins in a sample, as well as immunohistochemistry, a technique used to visualize the presence of certain biomarkers in a sample.

Given that our bodies naturally contain many different B cell clones, the pool of antibodies generated in response to a pathogen would be polyclonal by default, not monoclonal. While it is possible to isolate monoclonal antibodies from a person, this would occur outside of the human body and require human intervention in the form of selecting and purifying a sample to obtain a specific B cell clone.

Claim 4:

[Monoclonal antibodies] are a key tool in pathology. This is done via immunohistochemistry […] Therefore, in the absence of monoclonal antibodies to the novel coronavirus, pathologists cannot verify whether SARS-CoV-2 is present in the body, or whether the diseases and deaths attributed to it indeed were caused by the virus rather than by something else

This is demonstrably false. In its statement, the ESP clarified that “Monoclonal antibodies able to identify different components of the novel coronavirus (SARS-CoV-2) are certainly available. They are used by pathologists to demonstrate the presence of the virus in body tissues with immunohistochemistry and immunofluorescence studies.” Furthermore, the ESP also pointed to several published studies in the journals the Lancet, the New England Journal of Medicine, and the British Journal of Dermatology as evidence that pathologists have indeed imaged coronavirus in human tissues[6-9]. (Read the ESP’s full comment.)

In addition, the ESP webinar that the article refers to included a specific session dedicated to methods for detecting SARS-CoV-2 in human tissue. This session showed that pathologists are using a variety of techniques to determine whether a person was infected with SARS-CoV-2, including molecular techniques such as in situ hybridization (ISH). ISH uses nucleic acids (DNA and RNA) attached to a label, such as a radioactive isotope or fluorescent dye, that bind to viral nucleic acids in human tissue, thus signaling the presence of the virus. The webinar also describes the detection of SARS-CoV-2 in human tissue using immunohistochemistry (IHC) as demonstrated in another published study[10].

In summary, the article’s claim is false. Monoclonal antibodies for detecting SARS-CoV-2 are available and pathologists use a variety of techniques to detect SARS-CoV-2, as demonstrated in published studies.

Claim 5:

the novel coronavirus has not fulfilled Koch’s postulates

Koch’s postulates are a set of criteria used to determine whether a certain microorganism is the cause of a disease. They were originally developed by Robert Koch, a German physician who won the Nobel Prize for Physiology or Medicine in 1905 for his work on tuberculosis. The original postulates are as follows:

  1. The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms.
  2. The organism must be isolated from a host containing the disease and grown in pure culture.
  3. Samples of the organism taken from pure culture must cause the same disease when inoculated into a healthy, susceptible animal in the laboratory.
  4. The organism must be isolated from the inoculated animal and must be identified as the same original organism first isolated from the originally diseased host.

While these postulates remain an important foundation for establishing the cause of an infectious disease even today, scientists have also recognized that there are limitations to these criteria. Vincent Racaniello, a virologist and professor at Columbia University’s College of Physicians & Surgeons, wrote in his blog post that “Despite the importance of Koch’s postulates in the development of microbiology, they have severe limitations, which even Koch realized.” For example, Vibrio cholerae, the causative agent of cholera, could be isolated from both sick and healthy people, invalidating postulate #1.

Other notable exceptions to the original postulates that Racaniello pointed out are viruses, such as poliovirus, which causes illness of varying severity and does not manifest in the same way for all infected individuals. For example, fewer than 1% of individuals infected by polio are affected by paralysis. Additionally, “Postulates #2 and #3 cannot be fulfilled for viruses that do not replicate in cell culture, or for which a suitable animal model has not been identified.” Consequently, over the past decades, scientists have found it necessary to modify Koch’s postulates to adapt the criteria for the study of viral diseases[11-13].

Ian Lipkin, professor of epidemiology and director at the Center for Infection and Immunity of Columbia University’s Mailman School of Public Health, told Health Feedback that many published studies have already demonstrated that SARS-CoV-2 fulfills Koch’s postulates[14-16]. Specifically, researchers isolated SARS-CoV-2 from COVID-19 patient samples, propagated the virus in cell cultures in the laboratory, and infected non-human primates with the cultured virus. The infected primates displayed the same signs of COVID-19 as humans, including lung damage and pneumonia. Finally, the researchers were able to detect the virus in the infected animals. With these findings, all four of Koch’s postulates are met, demonstrating that SARS-CoV-2 is the cause of COVID-19.

Claim 6:

no one has died from the coronavirus

In its statement, the ESP refuted this claim, stating that:

As discussed in the two ESP webinars on the subject (May 8th and June 25th, 2020), the striking autopsy findings seen in the lungs and other organs of COVID-19 patients are unexplainable as the effect of any concurrent disease and support the novel coronavirus (SARS-CoV-2) as the cause of death in these cases.

In agreement with this, autopsy studies of COVID-19 patients have demonstrated the presence of the novel coronavirus (SARS-CoV-2) in a variety of tissues, mainly the lungs and the inner lining of blood vessels (endothelium).” (Read the ESP’s full statement.)

