Correcting Misinformation about SARS-CoV-2 Whole Genome Sequencing

Introduction

In a typical piece of hate mail that landed in my email inbox in mid-July, an angry reader called me “ignorant” and “stubborn” for saying that SARS‑CoV‑2 exists while alerting me to a video published on July 13, 2022, by Dr. Tom Cowan, a leading proponent of the claim that it does not. In the video, which my fan evidently found persuasive, Cowan responds to something I had written about the whole genome sequencing of SARS‑CoV‑2 and purports to explain why I was wrong. However, it is Cowan who is wrong and continues to misinform his audience about the existence of the coronavirus that causes COVID‑19.

Although Cowan was unaware of the origin, the specific quote of mine to which Cowan responds in the video was something I wrote in an email newsletter on June 16. In that email to my subscribers, I responded to an article written by Dr. Andrew Kaufman, another leading proponent of the claim that SARS‑CoV‑2 does not exist, in which he similarly attempted but failed to debunk statements I had made in an interview with journalist Bretigne Shaffer about counterproductive misinformation emanating from within the health freedom movement. (That interview was later cited by Dr. Joseph Mercola in an article at Mercola.com in which he expressed his agreement with my viewpoint, which is probably how Kaufman came to learn of it.)

As an example of how Kaufman attempted but failed to rebut my statements in that interview, he resorted to strawman argumentation, such as attributing to me the claim “that scientists do not yet have the technology to purify viral particles”, which he then rebutted by saying that they do. But that is a lie. I never said any such thing.

The rest of his arguments were of a similar nature, either logically fallacious or factually incorrect, as I discussed in my newsletter but will not get into here except for the part that’s relevant to Cowan’s rebuttal video.

Here is that relevant excerpt from Kaufman’s article:

Hammond claims that scientists can do genetic sequencing of the particles found in tissue cultures. . . . Hammond describes the method accurately, in that they start with lots of pieces of genetic material, and then a computer does sophisticated calculations and simulations to put them together. The problem—which Hammond does not describe—is that the starting material for these experiments is not a pure organism; it’s not just a virus. . . . [T]here are many sources of genetic material. When they put those little bits of genetic material into the computer, the computer doesn’t know which organism they’re from—since they are not starting with a pure virus, there’s no way to tell.

Kaufman is incorrect.

First of all, it isn’t true that scientists never purify a sample prior to doing whole genome sequencing. Depending on the type of sequencing being done, it may or may not be necessary to first isolate the virus. A typical process would be to purify the patient sample with filtration or centrifugation, inoculate cell culture with the supernatant and watch for viral replication and cytopathic effects in comparison to an uninoculated control, observe the virus under an electron microscope, and utilize whole genome sequencing technology to place the virus on its evolutionary family tree.

As an example, take a 2013 study published in Nature titled “Isolation and characterization of a bat SARS‑like coronavirus that uses the ACE2 receptor”. Here are a few relevant quotes:

• “PCR positive faecal samples(in 200 ml buffer) were gradient centrifuged at 3,000–12,000g and supernatant diluted at 1:10 in DMEM before being added toVero E6 cells.”
• “Virions from a 10-ml culture were collected, fixed and concentrated/purified by sucrose gradient centrifugation.”
• “Purified virions displayed typical coronavirus morphology under electron microscopy.”

Second, as I pointed out in my newsletter, Kaufman’s claim that you cannot sequence the whole genome of an organism or a virus unless it is separated from all other genetic material is false. Here is what I wrote in my newsletter:

Kaufman’s claims here about whole genome sequencing are also wrong. Apart from falsely claiming that no purification process is undertaken during the process of virus isolation, the claim that whole genome sequencing cannot be done if there is more than one source of genetic material in a sample is also false. It’s called “metagenomic” genetic sequencing. (You could mix up the pieces to dozens of different puzzles and still reassemble each puzzle because each piece only fits one other piece. You can’t start with a puzzle of an elephant and a bear and mix up the pieces so that you end up with a puzzle of a wooly mammoth.)

Just to establish that I am not also engaging in strawman argumentation, Cowan specifies the position he is defending as follows:

I’m not sure where he [Jeremy Hammond] originally wrote this [response to Andrew Kaufman], but this was in response to some of us saying there’s no way you can find the genome of a vir—I’ll try to be very careful about my wording here—find the genome of a virus if the pieces of genetic material that allegedly belong to the virus are mixed up with the genetic material of fungus and bacteria and human and fetal calf serum and monkey kidney cells and a whole lot of other genetic material.

