My Quest To Find Evidence That Viruses Actually Exist

I set up a community farm called Lovebrook here in Sussex in the UK. On Fridays I lead a community health session. I’m not medically trained but that doesn’t matter

The idea is that we tap into the deep pool of health knowledge and experience that the community already has.

We share what we know on a topic, support each other, work on the farm, and then share a wholesome lunch.

This question came up: ‘I know viruses exist, but how do we know that they exist?’. None of us had the answer, so I thought I should do the question justice and go away and try to answer it as well as I could.

I thought I’d probably be able to find a good lab image of a virus and come back to the group to explain the process of how the virologist isolated and identified it.

To my surprise, it didn’t quite turn out like that. Here’s what I found.

1. What are the techniques that virologists use to identify viruses?

I discovered a whole toolbox of methods that are used in virology — including filtration, cell culture effects, imaging, molecular detection, immune assays, animal studies, and metagenomics.

What surprised me was that all these different techniques already assume the existence of a virus. They don’t really test whether a virus exists — they start from that idea and then build everything on top of it

While these techniques differ technically, their results are interpreted within a framework that presupposes viruses – using techniques that rely on software models built from assumed viral genomes, or automatically interpreting toxicity and cell damage as biological invasion.

I found this confusing because I didn’t understand how this could be squared with the scientific method. If none of these methods can directly show that a virus exists, how can hypotheses about viruses be tested?

This was not a good start, so I decided to find out more about one major technique – CPE

2. How does CPE provide evidence?

I found out that CPE is the routine way to demonstrate the pathological properties of viruses in the lab. The technique is to add suspect virus samples to cells in culture. When the cells begin to die, we have the so-called “cytopathic effect” or CPE.

However, I found out that this technique was not what it seemed. According to Dr Mike Yeadon, a Biopharma research scientist and former Vice President at Pfizer, what he discovered about CPE was:

“so unbelievable that I rejected it for over two years after I was told about it. Cells die not because a clinical sample, thought to contain a virus was added, but because the researchers, following a 70-year-old recipe, radically reduce the growth factors necessary to keep the cells alive and add high concentrations of antibiotics (ostensibly to retain bacterial sterility).”

He goes on:

“You may be thinking ‘This cannot be right because, if it was, the control leg of such a study would report CPE even with no supposed pathogen’. Here’s the shock. None of the papers reporting, for example, “The isolation of SARS-CoV-2” ever include these controls. What this means is that, uniquely in virology, the scientific editors & peer reviewers have become accustomed to not expecting to see control legs and results.”

3. So we just need to do the proper control studies then?

I discovered that over the past two years, Jamie Andrews, Albert Mathews and a team of microbiologists and Geneticists at the Virology Control Study Project, has gone back to the root of this central method in virology and, using contract research organisations, performed the necessary control studies.

In every case, when they looked at the cells after growth factor dilution and addition of antibiotics, they see the cells begin to die off, that is, CPE occurs. They have repeatedly confirmed that it’s the protocol & not the purported “virus” which causes cells to die.

What this suggests is that the most important technique for “confirming the cytotoxic effect of viruses” has been carried out without controls since the first time it was reported on in the 1950s, (when it turns out a Nobel Prize was awarded).

4. Ok, regardless of whether we can confirm the effects of viruses, I’m sure I’ve seen actual images of them?

I initially looked into the technique regarded as the most advanced for visualising viruses – ‘cryo-electron microscopy’ (cyro-EM). This method freezes samples to produce high-resolution images of so-called purified ‘virions’ (viruses outside of the cell).

However, as I looked more closely, I found that purification and identification elements of this technique relied on prior selection, and agreement with genomic and immunological models – meaning the images only make sense once those assumptions are already in place.

The images of viruses that I have seen in the media would have been captured not through cyro-EM but through general electron microscopy (EM). This is the principal method used to visualise viruses at high resolution.

However this method is also not as simple as I thought. It requires cells or cell lines to be removed from their living context and subjected to extensive artificial preparation—including chemical fixation, dehydration, heavy-metal staining, sectioning, and vacuum exposure—meaning the resulting images depict static, highly processed specimens rather than intact, living biological systems.

