Why Virus Denial Is Wrong

Does this even need saying? That I should even feel moved to write this post, in this day and age, seems extraordinary. But an increasing number of people are latching onto the hoary old idea that there is no such thing as a virus – that viroloigists have been studying an artefact all this time; a product of the organism rather than an entity hijackiing host biology in order to spread between hosts.

Like many positions over the last few years, it is driven by Covid denialism taken to extremes – not only does SARS-CoV-2 not exist, none of them do. This seems a somewhat hyperbolic extension – scepticism over SARS-CoV-2 extended to dismissing the entire science of virology! This puts me in mind of the inhabitants of the planet Krikkit in Douglas Adams’s Hitchhiker’s Guide upon observing the glories of the Universe for the first time above their cloud-shrouded planet:

“It’ll have to go”

To anyone with even a basic grasp of molecular biology, this seems a ridiculous position to espouse. Not only is germ theory denial completely at odds with the understanding of the nucleic acid-protein relationship that developed in the latter half of the 20th century, viruses directly contributed to that understanding. It was a virus that gave some of the earliest evidence that nucleic acid was the genetic material. Viruses infecting bacteria – bacteriophages – had vital roles in elucidating the genetic code, in understanding the control of gene expression, and in genetic engineering. A virus was the first ‘organism’ to have its genome sequenced. The literature is full of ΦX174, T4, T7 and λ. All of this was only possible because they are clearly an entity separate from the organism they infect – in those instances, the ‘model’ bacterium Escherichia coli. Their genes are different, their proteins are different, they can be purified, crystallised, caught or interrupted in the act of infection… yet these people would have it that no virus has ever been ‘isolated’.

One might forgive online contrarians their ignorance. People classically do not know what they don’t know; only from a position of a reasonable grasp of molecular biology can one see how absurd the idea is in its light. Yet one or two people with a publication history in relevant fields have latched onto this. Notable among them are Stefan Lanka and Mike Donio. Both have published papers in their earlier careers that are quite orthodox. Here’s Lanka with a 1993 paper on the genome of a virus of marine algae. Donio, meanwhile, co-authored this paper on co-occurrence of Guillain-Barre virus and HIV, for example. Something must have caused an epiphany. Donio has now taken to Tweeting, almost daily:  “Today is […] and there still is no evidence that viruses exist!”.

A potted history

Viruses were first suspected in 1892 when Dmitri Ivanovsky demonstrated that ‘something’ in sap from infected plants was able to transfer tobacco mosaic disease to healthy plants after passing through filters fine enough to exclude bacteria.

In 1896, Ernest Hankin noted that ‘something’ in the waters of the Ganges, again able to pass through a fine filter, had a marked detrimental effect on the cholera bacterium. He had discovered the first bacteriophage.

The agents underlying these observations, whatever they were, were invisible to light microscopy, so remained speculative. At that stage, it was not possible to rule out the possibility that the phenomenon was due to some chemical agent in solution. So in about 1900, virus denial would have been a perfectly respectable position! But with the developments in electron microscopy and x-ray crystallography (only possible if a substance can be ‘isolated’ and purified) during the first half of the 20th century, we were finally able to visualise these agents, while developments in biochemistry enabled detail of their protein and nucleic acid components to be examined, as well as providing materials for investigation into the fundamentals of biochemistry itself. For example, plant viruses were observed to provide a useful source of pure RNA as far back as the 1930s, a chemically difficult separation using whole cells due to the close similarity of DNA and RNA.