So, as you can see, both Kaufman and Cowan, according to Cowan’s own carefully worded summation, really are arguing that it isn’t possible to find the genome of a virus if the genetic material of that alleged virus is mixed up with the genetic material of other organisms.

They are wrong. As I briefly and correctly noted in my newsletter, it is possible to find the genome of a virus—and to identify that virus—despite its genetic material being mixed up with the genetic material of other organisms.

Clarifying “Metagenomic” Versus “De Novo” Sequencing

To start out, in his video response to me, Cowan refers to “metagenomic sequencing or de novo sequencing”, thus conflating the two. To clarify for my own readers, “metagenomic” and “de novo” (Latin for “of new”) mean two different things.

“Metagenomic” sequencing refers to the sequencing of the genomes of multiple organisms or viruses simultaneously. Each organism does not need to be first separated from the rest in order to do this, and the sequencing can be performed directly from a patient or environmental sample, without first isolating each microorganism.

Here is a description of metagenomic next generation sequencing from a paper on the topic published in Annual Review of Pathology: Mechanisms of Disease on October 24, 2018 (with bold emphasis added):

Next-generation sequencing (NGS), also termed high-throughput or massively parallel sequencing, is a genre of technologies that allows for thousands to billions of DNA fragments to be simultaneously and independently sequenced. The applications of NGS in clinical microbiological testing are manifold and include metagenomic NGS (mNGS), which allows for an unbiased approach to the detection of pathogens. This review focuses on using mNGS methods to identify pathogens directly from clinical samples from patients. Untargeted mNGS approaches use what is known as shotgun sequencing of clinical samples or pure microbial cultures in which random samples of analyte DNA or RNA are surveyed en masse, in contrast to targeted approaches that utilize singleplex or multiplex polymerase chain reaction (PCR), primer extension, or bait probe enrichment methods, thus restricting detection to a list of specific targets.

. . . A chief advantage of mNGS is unbiased sampling, which enables broad identification of known as well as unexpected pathogens or even the discovery of new organisms.

On the other hand, “de novo” sequencing refers to genomic sequencing that is done without a reference strain, which is a genome sequence that can be used for comparison. For example, scientists might identify a viral variant by starting with a reference genome and then do a targeted sequencing of the variant based on that reference strain, whereas de novo sequencing is “unbiased” because it doesn’t depend on reference genomes and therefore “is fully agnostic to the pathogen that one is seeking.”

Obviously, every reference genome had to have originally been de novo sequenced; if it were true that whole genome sequencing cannot be done without having a reference genome to start with, logically, nothing could ever be originally sequenced. The technology of genome sequencing could not exist. But it does.

As noted in a paper on metagenomic sequencing published in the Yale Journal of Biology and Medicine on September 30, 2016, scientists “distinguish between de novo assembly – which involves reconstructing genomes directly from the read data, and comparative assembly – where the aim is to use the sequences of previously sequenced closely related organisms to guide the construction of a new genome.”

The most useful application of metagenomic sequencing is de novo sequencing of multiple genomes at once. However, de novo sequencing is not necessarily metagenomic sequencing; it could also be a targeted sequencing without a reference strain of an isolated organism or virus. Thus, the two terms should not be conflated.

Clarifying “PCR Test” Versus “Whole Genome Sequencing”

With that clarification out of the way, I need to also point out that whole genome sequencing is a different technology from the PCR tests that, yes, have been misused to perpetrate systematic scientific fraud. (For more on that, see my article “Facebook ‘Fact Check’ Lies about PCR Tests and COVID‑19 ‘Cases’”.)

I need to point this out, too, because I have seen the two technologies so frequently conflated by readers expressing their belief to me that SARS‑CoV‑2 does not exist.

The diagnostic PCR tests cyclically amplify specific RNA fragments present in a patient sample, with the “cycle threshold” for positivity being an imperfect proxy measure of viral load: a higher number of cycles required to obtain a positive result implies a lower amount of RNA in the sample, whereas a lower number of cycles implies a higher “viral load”. (This correlation does not always hold true. A high “viral load” could simply represent dead nucleotides, remnants of an effective immune response that has already eliminated the viral infection.)