I learned that the images we see in textbooks are cleaned up high contrast images, and what microscopists actually have to work with is a soup of variegated cell material. Areas of interest can be magnified to find particles that correspond to the size and shape of known viruses, and then this data is triangulated using other (model based) identification techniques.

Viruses where viruses shouldn’t exist

Intriguingly though, researchers such as Dr Stephan Lanka claim that they have identified structures with all the requisite size, morphology and location patterns of a bona fide virus, but in places where viruses definitely shouldn’t exist.

In 2025 The Virus Control Studies Project (VCSP) provided confirmation of this. They sent verified virus-free cell lines with all the requisite contamination controls to reputable labs and contracted them to explore the cell lines to identify potential viruses.

The labs were blind to the rationale for this routine investigation.

The Virology Controls Study Project

The results were striking. VCSP videos of these microscopy sessions were comprehensively and methodically recorded, video-recorded and published. They show that examples of many families of viruses were found by microscopists – oval shaped retroviruses, corona enveloped viruses, icosahedral herpes viruses, large ovoid pox viruses and even evidence of viral ‘budding’ and other phenomena you would expect to see in contaminated cell lines – all within a verified virus free cell line.

The obvious question here is if these are not viruses, what are microscopists seeing?

The researchers suggest that they can only be looking at dead and dying cellular debris — vesicles, blebs, and fragments produced during cell injury and death.

I discovered that microscopists say they routinely see ‘lookalikes’, but if VCSP’s research is correct (and this is relatively cheap to independently replicate and very easy for any curious virologist to confirm), this suggests that everything could just be a ‘lookalike’.

This is an extraordinary situation. If confirmed it would mean that for decades technicians have been expecting to see ‘known’ viruses and then doing nothing more than the equivalent of finding faces in clouds.

5. What about images of viruses in the blood?

I now knew that if I was going to find the solid evidence I was looking for, It would probably have to come from a process that avoided all the artificial preparation and complexities of electron microscopy and CPE.

I decided to find out what could be seen in the blood. I knew that Pox viruses were said to be blood borne, and I knew that it was possible to capture images of small structures in the blood because I had seen images of them.

The microscope technique used here is called light microscopy which is a much more direct process than electron microscopy. I found out that all sorts of structures inside cells in the blood such as mitochondria, and granules are directly visible through this apparatus – which was very promising since Pox viruses are the same size as these already seen structures at 200 – 300 nm.

Frustratingly however, these viruses are said to remain invisible to light microscopy not because of their size, but because they are said to be transient and lack contrast. Because of this, light microscopy wouldn’t be expected to see them.

6. Ok, so even if there are problems with lab techniques, there must be lots of experiments proving contagion?

I felt I was sure to find good evidence here, particularly with colds and flu being so common. However, again I came up against extraordinary claims such as this by Dr Tom Cowan in his book ‘The Contagion Myth’ co-authored by Sally Fallon Morell:

‘You will not find a single paper that directly proves natural human-to-human transmission of a virus’.

This sounded like the gauntlet was being thrown down here so I explored further. I then discovered that in the UK The Common Cold Unit in Salisbury produced 40 years worth of data that failed to demonstrate natural human contagion.

Mike Yeadon has discovered the same phenomenon. After a career specialising in respiratory diseases he created a Substack repository of every published study on attempted transmission of colds and flu.

These papers start in 1918 & continue until 2024. He claims that in not a single paper do healthy volunteers develop symptoms, after spending time with a symptomatic person, any more often than when the volunteers spent the same amount of time with a well person – suggesting that respiratory illnesses do not seem to be contagious.

Animal experiments

Even animal contagion experiments appear to be unsatisfactory. As Dr Andrew Kaufman has pointed out, even the most frequently cited animal “contagion” experiments typically involve injections of ground tissue, force-feeding of pathological material, and conditions of extreme confinement, stress, or deprivation – perhaps less proof of contagion, and more proof that you can make an animal sick by poisoning or injuring it.

