COVID-19 vaccines are in widespread use. Now we need to be even more vigilant to keep the coronavirus suppressed using what we have.

Of all the questions the COVID-19 coronavirus evokes, one has immediate practical implications.

Why is the virus spreading in the way it does?

Many other questions all have relevance. Questions like:

  • Where did SARS-CoV-2 virus come from?
  • What’s the best way to treat the disease?
  • Will vaccines reduce or even prevent transmission?
  • Will selection pressure from those same vaccines bring about vaccine-resistant variants?
  • How long will immunity last?

Yet I see most immediate value in determining why the virus is spreading in the way it does. Knowing that would provide more choices.

Even ‘spreading’ brings a new perspective.

The usual view is that we are talking about coronavirus spreading between people. Masks, hand hygiene, social distancing, lockdowns and vaccines all play an important part. The aim is to reduce the R value, the number of people any one infected person infects. Reducing the R value reduces spreading between people.

The other perspective for ‘spreading’ is between cells in the lungs of an infected person. Reducing that reduces the number of virus particles available to spread between people.

I propose we call the R value for spread between people the outer R, and spread between cells the inner R.

A lot of time and money goes into reducing the outer R. Yet leaving the inner R unresolved puts more virus particles into the environment to thwart efforts on the outer R.

Ignoring the inner R means ignoring the source of the problem. All the strenuous efforts in reducing the outer R can be overwhelmed when there are just too many coronavirus particles present.

New virus variants arise within people rather than between people, making it even more important to give due regard to the inner R.

Humans have 23 billion (that’s 23,000,000,000) Alveolar Type 2 cells in their lungs, the ones this coronavirus attacks leading to COVID-19 disease. When a new virus particle is released from an infected cell, it will find 23 billion target cells within the same person. It’s much easier for the virus particle to infect one of those cells than it is to venture outside and infect another person. When we place our efforts into reducing the outer R while ignoring the inner R, we are giving the virus odds of 23 billion to 1 against us. Those odds favour the virus.

Before coronavirus can spread between cells, it must infect a cell. We know which receptor on the outside of the target cell the virus attaches to allowing it to enter the cell. We know what happens from then until the infected cell releases multitudes of new virus particles. Yet we have another fundamental question.

Why was it able to reach the receptor in the first place? There is a mucus layer over the cells which should prevent the virus reaching the receptor. That mucus has been proven to provide protection against attack by viruses. Is there something making the protective mucus less effective against this coronavirus? Yes, which raises yet another really relevant question.

Are we making it easier for the virus to attach?

Yes, I suggest we are. Regarding the first overriding question of why the virus is spreading as it does, the simple answer is we are helping it.

The ACE2 receptor which the virus attaches to is found on many different types of cells in the human body. Here I will focus on the cells within the alveoli, the tiny air sacks deep within the lungs. Those alveoli expand and contract each time we breath. The walls of the alveoli are extremely thin to allow oxygen to pass into the blood and carbon dioxide to pass out. To protect the delicate walls, a specialised type of lung cell makes a mucus to help the walls as they expand and contract. That mucus, called pulmonary surfactant, covers the cells keeping them moist and provides defences against attack by infectious agents like viruses.

The COVID-19 coronavirus attacks alveolar type 2 cells (AT2 cells), the very cells which make that protective mucus.

Solvent vapours can dissolve the mucus weakening the innate protection the mucus should be providing to the cells this coronavirus attacks.

Alcohol vapour rising from hands treated with alcohol hand sanitisers is a solvent vapour. In 1952 it was proven, in patients, that alcohol vapour dissolves this mucus.

We’ve known for decades that alcohol vapour from hand sanitisers passes all the way through the lungs into the blood. It therefore reaches and passes through the mucus which should be protecting the target cells from coronavirus attack.  It is also well known that alcohol we drink, which passes out through the same mucus layer, can damage the mucus.

It therefore follows that solvent alcohol vapour could increase this coronavirus’ access to ACE2 receptors allowing the virus to infect AT2 cells. Each infected cell is believed to make, and release, about 1,000 new coronavirus particles.

Even worse, every AT2 cell the virus attacks and turns into a factory making more virus, is one less AT2 cell making mucus to defend neighbouring AT2 cells.

For absolute clarity and the avoidance of doubt, I propose that alcohol vapour rising from hands makes it easier for the coronavirus to infect cells. Each infected cell stops making mucus thereby weakening the defences of other cells and SIMULTANEOUSLY releases many new virus particles in the immediate vicinity of cells with less protection because there is less mucus.

Could alcohol vapour be why the virus is spreading as it does?

Since that is scientifically plausible, it means an artificial factor is helping the coronavirus spread. We are helping it.

What happens if alcohol vapour is present in hospital wards where patients are being treated for the disease COVID-19?

  • The patients have lung cells which are releasing innumerable new coronavirus particles.
  • Less defensive mucus is being made as fewer AT2 cells are able to make mucus.
  • Target cells have reduced protection.
  • More virus particles are present to infect more cells.
  • Each new cell infected means less mucus and more virus.
  • When sufficient AT2 cells are infected the patient dies from COVID-19.

On the journey to death, infected patients breath out many new coronavirus particles. If we want to prevent the new virus infecting AT2 cells in another person it would be wise to ensure there were no solvent vapours for the new person to breath in. That is particularly relevant for healthcare workers, many of whom are working in a coronavirus-rich setting during this pandemic. If it is also a solvent-rich setting, the virus is being helped to spread, infect and kill.

How much alcohol vapour is too much? To answer that would involve prolonged studies while the number of COVID-19 deaths continues to rise. We already have over two and a half million deaths making further delay needlessly costly. Existing proven science is there to be utilised and as we approach 3 million COVID deaths it is easier to use the science we have than generate more.

A better choice is to ensure NO alcohol vapours by simply substituting alcohol hand sanitisers with effective products which do not liberate solvent vapours. Such products which kill the coronavirus are already being used in medical settings around the world. NewGenne has one and I am happy to provide the names of others.

For decades there have been ample well known medical, safety and efficacy reasons to justify substituting alcohol sanitisers with safer products. The current pandemic is simply the latest. More on this topic can be found in my nonfiction book Coronoia® Alcohol sanitisers fuel the pandemic? which is available from the shop on this website and Amazon.

This is an evolving thesis presented to generate debate. Who would benefit from being involved in the debate? Certainly anyone who employs people where this coronavirus is likely to be present. That is a huge number of employers. They all have legal obligations to safeguard the health of their employees at work. Any employer who allowed alcohol hand sanitisers to be used by their staff would be unable to defend themselves if staff died from COVID-19 after being infected at work.

Occupational deaths are a very serious matter and they are still happening.

Numerous healthcare workers have died of COVID-19, as have many other workers who were required to work in settings that were both virus-rich and solvent-rich.

This web-page is updated regularly and always ends with a date. The logic supporting the thoughts is being made universally available. If that makes any employer uncomfortable they have the option of removing alcohol vapours from any work environment they control.

If alcohol vapours are helping the virus spread to new victims and if alcohol vapours are advancing some of the infected people to an early death, then a high level of fear is warranted. Fear among workers who rightly fear for their lives. And hopefully fear among their employers who know from this web-page that they are allowing it to happen when they have perfectly safe and effective alternative products.

Now we can return to what I consider to be the most pressing question.

Why is the virus spreading in the way it does?

If part of the answer is the use of alcohol hand sanitisers, we can stop that immediately.

Dr Harley Farmer PhD BVSc(hons) BVBiol(Path) MRCVS

CEO NewGenne Ltd +44 (0) 7876 747700

24th March 2021