How does the virus invade?
The coronavirus is a sphere with club-ended spikes all over it. The end of the club has a protein on it called Protein S. It’s about 3000 amino acids long and has a weak spot in the middle called a cleavage site. It’s the feature photo for this post.
A part of the Protein S has a stretch of 60 or 70 amino acids that bind to a complementary stretch of amino acids on the surface of a gut or lung cell called the ACE2 receptor site. So the virus gets stuck on the surface of the cell when its Protein S happens upon an ACE2 receptor.
As the virus lies stuck to the human gut or lung cell, various enzymes in the fluid around the cell can float by and eat away at the cleavage site. The weak spot in the Protein S region of the virus membrane breaks and so does the cell membrane. The virus particle and the human cell now share their insides. The RNA of the virus has full access to all the substances in the human cell that allow it to breed freely, make many copies of itself and coat them in the spherical capsule. It will then rupture the cell and release hundreds of offspring to go on and infect other cells.
Why is there often such a vicious lung reaction?
My theory takes its inspiration from the early ACE inhibitors of the mid 80’s. Enalipril in particular. The new ones don’t have the cough problem.
These blood pressure drugs bind to (slightly different) ACE receptors and block the conversion of Angiotensin one to Angiotensin two. Angiotensin one raises blood pressure a little, but Angiotensin two raises blood pressure a lot more. They were very successful at lowering blood pressure but in the occasional person they were associated with a dry cough that sounded allergic. This virus binds to an ACE receptor site as do ACE inhibitors. Is the virus creating a super version of the allergic cough we saw with those early ACE inhibitors?
Known causes of an enhanced inflammatory response in the lungs of those who have died
These include chronic occupational exposure to the virus – this may be an example of epigenetic stimulation of the genes that produce the ACE2 receptors
The number and availability of the ACE2 receptor sites influences how easily a coronavirus can attack, invade and take over our lung or gut cells.
The expression of the ACE2 gene increases with age leading to more ACE2 receptors on cells.
There is a suggestion that exposure to caffeine and alcohol increase the risk by doing the same – it’s called up-regulation of the genes. An external agent – alcohol, caffeine, maybe a virus – they don’t change the gene; they make it work harder. This means more ACE2 receptor sites on the surface of the cell for the virus to bind to and invade.
I don’t have a reference for that theory. It’s from animal studies. The good thing is that if the alcohol or coffee is stopped, after two weeks the effect wears off and the gene is no longer up-regulated. Less receptor sites. Less targets for the virus to land on. Less ACE2 receptors in the lung means a less severe Sudden Acute Respiratory Syndrome. Better survival. Less targets on the cells that line the heart and blood vessels – less likelihood of dying from heart failure. Strong message here about those lifestyle factors.
What to do now?
Self isolate or isolate your child for 2 weeks if there is a case at your Uni or school.
Keep social distancing.
Keep up the physical exercise
Future vaccines and drugs
I think that some of the current ACE inhibitors may be modified to compete with the virus for binding to its target sites, lessening the speed of invasion. Or they may attack the Protein S.
Vaccine development will be aimed at the Protein S that the virus uses to attack us.