In the first half of the 1900’s, it was not known whether protein or nucleic acid carried the genetic material. Two landmark experiments, familiar to anyone who has ever taken a molecular biology class, established that it was definitely nucleic acid. Firstly, Oswald Avery in 1944 showed that the material causing transformation in pneumococcal bacteria – making infectious particles from uninfectious components – was most likely DNA. However, they could not discount the possibility of microscopic impurity. The matter was largely settled by Alfred Hershey and Martha Chase in 1952 using viruses. Bacteriophages have a protein coat with nucleic acid inside. By separately labelling proteins with radioactive sulphur, and nucleic acids with phosphorus, they established that, on infection, the protein stayed outside the cell and the nucleic acid went in, causing the subsequent death of the cell. Later, tobacco mosaic disease was shown to be caused by its RNA component alone, indicating that plant viral diseases, at least, had a similar basis to phage-induced cell death.

Within a year of Hershey-Chase, the Watson-Crick structure of nucleic acid was published, with its famously laconic observation

“It has not escaped our notice that the specific pairing we have postulated immediately suggests a possible copying mechanism for the genetic material.”

This ‘pairing’ refers to the pairwise affinity of the 4 DNA bases for each other: A binds to T, and G binds to C. Thus, if you know the sequence of one strand, you automatically know the sequence of the other. You can use the one as a template for the other. More than that: a template is always used. Barring occasional single-base insertion, or monotonous polynucleotides, any nucleic acid sequence always ultimately derives from template-directed synthesis, not from stitching together bases de novo. This is important for the question ‘are viruses real?’, as we shall see.

Further progress was made by Crick in the elucidation of the genetic code, the set of 64 different triplets that specify the amino acid sequence of proteins. This work made elegant use of a virus, bacteriophage T4, to establish that the code was triplet in nature. In these pre-sequencing days, the work relied upon a prior map of the ‘phage’s genome derived by Seymour Benzer. This map was only made possible by the way in which the phage infects its hosts – phages are not simply breakdown artefacts, as deniers suppose viruses to be.

Following this, the coding table was gradually filled in by Nirenberg – first the easy ones, poly-U etc, then simple alternates giving 2-acid mixtures, and so on. The triplet code was thus independently confirmed.

In parallel with this work, viruses contributed to a fuller understanding of gene expression control. A gene in DNA consists of a sequence transcribed into RNA, but flanked by ‘upstream’ and ‘downstream’ sequence that is not transcribed. The RNA is processed before being translated into protein, 3 RNA bases coding for each amino acid. Again ‘upstream’ and ‘downstream’ sequence is not translated, but is required for proper processing. Without these flanking sequences, the gene does nothing. Much of this picture came initially from studying and utilising viruses.

“Ah”, says the denier. “I accept the existence of bacteriophages, so you’ve wasted your time”. But why? What is fundamentally different about bacteriophages? Is it simply that they are harder to deny? By what criteria do you accept the ‘isolation’ of phages infecting prokaryotes, but reject that of viruses infecting eukaryotes? It’s fairly easy to see phages in action. You can use a cell counter, and observe the bacteria blebbing out in real time, as they burst forth their cargo of replicated virions. But then, you can do similar with single-celled eukaryotic protists. It becomes a shade harder with multicellular organisms, but not much. Point is, the techniques and observations in use at a level one does accept are different only in detail from those used at a level one does not. I think this is why people latch onto a ‘hardline’ version of virus denial. Concede on one, there’s a foot in the door and you have to let ’em all in!

It is not simply bacteriophages that have contributed to the above understanding. For example, in determining that eukaryotic cells process mRNA, poliovirus was used, specifically because it multiplies in HeLa cells, and redirects their protein synthesis to itself. It is not a breakdown product of those cells. Similarly, DNA viruses herpes simplex and mouse virus SV40 (which integrates into chromosomes) were used to investigate the path from nuclear RNA to cytoplasmic processing, and indicating the mechanisms by which viruses can cause cancers. Vaccinia virus gave the earliest indication that mRNA acquired a ‘poly-A tail’ – a very useful ‘handle’ for grabbing hold specifically of mRNA for further investigation. Other viruses such as vesicular stomatitis virus, reoviruses and adenovirus also helped supply key elements of the emerging picture, in a manner that depended entirely on their cellular infectivity and reproduction.