While genomic sequencing may involve the use of polymerase chain reaction (PCR) technology to amplify RNA or DNA, whole genome sequencing is a different technology from the diagnostic PCR tests misused by “public health” officials to perpetrate systematic scientific fraud in the counting of “COVID‑19” cases.

Scientists were able to develop PCR tests to detect RNA from SARS‑CoV‑2 in patient samples precisely because the whole genome of the virus had already been sequenced. It is true, as virus deniers commonly point out, that the developers did not themselves have access to a virus isolate, but they didn’t need to; they developed their tests to detect specific RNA sequences based on the published whole genome of the target virus. (What their non-possession of a virus isolate meant for the validation of the tests they developed is a different issue.)

On that note, I need to also remind that it isn’t true that the CDC has “admitted” that SARS‑CoV‑2 was never isolated. I corrected that viral misinformation in my December 2020 article “No, the CDC Did Not Admit That SARS‑CoV‑2 Has Not Been Isolated”.

That false claim, to my knowledge, was not propagated by Tom Cowan. Incidentally, though, in that article of mine, I also corrected another piece of misinformation that did originate from Cowan, which was his false claim that a CDC study proved that “the SARS‑CoV‑2 virus is harmless to human beings” and was only capable of infecting monkey cells.

Cowan made that claim in an article titled “Only Poisoned Monkey Kidney Cells ‘Grew’ the ‘Virus’”, published on his website DrTomCowan.com on October 15, 2020. (Trying to access that article on his site now results in a “404 Page Not Found” error, but the link I’ve provided is to a webpage snapshot accessible on the Internet Archive’s Wayback Machine.)

Note that Cowan’s argument that SARS‑CoV‑2 can only infect monkey cells, not human cells, directly contradicts his argument that SARS‑CoV‑2 does not exist. This logical inconsistency is characteristic.

Metagenomic Sequencing Explained

Coming back to Kaufman and Cowan’s mutual claim about whole genome sequencing, the standard method of isolating viruses is cell culture, and it is not necessary to first grow the virus in a culture medium for metagenomic sequencing to be done. That is to say, it is not necessary to first purify and isolate the virus to sequence its whole genome. Nor does it require specific amplification via PCR.

Here is more relevant information about metagenomic sequencing from a paper on the topic published in Frontiers in Cellular and Infection Microbiology on September 9, 2021 (bold emphasis added):

[T]the detection of pathogens by antigen and/or antibody immunology and PCR must be based on the genetic sequence of known pathogens, and unknown pathogens cannot be detected.

Metagenomic next generation sequencing (mNGS) is a method that can directly utilize the patient specimen for pan-nucleic acid detection; all nucleic acids in the specimen are extracted and sequenced in parallel, so as to obtain the sequence of host and microorganisms.

. . . mNGS does not rely on traditional microbial culture, nor does it require specific amplification. . . . mNGS can be applied to a wide range of specimen types (sputum, throat swab, blood, alveolar lavage fluid, pleural fluid, cerebrospinal fluid, pus, tissue specimens, etc.), and it can directly detect nucleic acids in clinical samples without distinction and selectivity for high-throughput sequencing. Comparing and analyzing with the known microbial sequence database, and judging the types of microorganisms contained in the sample based on the sequence information, it can unbiasedly detect pathogenic microorganisms in clinical samples, including viruses, bacteria, fungi, and parasites.

Here is another description of metagenomic sequencing from the 2016 paper in the Yale Journal of Biology and Medicine:

The use of high throughput sequencing in the analysis of microbial communities has led to the creation of a new scientific field – metagenomics – the analysis of the combined genomes of organisms co-existing in a community. A critical step in such analyses is metagenomic assembly – the stitching together of individual DNA sequences into genes or organisms.

Recall that the original statement of mine that Kaufman was attempting to dispute was my observation that scientists can do whole genome sequencing of multiple microorganisms simultaneously. As I have just shown, what I said is correct, and Kaufman was mistaken in his attempted rebuttal.

As I have also just shown, it is also untrue that “there’s no way to tell” what organisms are being sequenced when this is done.

For example, following metagenomic de novo sequencing, the genomes of newly sequenced organisms can be compared to previously sequenced organisms and classified according to their “phylogenic tree”, which you can think of as a family tree showing the evolutionary ancestry of a species with all its branches.