If the article’s claim were true, then the number of deaths that have occurred since the beginning of the outbreak would be similar to that of previous years before the emergence of COVID-19. However, this is not the case. For instance, an earlier Health Feedback review reported that we are seeing a higher number of deaths in 2020 compared to previous years in the U.S. (see figure below).

Figure 1. Weekly excess deaths in the U.S., as calculated by the U.S. CDC&. The bars represent the weekly number of deaths from all causes, which include deaths attributed to COVID-19 and to other causes. The orange curve is the threshold above which the number of deaths exceeds the number of deaths normally expected at that time of year, based on records from previous years. Note the excess deaths detected in January 2018, which occurred during the 2017-2018 flu pandemic, and in early 2020, which is attributed to COVID-19.

A Financial Times report also showed the same pattern of excess mortality in other countries like Belgium, France, and Italy. The excess mortality observed across the world in 2020 can only be attributed to the COVID-19 pandemic, as there is no other factor which can explain this sudden increase in mortality compared to previous years when COVID-19 was not present.

Claim 7:

the inability to identify monoclonal antibodies for the virus suggests there is no basis for the vaccines, serological testing, and immunity certificates being rolled out around the globe

This is inaccurate for several reasons. As we explained earlier under Claim #2, monoclonal antibodies which bind to SARS-CoV-2 have indeed been identified[1,2]. Additionally, immunity is not dependent on monoclonal antibodies. The body has many different B cell clones, meaning that the antibodies produced in response to a pathogen would be polyclonal by default—even so, our immune system remains functional. Furthermore, while antibodies are an important part of the immune response, other factors which can be enhanced by vaccination, such as the T-cell mediated immune response, are also relevant in mounting an effective defense against infection.

Finally, immunity certificates are not being “rolled out around the globe” at the moment. Countries including Germany and the United Kingdom have discussed its use as a potential tool for returning to normal life, but whether immunity certificates will be implemented is still an open question given the practical and ethical implications, some of which are discussed in this 21 May Nature news article.

Claim 8:

Among the myriad ways the WHO is creating [worldwide] chaos is by prohibiting almost all autopsies of people deemed to have died from COVID-19

The World Health Organization has not prohibited such autopsies and the article produces no evidence to support this claim. In fact, the aforementioned ESP webinar openly discusses findings from the autopsies of COVID-19 patients. Furthermore, several studies on COVID-19 autopsy findings from countries such as the U.S., Germany, and China have been published[17-20].


W. Ian Lipkin, Professor of Epidemiology, Mailman School of Public Health, Columbia University:
Conspiracy theorists are not persuaded by data. There are many studies on SARS-CoV-2 that fulfill Koch’s postulates[14-16].

European Society of Pathology:
[The following statement was co-signed by ESP president Prof. Holger Moch, ESP Director-General Dr. Raed Al-Dieri, and ESP Secretary Prof. Aurelio Ariza]
In response to some of the claims made by the article “No one has died from the coronavirus,” the European Society of Pathology (ESP) offers the following comments:

Claim by the article: “No one has died from the coronavirus”

Comment by the ESP: As discussed in the two ESP webinars on the subject (May 8th and June 25th, 2020), the striking autopsy findings seen in the lungs and other organs of COVID-19 patients are unexplainable as the effect of any concurrent disease and support the novel coronavirus (SARS-CoV-2) as the cause of death in these cases.

In agreement with this, autopsy studies of COVID-19 patients have demonstrated the presence of the novel coronavirus (SARS-CoV-2) in a variety of tissues, mainly the lungs and the inner lining of blood vessels (endothelium). There is evidence of a specific COVID-19-associated coagulopathy that can cause deadly thromboembolism.

Claim by the article: “In the absence of monoclonal antibodies to the novel coronavirus, pathologists cannot verify whether SARS-CoV-2 is present in the body, or whether the diseases and deaths attributed to it indeed were caused by the virus rather than by something else”

Comment by the ESP: Monoclonal antibodies able to identify different components of the novel coronavirus (SARS-CoV-2) are certainly available. They are used by pathologists to demonstrate the presence of the virus in body tissues with immunohistochemistry and immunofluorescence studies.

Other techniques (such as in situ hybridization and RT-PCR) can detect viral RNA in tissues. Additionally, electron microscopy neatly allows the visualization of the spike-crowned virus (hence the name coronavirus) in the diseased organs.

Coronavirus images as observed by pathologists in human tissues may be seen in the articles by M. Ackerman et al. (NEJM 2020)[6], I. Colmenero et al. (Brit J Dermatol 2020)[7], V.G. Puelles et al. (NEJM 2020)[8] and Z. Varga et al. (Lancet 2020)[9], among others.

The above comments briefly summarize the official position of the European Society of Pathology (ESP), which is not responsible for the claims and opinions of its individual members.


&: The number of deaths in Figure 1 are labeled “predicted number of deaths” because the raw number of deaths counted in a given week by the CDC are typically not finalized until weeks to months after the week in question due to a lag in reporting of death certificates. More details are available in this technical note.