Are we to suppose that these scientists were all completely misled by artefacts? One wonders how molecular biology survived these errors!

Genome or ‘genome’?

Virologists think they recover viral genomes from sick patients. Deniers do not. And here’s the nub of the problem: if the virologists aren’t looking at ‘real’ viral genomes in the disputed part of the set, what are they looking at? Some argue that these ‘pseudogenomes’ are an artefact of extraction, constructed from the host DNA. This is highly implausible. These ‘pseudogenomes’ have a consistent size and structure for a given ‘virus’, nonetheless distinct from those produced by other ‘viruses’: for a given species the same genes appear in the same order with largely the same sequence. Yet among those distinct constructs, there are relationships. The ‘coronaviruses’ cluster together, the ‘rhinoviruses’ likewise, while even within a given cluster different variants appear. It looks for all the world like a nested hierarchy: a product of a branching process of replication. Why would a process of host DNA randomisation produce a nested hierarchy? You would expect every instance to be different, random, and be more closely related to the host genome than to each other.

Furthermore, some of these ‘pseudogenomes’ are RNA, some DNA. So we need (at least) two processes here: one to reassemble DNA in the nucleus, the other operating on RNA transcripts. Within those, we need mechanisms to separately construct adenovirus, rhinovirus, coronavirus, rabies, etc etc.

Not only that, these reassemblies need to generate viable functional genes – because the genes of viruses are functional. They can be transcribed (DNA viruses) and/or translated (both) into a consistently folded protein product indistinguishable from that in an intact virion. As we can see from the picture above, a DNA gene needs specific control sequences to be translated at all, and it needs to contain control sequences for subsequent processing when it has been copied into RNA. There’s even the restriction that the first triplet a specific distance downstream of the RNA control sequence is AUG.  Getting this tight specification from random assembly is a tall order – like getting the bitmap of a horse, and the header detail that tells the rendering software what it’s looking at, by flipping coins.

Yet there is absolutely no evidence of such reassembly. Bear in mind that, as noted above, a nucleic acid strand always derives from a template somewhere. There is no known mechanism that generates non-monotonous stretches of nucleic acid without using a template, or which obliterates all information regarding that template in the process. Apart from occasional single-base insertions, DNA sequence always comes from a prior DNA/RNA sequence, RNA likewise, even when there is recombination. Yet there is little or no sequence similarity, even fragmentary, with the host in these genomes. Conversely, there’s a great deal of sequence similarity with other instances of the viral sequence. So why not infer that they have a common origin with each other? It is far more likely … surely?

There is an echo of arguments with Creationists in all this. If I see a host of nucleic acid strings of common sequence, forming nested hierarchies, my go-to explanation is that these are most likely commonly descended, by template copying. This is the general principle behind molecular phylogenetics, which establishes relationships between species using genes, and also can be used to track diseases. But no, these latter-day Creationists would have it, these genomes are ‘separately created’ from the host in some way that nonetheless generates functional genes and nested hierarchies.

If your hypothesis demands an unknown mechanism to keep it afloat, and ignores a more obvious, known cause, so much the worse for your hypothesis. On the other hand, if such a mechanism were discovered, there would be a Nobel in it. Leading lights of the ‘no-virus’ movement seem more interested in issuing theatrical monetary challenges to the mainstream than in investigating this. In John Baez’s prescient 1998 ‘crackpot index’, that’s a 10-pointer.

45 thoughts on “Why Virus Denial Is Wrong

  1. Allan,
    Have you been following Steve Kirsche’s blog on substack?
    Please confirm.
    J-mac

  2. Neil Rickert: This does not appear to be at all relevant to the issue being discussed.

    Really?!
    I know you don’t have a good explanation as to why whether viruses are alive or not is relevant to this, or any other issue, so I’m not going to make you come up with a bad one and make as all suffer reading it…

  3. J-Mac:
    Allan,
    Have you been following Steve Kirsche’s blog on substack?
    Please confirm.
    J-mac

    Absolutely not! The man is a loon.