Scientists can search international genomic databases to find other previously sequenced genomes that most closely match the newly sequenced genome. They can tell whether the genome is from a virus, a fungus, a parasite, a bacterium, etc., and they can place the organism into its phylogenic tree by comparing its genome with the genome of other known organisms.

One international database for genomic sequences is GenBank, accessible on the website of the National Center for Biotechnology Information (NCBI) under the National Institutes of Health (NIH). Another is GISAID. A visualization of the phylogenic tree of SARS‑CoV‑2 based on GISAID data is accessible at Nextrain.org (also at GISAID.org.) Additional visualizations of genomic data from GISAID are accessible at CovidCG.org.

Of course, again, any reference or comparison genome had to be originally identified and classified in the first place, which is where de novo sequencing comes in. Scientists have numerous means at their disposal to characterize newly discovered organisms, including isolation, electron microscopy, and whole genome sequencing.

Tom Cowan’s Arguments about Metagenomic Sequencing

In his attempted rebuttal of my response to Kaufman’s false claim, Cowan presents four arguments, each logically fallacious and/or factually incorrect.

First, he repeats essentially the same falsehood as Kaufman. When they put those little bits of genetic material into the computer, Cowan argues, the computer doesn’t know which organism they’re from. Since they are not starting with a pure virus, he says, there’s no way to tell.

Again, that is untrue. Metagenomic sequencing allows whole genome sequencing of many microorganisms simultaneously, and scientists can identify a species by its observable characteristics, including its full-length genome. Hence, they are able to place the newly discovered virus or organism into a phylogenic tree, which is like a family tree showing the evolutionary branches of a virus or a living organism.

As an example of how this claim from Kaufman and Cowan is false, metagenomic sequencing has been used to characterize microorganisms in the human gut, which are estimated to be one hundred trillion in number. In a study published in February 2021, scientists used metagenomic sequencing to identify more than 140,000 virus species in the human gut.

Second, Cowan takes issue with my puzzle analogy. My analogy is incorrect, he argues, because somebody knew what the elephant looked like, whereas with a virus mixed up with other genetic material, you don’t know what’s in there.

However, this argument of Cowan’s is a silly non sequitur fallacy because we can assume that the person assembling the puzzle has never seen an elephant before and my analogy holds. If you give me the mixed-up pieces to a puzzle of a crazy space alien without showing me the box cover, I could assemble the picture despite not knowing in advance what the product is going to look like.

Third, Cowan also argues that there are not different “types” of DNA (or RNA in the case of RNA viruses) for viruses, bacteria, and other organisms; they are all basically the same. This is true inasmuch as DNA is comprised of strands of nucleotides constructed from four nucleobases: adenine (A), cytosine (C), guanine (G), and thymine (T). That is, the basic building blocks of all DNA is the same regardless of whether it comes from a human, an animal, a plant, a bacterium, or a virus.

However, Cowan does nothing to invalidate my analogy by pointing out this fact. Since I did not claim that virus DNA (or RNA) is of a different “type” than bacteria DNA, it amounts to a strawman fallacy. It is the sequence of nucleotides that is different whether you are talking about different organisms (like viruses versus bacteria) or different strains of the same organism; and, again, scientists can place a newly identified virus into its phylogenic tree based on its whole genome sequence.

Cowan’s fourth argument is by his own description the “most important”. I haven’t taken the time to ensure a verbatim transcript, but accurately paraphrased if not directly quoted (you can watch his video to verify), his argument goes like this:

When they do de novo sequencing, when they sequenced SARS-CoV-2, you have no idea what’s in there, so the computer starts assembling the puzzle pieces based on how they fit together, overlapping nucleotides. Unlike the puzzle, where you get one picture only, the computer came up with a million different options. In other words, the computer came up with a million different possibilities for which is the “correct” viral genome. The puzzle computer said there are a million different ways to assemble these pieces into a picture.

If you’ve never seen an elephant and you don’t know elephants exist, how do you decide which particular picture is the actual elephant? I can’t think of anything that could guide you in choosing which is the correct picture. In fact, what they did is they said, “This one, which is the longest, is about the same size and the same sequence as a previous coronavirus” that was, by the way, made in the exact same process, without any guiding picture or any guiding genome to guide the process.

