Discover more from Unrestrained Inquiry
Covid Virus or No Covid Virus?
My Thoughts on the Cowan/Kaufman Theory That Viruses Don't Exist
The theory advanced by Dr. Cowan and Dr. Kaufman that viruses don’t exist (and by extension the COVID virus) has generated a lot of controversy. There are those who are convinced by their arguments and those that find the theory ridiculous. The path I advocate is taking is critical thinking and an examination of the evidence.
Independent journalist Jeremy Hammond has written an excellent piece that aims to settle the matter:
Thanks for reading Unrestrained Inquiry! Subscribe for free to receive new posts and support my work.
The article is a tour de force on the matter, and it is amazing just how much virology Mr. Hammond has learned in the course of writing this article.
I do think that his language characterizing Cowan as "spreading misinformation" is a bit strong. The target audience of the articles are people in the health freedom who have been battered by charges of misinformation by the media and are tired of hearing it.
Moreover, spreading misinformation is a deliberate, willful act, and I don't think Cowan/Kaufman is doing that. I think they believe in their theory and will defend it to the bitter end (but not out of maliciousness). Some brilliant academics have done the same with their established views (i.e., Milton Friedman and efficient markets in light of behavioral economics).
But let’s get back to the important questions here:
1) How scientifically viable is the no-virus hypothesis?
2) Is the no-virus hypothesis good or bad for the movement from a practical standpoint?
Regarding #1, we can apply the Bradford-Hill criterion to it to examine it. If you aren't familiar with this criterion, read the link below. It is an essential thing to know to make sense of conflicting info.
Mr. Hammond makes some devastating points in his article:
1) Consistency with other scientific tools that allow us to look at evidence of viruses:
"But that's untrue, too, just as it isn't true that the de novo genomic sequencing was the scientists' only means of characterizing SARS‑CoV‑2. Scientists have a variety of means of characterizing and classifying microorganisms, which is how reference genomes become reference genomes in the first place. Scientists can purify and isolate the organism, observing any replication and cytopathic effects in a culture. They can observe and characterize the entity with electron microscopy. They can inoculate animals with the virus to observe viral infection and pathogenesis of disease. They can characterize the proteins of the virus and test the binding of different antibodies to various of its epitopes. Multiple methods and lines of evidence are used together to identify organisms and place them in their family tree and to determine their role, if any, in the pathogenesis of disease."
2) Consistency with the evolution of viruses
“Designating this virus "WH-Human 1 coronavirus (WHCV)", later renamed "SARS‑CoV‑2", the authors reasonably concluded (bold emphasis added):
Here we describe a new coronavirus—WHCV—in the BALF [bronchoalveolar lavage fluid] from a patient who experienced severe respiratory disease in Wuhan, China. Phylogenic analysis suggests that WHCV is a member of the genus Betacoronavirus (subgenus Sarbecovirus) that has some genomic and phylogenetic similarities to SARS‑CoV, particularly in the RBD [receptor binding domain] of the spike protein. These genomic and clinical similarities to SARS, as well as its high abundance in clinical samples, provides evidence for an association between WHCV and the ongoing outbreak of respiratory disease in Wuhan and across the world. Although the isolation of the virus from only a single patient is not sufficient to conclude that it caused these respiratory symptoms, our findings have been independently corroborated in further patients in a separate study. [emphasis Hammond]”
3) Experimental evidence that shows consistency to previously known viruses
“That study similarly describes the whole genome sequencing of SARS‑CoV‑2—which at the time they called "2019-nCoV"—using metagenomic technology. As described in the abstract (bold emphasis added):
Full-length genome sequences were obtained from five patients at an early stage of the outbreak. The sequences are almost identical and share 79.6% sequence identity to SARS‑CoV. Furthermore, we show that 2019‑nCoV is 96% identical at the whole-genome level to a bat coronavirus. Pairwise protein sequence analysis of seven conserved non-structural proteins domains show that this virus belongs to the species of SARSr‑CoV. In addition, 2019‑nCoV isolated from the bronchoalveolar lavage fluid of a critically ill patient could be neutralized by sera from several patients. Notably, we confirmed that 2019‑nCoV uses the same cell entry receptor—angiotensin converting enzyme II (ACE2)—as SARS‑CoV.”