W. Ian Lipkin
Professor of Epidemiology, Mailman School of Public Health, Columbia University


Flora Teoh
Science Editor, Health Feedback



Viral Realities Revealed: Dr John Lee, Pathology Professor

•Jun 30, 2020

Ivor Cummins

Excellent conversation with a hero of mine - retired Professor of Pathology Dr. John Lee. He has written such common-sense and yet exceptionally scientific articles on this seasonal viral challenge in The Spectator Magazine, since late March.  I found these articles and realized there was at least one other person in UK/Ireland who understood what the hell was going on - a relief I must say! We cover mortality risk realities, the evidence supporting Lockdown being an effective intervention, the ethics and philosophy of it all - and exactly WHY such challenges remain. The technical reality is nothing like that portrayed in the media - that's for sure.


12 COVID-19 Autopsy Cases Reveal the TRUTH How COVID-19 Patients Dying - Doctor Explains

•May 14, 2020


Doctor Mike Hansen

621K subscribers


12 COVID 19 Autopsy Cases Reveal the TRUTH How COVID 19 Patients Dying - Doctor Explains In all 12 COVID 19 Autopsy cases, the cause of death was found within the lungs or the pulmonary vascular system. Those who did not die of large pulmonary emboli died of extensive inflammation, meaning pneumonia with ARDS. In these COVID 19 Autopsy cases, the lungs were wet and heavy, much like a saturated water sponge. The lung surfaces often had a distinct patchy pattern, with pale areas alternating with slightly protruding and firm, deep reddish-blue Hypercapillarized areas. This indicates areas of intense inflammation, with endothelial dysfunction that can be seen at the microscopic level. When they look at the lungs' slices under the microscope, they found diffuse alveolar damage in 8 COVID 19 Autopsy cases. Specifically, they saw hyaline membrane formation, tiny clots in the capillaries, capillaries engorged with red blood cells, and other inflammatory findings. All these findings represent ARDS. They also found lymphocytes, a type of white blood cell, infiltrated these areas of infiltration. This fits the picture of viral pathogenesis.

⏩ Timestamps, click to skip ahead:

12 COVID 19 Autopsy Cases Reveal!

00:00​ - Introduction

02:38​ - The starting point of the COVID 19 Autopsy Analysis

04:10​ - Why we get COVID 19 false Negative Test

04:34​ - Rest of the Part of COVID 19 Autopsy Analysis

09:45​ - Big Takeaway's from the Findings in this COVID 19 Autopsy Study

12:30​ - Minimize the chances of having the severe disease if you were to get COVID 19

This is the link to the main study in this video: https://www.acpjournals.org/doi/10.73...

They also looked at the pharynx of these COVID 19 patients, meaning in their throat. The lining of the throat, or mucosa, was hyperemic, meaning very red and irritated. At the microscopic level, they saw lymphocytes invading there, which is consistent with a viral infection. In one COVID 19 case, a COVID 19 patient had lymphocytes invade his heart muscle, findings that are consistent with what we call viral myocarditis. More than half of the COVID 19 patients in this study had large blood clots. One-third of the COVID 19 patients had pulmonary embolism as the direct cause of death. All the others died of intense inflammation in their lungs related to pneumonia with ARDS (Acute Respiratory Distress Syndrome). Recently, studies show that about 1/3rd of COVID 19 patients with severe COVID 19 have blood clots. In another study of 191 COVID 19 patients, half of those who died had clots, compared with 7% of survivors. And levels of D-dimer that were greater than 1000 µg/L were associated with a fatal outcome. So it's pretty clear now that the COVID 19 has caused many clots to form in moderate to severe COVID 19 disease.

How is this happening?

It's likely a combination of reasons that have to do with downregulation of the ACE2 receptor in the lung alveoli, with a subsequent shift towards having more angiotensin II in the lungs, and less angiotensin 1-7 and 1-9 in the lungs, and when this happens, this leads to more cytokine storm with more inflammation, more constriction of pulmonary arteries, and more clots that develop. That, in turn, leads to more endothelial dysfunction in the capillaries that surround the alveoli. Also, there is evidence that the virus attaches to the ACE2 receptors of those endothelial cells that line those capillaries, which further propagates inflammation and clotting. And in the cytokine storm that develops there, RANTES, a chemokine, binds to the CCR5 receptor of CD4 and CD8 lymphocytes, and that causes those lymphocytes to infiltrate those areas of inflammation, and in doing so, further contributes towards the inflammatory reaction. This is why we are seeing low levels of CD4 and CD8 lymphocytes in severe COVID 19. Endothelial damage can also lead to the development of antiphospholipid antibodies, and these antibodies are bad because they trigger blood clots formation. That’s why COVID 19 patients who have clots with antiphospholipid antibody syndrome need to be on blood thinners.

11 out of the 12 COVID 19 patients in this study had underlying heart disease and were obese. These are known risk factors for cardiovascular disease and known risk factors for endothelial dysfunction and are known risk factors for COVID 19. So the big takeaways from the findings in this study are that most people who die of COVID 19 are primarily lung problems. Either related to inflammation with ARDS and/or blood clots.

Antiphospholipid syndrome might be a commonality among patients with thrombosis in COVID 19 patients.

Doctor Mike Hansen, MD Internal Medicine | Pulmonary Disease | Critical Care Medicine

Website: https://doctormikehansen.com/