. . . So, we’re talking about a million different pictures and no way to know which is the correct picture. So they basically chose the longest, said it was 90% similar to the original one, fiddled, took out some of the sequences, added something to the end, and then rearranged things a little bit, and said, “Look, it’s an evolution from the original SARS-CoV-1.”

If the pieces of the puzzles fit together a million different ways, could you assemble them? No. So unless someone can give me a “Here’s how you choose” scenario, I am going to stick with my conclusion that this is an in silico—a computer derived—sequence that is not sequenced; it’s assembled or aligned, and it has no relationship to a reality of an organism because it did not come from the organism. The organism was never seen, and so there’s no guiding principle to say “this” as opposed to “this other one was the correct genome”.

The underlying premise of Cowan’s argument here is that when they first sequenced the genetic material that was eventually labeled “SARS‑CoV‑2”, the result was a million different sequences, and the scientists in China who did that work simply selected the longest one, manipulated it, and called it a novel coronavirus without any way of knowing whether the genetic material actually even came from a virus.

However, Cowan’s premise is false. The result of the whole genome sequencing that was done was not a million different options from which scientists selected one on the arbitrary criterion of length.

Rather, it just so happened that the longest sequence turned out to be from a previously undiscovered virus belonging to the Betacoronavirus genus, and it made perfect sense to point to this virus as the likely culprit in the pathogenesis of the observed disease.

The initial whole genome sequencing of SARS‑CoV‑2 is described in a paper by Fan Wu et al. titled “A new coronavirus associated with human respiratory disease in China”, which was published in Nature on February 3, 2020. Here is a relevant excerpt from the study abstract (bold emphasis added):

Here we study a single patient who was a worker at the market and who was admitted to the Central Hospital of Wuhan on 26 December 2019 while experiencing a severe respiratory syndrome that included fever, dizziness and a cough. Metagenomic RNA sequencing of a sample of bronchoalveolar lavage fluid from the patient identified a new RNA virus strain from the family Coronaviridae, which is designated here ‘WH-Human 1’ coronavirus (and has also been referred to as ‘2019-nCoV’). Phylogenetic analysis of the complete viral genome (29,903 nucleotides) revealed that the virus was most closely related (89.1% nucleotide similarity) to a group of SARS-like coronaviruses (genus Betacoronavirus, subgenus Sarbecovirus) that had previously been found in bats in China.

Metagenomic sequencing of the sample turned out 56,565,928 reads, or substrings of a genomic sequence (short base-pair sequences), that were de novo assembled into 384,096 “contigs”, or contiguous linear strands of RNA. (For a helpful glossary of terminology related to genomic sequencing, see here.)

The Chinese researchers did this using software known as “Megahit”, which is described in a separate paper referenced by the authors as “a NGS [Next Generation Sequencing] de novo assembler for assembling large and complex metagenomics data in a time- and cost-efficient manner.” That paper about Megahit further explains (bold emphasis added):

Next generation sequencing technologies have offered new opportunities to study metagenomics and understand various microbial communities such as human guts, rumen and soil. Due to the lack of reference genomes, de novo assembly of metagenomics data (short reads) is a beneficial and almost inevitable step for metagenomics analysis.

Note that assembling a genome without a reference is precisely what Cowan is claiming cannot be done.

The output of 384,096 contigs does not mean that “the puzzle computer said there are a million”—(or hundreds of thousands of)—“different ways to assemble these pieces into a picture” or that “the pieces of the puzzles fit together a million”—(or hundreds of thousands of)—“different ways”. It means that the “puzzle computer” assembled 384,096 different “pictures”, with each fitting together in only that one way—just as I originally described with my puzzle analogy.

It is also not true that the Chinese researchers had those 384,096 pictures and no rational basis for determining whether any of them might be a virus and whether one of them might have been the cause of the patient’s symptoms.

It is true that of the 384,096 contigs assembled, the one later named “SARS‑CoV‑2” was the longest, consisting of 30,474 nucleotides. The scientists then used polymerase chain reaction technology—again, not to be confused with the diagnostic PCR tests misused to perpetrate systematic scientific fraud in the counting of “COVID‑19” cases—and reference genomes of known coronaviruses that were genetically similar to determine the genome organization of the newly discovered coronavirus, with the result being a full-length genome sequence consisting of 29,903 nucleotides.