    (Edit: at least I see on this one we’re on the same side).

  4. J-Mac:
    Are viruses alive ?

    Sometimes I think ‘yes’, but I can accept the argument for ‘no’.

    Nonetheless, in the context of my essay, to have a view either way one would first have to agree they exist.

  5. Something about this whole thread reminds me of the joke about the agnostic dyslectic insomniac who lies awake at night wondering, is there a dog?

  6. It’s interesting that arch-contrarian Kirsch has come down on ‘the right side’ on this one, since it’s an idea that has considerable traction among antivax types. But of course there are many positions and permutations, so I shouldn’t fall prey to the black and white thinking I often criticise. It is perfectly possible to be a vaccine-sceptical Covid-accepter. Which explains the ridiculous shopping list of drugs, supplements and drenches Kirsch chugged when he got it.

  7. A bit late to the party, the heat got to me. Now we’re getting a wetting and the humidity is horrendous!

    Wow, Allan, you have the essence of a textbook there. Such clarity, such style!

    That I should even feel moved to write this post, in this day and age, seems extraordinary.

    Almost the opposite effect on me. That all my old certainties seem under threat has rendered me (almost) speechless, and possibly incoherent.

  8. Currently I am reading Michael G. Cordingly’s Viruses: Agents of Evolutionary Invention, which is a enjoyable and accessible introduction into the tremendous diversity of our invisible parasitic friends.

    Amusingly, as it pre-dates the outbreak of the COVID19 pandemic by 2 years it declares influenza to be the greatest threat for a next pandemic:

    Moreover, although new zoonotic viruses will challenge us on occasion (e.g., the SARS outbreak), the emergence of a pandemic human influenza virus is justifiably our greatest preoccupation.

  9. Having personally sequenced thousands of COVID samples and gotten results that are a few mutations away from the Wuhan reference, I would have the same questions that Kirsch has had on his website. I have also sequenced negative controls and gotten back zero sequence (or just a few hundred random sequences compared to millions of amplicons/reads from the positives).

    The sequences I get back are not found anywhere in the human genome. They are also transient, meaning that these sequences come and go. They occur after close contact between people. We can also measure increases in the number of mutations over time. We are also sequencing from RNA template, not DNA, so that RNA has to come from somewhere.

    So if it isn’t a virus, then what in the hell is it? Why are nasopharyngeal swabs from symptomatic people transiently positive for these RNA sequences? Why do these RNA sequences increase in number in cell culture and create plaques?

  10. T_aquaticus: The sequences I get back are not found anywhere in the human genome. They are also transient, meaning that these sequences come and go. They occur after close contact between people. We can also measure increases in the number of mutations over time. We are also sequencing from RNA template, not DNA, so that RNA has to come from somewhere.

    So if it isn’t a virus, then what in the hell is it? Why are nasopharyngeal swabs from symptomatic people transiently positive for these RNA sequences? Why do these RNA sequences increase in number in cell culture and create plaques?

    Do you have access to the viral sequences that killed an estimated 20 plus million people during the Spanish Flu pandemic In 1918?

  11. My whole family has recently tested positive for convict-19. What a joke!
    My oldest son had a cough for 3 days a bit of fever 37 plus. My younger son had a typical stomach flu that was treated with a combination of some Eastern European/North American remedies. It worked within 6 hours.
    My wife (vaxxed March 2021) lasted the longest…
    I had chills after getting out of the shower for few days…

  12. Flint:
    Something about this whole thread reminds me of the joke about the agnostic dyslectic insomniac who lies awake at night wondering, is there a dog?

    You must be commenting on the wrong thread…as usual…No, don’t change that chronic diseases. Even skeptics here pray for a good laugh from time to time…

  13. J-Mac: You must be commenting on the wrong thread…as usual…No, don’t change that chronic diseases. Even skeptics here pray for a good laugh from time to time…

    As you once again demonstrate, you have mastered the art of missing the point.