4) Confirmation of the proposed mechanism of infection via a challenge
“That work was done later. For example, a study published in Clinical Infectious Diseases on March 26, 2020, described the clinical and pathological manifestations of COVID‑19 in golden Syrian hamsters, which were identified as a good candidate for fulfilling Koch's Postulates due to their cellular expression of ACE2 (suggesting that it might be possible to infect them with SARS‑CoV‑2). Using a control group of mock-infected hamsters (injected only with phosphate-buffered saline, which was "used to dilute virus stocks to the desired concentration" in the experimental group), they challenged the animals with the virus, observed infection as well as clinical and pathological manifestations of disease, and observed the development of anti-SARS‑CoV‑2 antibodies in all of the hamsters after recovery. (All the hamsters survived the disease.)”
5) Independent replication of challenges
“In a study published in Nature on May 7, 2020, another team of researchers described a viral challenge with mice genetically modified to express ACE2. Again comparing findings with a control group of mock-infected animals, their findings were similar to the hamster study: the animals in the experiment group became infected, developed disease, and developed antibodies specific to the spike protein of SARS‑CoV‑2.”
6) Independent replication of challenges in a model that is closer to humans
“A study published in Cell Research on July 7, 2020, performed a similar viral challenge experiment using rhesus macaques. Once again, in comparison to a control group of uninfected monkeys, the researchers observed that exposed animals became infected, developed disease, and developed antibodies to the virus.”
Dr. Cowan recently created a video rebuttal:
But he still doesn't address the above problems nor Jeremy's more detailed arguments about how genome sequencing works.
It’s not hard to ask more questions that Cowan/Kaufman do not have answers for:
There are critical questions that Cowan, Kaufman, and Lanka fail to answer:
If there is no virus, then what is causing COVID-19 symptoms?
If there is no virus, then what exactly was being done with gain-of-function research at Wuhan?
If there is no virus, then what exactly are front-line doctors treating?
If there is no virus and this is merely the flu, then why are there so many reports that standard flu protocols are failing to treat COVID-19?
If there is no virus, why is there a spike protein that has been purportedly been found?
If there is no virus, then does that mean all the papers on SaRs-CoV-2 reflect a collective delusion on the part of virologists and immunologists?
If there is no virus, why is there a larger body of work that points to SaRs-CoV-2 being man-made?
If there is no virus, why are there papers that COVID vaccination have some (short-term) effect at reducing severe COVID?
If COVID is "just a toxin" then why does it appear to spread "like a virus" with a high R0?
If there is no virus, then what about other diseases like the common cold, flu, chicken pox, measles, shingles, etc.?
Are antibodies to these viruses part of a collective delusion?
How do they explain that vaccinations (say measles vaccines) seem to have some effectiveness at reducing infectious disease incidence?
There’s just too many questions. So for now, I find the no-virus hypothesis to have too many holes to be scientifically viable.
Regarding the second question I brought up: is the no-virus hypothesis good or bad for the movement from a practical standpoint?
In his video, Cowan calls out CHD for failing to include him in a conference designed for unity. Still, I think his plan of spreading the no-virus hypothesis to a larger audience is evident.
This is a morally tricky situation. But we must think like strategists about our opponent's moves: how will our opponents respond if we advance the no-virus hypothesis?
Unfortunately, any way you look at it, advancing the no-virus hypothesis gives our opponents a gift - we give them an evidential reason to crush our movement as a danger to society (denial of pandemics is a core threat to national health security).
We know they are making moves already using the strategic line. The CA bill aimed at controlling doctors is a prime example. I foresee them getting bolder with it.
I would caution our movement groups against giving a broader audience to the no-virus hypothesis; even an open debate would not be good.
If we maintain silence, I think the doubts about the no-virus hypothesis would naturally fall by the wayside.
While I hate to advocate for using a tool that our opponents directly use, I think it is best for the long-term health of the movement.
I do admit that it might be possible (though I think it is remote) that Cowan/Kaufman might be ultimately correct. But it would be up to them to enlist the researchers and scientists in academia to show that their theories are correct.
Their message aimed at average movement members is not the right venue for their sophisticated pet theory that seeks to upend the establishment.
They have plenty of work to do. Let’s not spread their message until it is ready.
Thanks for reading Unrestrained Inquiry! Subscribe for free to receive new posts and support my work.