However, the researchers did not arbitrarily select that one contig simply due to its length and essentially fabricate the rest from there, as suggested by Cowan. Rather, they first screened the results “for potential aetiological agents”, meaning that they were specifically looking to see if any of the sequences were of a pathogen such as a bacterium or virus that might have caused the patient’s respiratory disease. The longest contig also had “a high abundance” in the patient sample, and phylogenic analysis identified it as being “closely related to a bat SARS-like coronavirus (CoV) isolate—bat SL‑CoVZC45 (GenBank accession number MG772933)—that had previously been sampled in China, with a nucleotide identity of 89.1%.”

The abundance in the sample and the genetic similarity to a known SARS-like coronavirus were reason enough to suspect the longest contig of being the potential culprit in the development of the patient’s respiratory disease.

Note again that the resulting number of contigs was 384,096, not one million. Also, the 89% match was with a SARS-like virus, not SARS itself (which was less of a match), although these are both errors of no consequence as far as the fundamental logic of Cowan’s argument is concerned. (We could correct these misrecollections in his verbal argument and his conclusion would remain the same.)

More importantly, note that it isn’t true that they arbitrarily selected the longest contig and labeled it a coronavirus without having any frame of reference to even identify it as a virus, much less a coronavirus.

Correcting for his inconsequential misrecollection of details, Cowan deals with this by saying that the SARS-like coronavirus that had 89.1% similarity to the longest contig from the patient sample had also been arbitrarily determined to be a coronavirus—essentially, an accusation that the researchers engaged in scientific fraud by simply fabricating the existence of both the newly discovered coronavirus and the genetically similar strain previously identified.

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.

It’s important to note that the question of whether the newly discovered coronavirus had caused the individual’s disease was not answered by this study describing the sequencing of its whole genome. 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.

Note that the length of the genome was not among the specified criteria used to pinpoint SARS‑CoV‑2 as the likely culprit in the pathogenesis of the patient’s disease.

The separate corroborative study mentioned is titled “A pneumonia outbreak associated with a new coronavirus of probable bat origin“, which was also published in Nature on February 3, 2020.

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.

The paper describes metagenomic analysis of a patient sample, which resulted in 10,038,758 reads. However, most of that genetic material was from the patient. After “filtering of reads from the human genome”, only 1,582 reads were retained.

This again demonstrates the untruth of the claim that scientists cannot know what the genetic material belongs to, a corollary of which is that they cannot distinguish human genetic material from viral genetic material. Of course they can distinguish between the two since humans and viruses have different genetic makeups, and scientists have the technology to determine the genetic makeups of living organisms as well as viruses (which are debatably not “alive”).

Of those 1,582 reads, 1,378 sequences “matched the sequence of SARSrCoV”, or severe acute respiratory syndrome-related coronavirus, which is the name of the species of coronavirus capable of binding to the ACE2 receptor. This species of coronavirus is a member of the genus Betacoronavirus.

With de novo sequencing, they obtained a 29,891-base-pair coronavirus genome. They then obtained four more full-length genomes from four other patient samples, each 99.9% similar, but with “less than 80% nucleotide sequence identity to SARS-CoV.”

There is actually a great deal of controversy about this paper in the scientific community as it relates to that other coronavirus with 96 percent similarity to SARS‑CoV‑2, which is named in the paper as “BatCoV RaTG13”. However, the controversy relates to whether SARS‑CoV‑2 is of zoonotic or lab origin, not whether the authors of the study identified a novel coronavirus or not.

Also, although the authors made the unproven claim in their abstract that the newly identified coronavirus “caused” the epidemic of acute respiratory syndrome in Wuhan, China, they rightly noted further into the paper that “The association between 2019‑nCoV and the disease has not been verified by animal experiments to fulfill the Koch’s postulates to establish a causative relationship between a microorganism and a disease.”

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.)

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.

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.

The role of SARS‑CoV‑2 as a necessary but insufficient factor in the pathogenesis of COVID‑19 is a separate topic from the point of this article, though. The question we are concerned with here is whether scientists have actually proven the existence of this novel coronavirus, and the answer is that they have, including through the use of metagenomic sequencing.

Summary of Opposing Arguments

The mutual argument presented by Kaufman and Cowan leads inevitably to the corollary that whole genome sequencing is a scientifically invalid method that cannot be used to identify viruses or microorganisms.