  14. Steve Kirsch says:

    If you ask 436 people for their pro or con vaccine story and none of them have an anecdote where the vaccines had superior mortality and morbidity. This is a statistically impossible outcome if the vaccines are neutral or beneficial.

    he calculated a p value 😃

  15. According to Steve Kirsch, no-one has looked at All-cause mortality by vaccination status.
    I found this rather surprising, so I pulled up the first data set I could find, for the UK from Jan 1 to May 31 this year.
    I was shocked, shocked to discover that the all-cause mortality rate was 2.44 fold higher in the unvaxxed (=2,337 /100,000PY) versus the ever vaxxed. (=957 / 100,000PY).
    Hey, maybe the time period was too late to capture all those vax-related deaths… So I checked Jan 1 to December 31 of 2021 – that’ll cover most of the vaccinations…
    Rate = 2,463 for the unvaxxed, and 920.3 for the ever vaxxed.
    That’s a 2.68-fold faster death rate.
    We explained this back in March.
    Do I get a million dollars?
    ROFL

  16. Corneel: Sometimes J-Mac appears to be saying that COVID19 cases are (deliberate?) misdiagnoses of influenza infection. At other times he appears to believe that the flu is caused by human (non-SARS-CoV-2) coronaviruses. Perhaps he believes both to be true. One never can tell with J-Mac.

    That’s ridiculous. We have the entire viral genome sequence for these cases, and they are correlated with positive PCR COVID tests. Only someone ignorant of infectious diseases, viruses, and molecular biology would make such baseless claims.

  17. T_aquaticus: Only someone ignorant of infectious diseases, viruses, and molecular biology would make such baseless claims.

    Surely J-Mac will return to explain his position and give some insightful and compelling arguments.

    There is a first time for everything.

  18. Corneel: Surely J-Mac will return to explain his position and give some insightful and compelling arguments.

    There is a first time for everything.

    SURELY!!!

    He could also explain why immunizing against the S-protein from the Wuhan strain of SARS-CoV-2 greatly reduced hospitalization for SARS-CoV-2 positive patients. If the cause were influenza then there is no reason why 95% of hospitalizations should be amongst the minority of Americans who were unvaccinated. The S-protein vaccination rates in hospitals should have mirrored the vaccination rates in the general population if the cause were influenza since influenza does not have an S-protein.

    Surely he has an answer for this.

  19. dazz:
    Viruses don’t exist, but when they do, their origin must be in a lab. Right? right?

    The Huanan Seafood Wholesale Market in Wuhan was the early epicenter of the COVID-19 pandemic

    Sorry, kind of offtopic, but there it goes.

    I’m not sure this means anything in the absence of some non-human vectors. I mean, actual animals, actual lineages.

    The animals suggested as the cauldron of origin — pangolins and bats — simply did not exist in the Wuhan markets.

    So it’s a mystery.

  20. If viruses don’t exist as described, the so called vaccines wouldn’t work, would they?
    Thank God they….do..?

  21. Steve still hasn’t responded to my challenge of proving that SARS COV2 is not only real and not rebranded seasonal mostly upper respiratory infections called the flu. All I’m asking for is to buy the samples of SARS COV2 virus and infect some mice vs controls. Since SARS COV2 virus is supposed to be extremely infections and lethal, there should be no problem at all to distinguish the virus infections from controls.
    Unfortunately, nobody I know about, has even attempted to do this simple experiment. The $1M reward stands..
    I’m sure joke_dna lab has done those very experiments and their data is publicly available…😉

  22. J-Mac: All I’m asking for is to buy the samples of SARS COV2 virus and infect some mice vs controls. Since SARS COV2 virus is supposed to be extremely infections and lethal, there should be no problem at all to distinguish the virus infections from controls.