Contagion papers

If contagion is being asserted, then it seems obvious that I should be looking for evidence that shows natural transmission under ordinary, non-coercive conditions. When I drilled down into specific papers the human transmission studies topic became even more intriguing.

For example,

HIV: In the longitudinal study by Padian and Padian researchers followed sexually active couples, where one partner was HIV-positive and the other HIV-negative, but under the conditions of this study found no documented cases of HIV transmission between partners.

SARS-CoV-2: In one of the most widely discussed human challenge studies of COVID-19 at Imperial College London, healthy volunteers were deliberately exposed to SARS-CoV-2. Most developed either no symptoms or only mild rhinitis symptoms. Some commentators have noted that participants underwent frequent nasal sampling. Though not identified as a causal factor in the study itself, they speculate that this was the cause of the observed rhinitis.

INFLUENZA: In a 2020 human challenge-transmission study led by Jonathan S. Nguyen-Van-Tam and colleagues, healthy volunteers infected with influenza A (H3N2) were exposed to other participants in a controlled setting, but there was ‘minimal’ evidence of transmission under those conditions (1 in 75 participants).

In a subsequent follow-up human challenge study published in 2026 by Jainyu Lai and other notable virologists and epidemiologists, it was reported that ‘no recipient developed influenza-like illness, PCR-positive respiratory samples, or serological evidence of infection following controlled exposure to infected donors.’

This theme is echoed throughout Daniel Roytas’ book ‘Can you catch a cold?’ (2024). He reveals that he spent years searching for all the studies he could find on human to human transmission of viruses.

It turned out that none of the more than 200 studies that he found showed transmission.

7. But I have seen evidence of contagion with my own eyes!

Like everyone else It feels obvious to me that we “catch colds” from other people. I’ve noticed the sequencing of illnesses happen in ways that are consistent with contagion. However if I really have to think about it, that’s all it is, consistent with contagion but not proof of it.

So in the spirit of the question ‘how do we know that viruses exist?’ I realise that while I’ve witnessed what looks like contagion in my household, I know that I also routinely witness close contact resulting in no transmission.

Similarly, I have come across anecdotes from doctors and health workers reporting that they spent whole careers working with infectious disease patients while also remaining mysteriously ‘immune’.

Patterns from events

I noticed that I form patterns from events. When I develop a cold, I remember recent contact with someone who had a cold, but I never consider that contact if it didn’t lead to me catching a cold. My expectations seem to be central to this too.

For example I’d never find myself wondering who I might have caught a headache from as I already know that headaches are not contagious. So although I may think I am observing patterns of disease due to pathogenic contagion, in reality I can’t rely on this as evidence of contagion.

8. So what is making us sick then? If there’s no good alternative theory for colds and flu then it must be a virus, right?

The virus explanation has framed my understanding of sickness for as long as I can remember, so removing it to consider an alternative felt a bit like like stepping into conceptual thin air at first.

This is where I learned about ‘Terrain theory’ as an alternative to ‘Germ theory’. This holds that people become ill because their internal environment is compromised, not because they are attacked by external pathogens.

In terms of specific alternative causes for viral disease, like most people I was under the impression that there weren’t any. However it turns out that there is actually no end to the list of proposed non-virus causes, eg toxic exposures (chemicals, pesticides, pollution, pharmaceuticals), Nutrition, Poor diet (ultra-processed foods, seed oils, sugar, alcohol), Dehydration, Chronic stress, Emotional shock, Unresolved trauma, Poor sleep, Lack of sunlight and fresh air, Poor gut function, Accumulated cellular waste, Metabolic stress, Poor circulation, Mold and biotoxins, Physical injury, Early years separation anxiety, Medical interventions, Psychological conflict, Fear, Noise, EMFs, Radiation, Temperature extremes, Social stress, Loneliness, the list goes on..

This is taken from a long document, read the rest here substack.com

Header image: Live Science

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Comments (1)

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    Tom

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    …”What surprised me was that all these different techniques already assume the existence of a virus.”…it is assumed because they do not want anyone questioning their science fiction lies and propaganda. Realize how much of the medical mafia is constructed around the fake existence of viruses. Those pictures could be anything.

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