After all, there could not possibly have been a reference genome for the very first coronavirus ever whole genome sequenced. If no valid results can be obtained without a reference genome, then no valid reference genome can possibly be obtained in the first place; the technology known as “de novo” sequencing cannot exist.

The logical corollary of their argument is thus that whole genome sequencing cannot possibly exist; it is a scientific hoax.

This is a puzzling self-contradiction given the acknowledgment in Kaufman and Cowan’s “Statement on Virus Isolation” that the genetic makeup of particles can be “characterized by extracting the genetic material directly from the purified particles and using genetic-sequencing techniques, such as Sanger sequencing, that have been around for decades.”

That part of their “Statement on Virus Isolation” is correct: whole genome sequencing does exist as a technology, and it is a valid technology. Consequently, their mutual argument in response to me is falsified by their own public declaration.

Scientists do have the technology enabling them to identify the nucleotide sequences of particles of genetic material known as “viruses”, which is done by assembling the unique pieces into a whole much like how you certainly can assemble a puzzle without having any foreknowledge of what the finished puzzle will look like. (Don’t cheat by looking at the box cover before assembly!)

The claim that the pieces of the puzzle can be fit together a million different ways so that you never know what you are going to get is incorrect. The assembly of a full-length genome is not random guesswork on the part of the computer but an application of logic much like the logic you use to assemble a puzzle (regardless of whether you know what the puzzle is supposed to look like when you’re done). It is not random or arbitrary but determined logically by the uniqueness of overlapping nucleotide sequences.

This is not to say that errors are not possible and don’t occur. But it is one thing to suggest that a published viral genome contains sequencing errors and quite another to suggest that the entire genome was essentially fabricated by scientists arbitrarily, a perpetration of scientific fraud based on a hoax technology.

In addition to genomic sequencing and phylogenic analysis, scientists have other means of characterizing viruses, and by using a combination of methods, they are able not only to determine that a sequenced genome is that of a virus but to identify the specific strain or variant of that virus. They are then able to map the ancestral relationships of different strains or variants using phylogenetic analysis, creating visualizations of the evolutionary path of the virus.

Conclusion

In sum, Kaufman claimed that I failed to point out a problem with whole genome sequencing in my interview with Bretigne Shaffer, which is that “there’s no way to tell” what organism an assembled genetic sequence is from without first having separated that organism from any other genetic material.

In my newsletter response to Kaufman’s article, I pointed out that, in fact, scientists can use metagenomic sequencing technology to determine the genetic makeup of numerous organisms simultaneously and directly from a patient sample, without having to first isolate each organism, and they can use other methods along with what they already know about similar previously identified organisms to also identify each new source of genetic material.

Cowan in turn took issue to my having pointed out Kaufman’s error, and in his video response to me, Cowan essentially repeats the same false claim that without first isolating an individual virus or organism, there is no way to identify the source of a full-length genome assembled.

In truth, since different organisms are essentially defined by their different genetic makeups, scientists most certainly can identify the source of a genome assembled using metagenomic sequencing and by conducting a phylogenic analysis to map its evolutionary relationship to other known organisms.

SARS‑CoV‑2 exists. The pervasive virus denialism that has regrettably penetrated the health freedom movement is harmfully counterproductive. To combat the threat of medical tyranny accompanying the COVID‑19 pandemic by denying the virus’s existence is to legitimize accusations leveled by the advocates of authoritarianism that misinformation is emanating from within the health freedom movement.

It is also irresponsible to mislead people into believing that a potentially deadly virus does not exist since anyone espousing that belief will naturally feel it unnecessary to take any steps to protect themselves or their loved ones. The message to the public harmfully becomes, for example, that there is no need to get more sunshine or supplement vitamin D to support your immune system against SARS‑CoV‑2 since the virus doesn’t exist!

For another example of how counterproductive this is, the message becomes that the SARS‑CoV‑2 spike protein that mRNA from COVID‑19 vaccines cause human cells to produce is incapable of causing harm to people because the SARS‑CoV‑2 spike protein does not exist!

We must do the hard labor of fighting the medical tyranny with effective arguments rather than lazily contenting ourselves with self-delusion. There’s much work yet to be done to protect ourselves and future generations of humanity from medical tyranny. I beg my readers, please, let’s get to it.