    Yes, we have all heard how the global mouse population has been decimated by the onslaught caused by COVID19. When was the last time you saw a mouse? eh? eh?

  23. J-Mac:
    Steve still hasn’t responded to my challenge of proving that SARS COV2 is not only real and not rebranded seasonal mostly upper respiratory infections called the flu. All I’m asking for is to buy the samples of SARS COV2 virus and infect some mice vs controls. Since SARS COV2 virus is supposed to be extremely infections and lethal, there should be no problem at all to distinguish the virus infections from controls.
    Unfortunately, nobody I know about, has even attempted to do this simple experiment. The $1M reward stands..
    I’m sure joke_dna lab has done those very experiments and their data is publicly available…

    Although I agree with your sentiment, that isn’t a fair challenge. First, you need to be registered as a BSL3 facility before you can receive viral samples like the ones you describe. You also need to be a BSL3 facility in order to house the infected animals. Also, mice are not a permissible host, but hamsters are, so they would be the species of choice.

    It is worth mentioning that mink are a very permissible host for SARS-CoV-2, and mink farms have been seeing mink die from the virus. In addition, transmission from human to mink and then back from mink to human have been recorded at mink farms.

    https://www.science.org/doi/10.1126/science.abe5901

  24. dazz:
    Viruses don’t exist, but when they do, their origin must be in a lab. Right? right?

    The logical contortions of antivaxxers/virus deniers merit a thread of their own.
    – Not worth worrying about but ivermectin/hcq/vit D/zinc are vital.
    – PCR doesn’t work but ivermectin is great as shown by its effect on PCR positivity.
    – Vaccines don’t work but select for immune escape.
    – keep vaccinating and variants will get more virulent, but variants are also getting milder.
    – Government data is a lie, but look at this Government data.

  25. In Canada, we seem to have different virus and therefore the reliable government data is showing that the Omni-com wave had negative impact on mortality. What do you see, objectively.?

  26. J-Mac: In Canada, we seem to have different virus and therefore the reliable government data is showing that the Omni-com wave had negative impact on mortality. What do you see, objectively.?

    Really? Looks like 2022 is higher than every year. Well, except April in 2020 and 2021.
    Care to support your random factoid with data?

  27. Allan Miller: The logical contortions of antivaxxers/virus deniers merit a thread of their own.
    – Not worth worrying about but ivermectin/hcq/vit D/zinc are vital.
    – PCR doesn’t work but ivermectin is great as shown by its effect on PCR positivity.
    – Vaccines don’t work but select for immune escape.
    – keep vaccinating and variants will get more virulent, but variants are also getting milder.
    – Government data is a lie, but look at this Government data.

    Yes, I’ve seen those twitter threads. But they’re the true critical thinkers, you know. Or so they say.

  28. If viruses don’t exist, how do you explain monarchs and aristocrats? huh?
    I bit opportunistic, I know, but still 😄

  29. What I meant to say in my last comment is that the Omni-con wave had negative excess deaths in Canada and it looks like in UK….
    Now SADS and unknown causes of deaths took over, especially in Alberta…
    At my wife’s hospital 5 young doctors died within few weeks.. 1 had cancer but didn’t die from it…

  30. Just looked at the stats.

    Case fatality rate for the world, for the duration, is about one percent.

    For New Zealand, about 0.17 percent.

    I watch New Zealand because it was 95 percent vaccinated before the plague hit.

    For whatever reason, they gave delta a complete miss.

  31. J-Mac:
    What I meant to say in my last comment is that the Omni-con wave had negative excess deaths in Canada and it looks like in UK….

    Good old vaccination.

    Now SADS and unknown causes of deaths took over, especially in Alberta…

    Including long term sequelae of Covid. AVs seem to think there’s a statute of limitations on Covid as a cause but vaccines are indefinitely responsible.

    And now, an anecdote:

    At my wife’s hospital 5 young doctors died within few weeks.. 1 had cancer but didn’t die from it…

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