COVID Second Wave; Of Hares and Foxes; Primer for Policy Makers, Part 5

We continue from COVID Second Wave; Of Hares and Foxes; Primer for Policy Makers, Part 4. The second question on our list is:

  • What drives virulence, and what holds it back?

We noted that even though viruses don’t have brains, they appear to have intelligent strategies. It comes from randomness at the molecular level, resulting in mutations. We see only the successes.

Since a virus is very small and simple compared to a living cell, the possibilities of change, of becoming a “better virus”, have limits. The limits can be roughly estimated from the structure of the virus.  But more weight is given to “reputation”. For example,

  • Baculoviruses infect insects, and are so specific that they typically  infect a single species of insect. Because they are made of double strand DNA, which is durable stuff, the chance for a baculovirus to find a new game is thought to be small.
  • Pox viruses, which include smallpox, manage to mutate even though their structures should be stable.
  • Different species of rhabdoviruses infect an incredible range: tomatoes, potatoes, and all kinds of vertebrate animals. The rabies virus is a rhabdovirus. These viruses are made of unstable RNA,  enabling rapid evolution. They have a highly adaptable plan, more so than a coronavirus.
  • Adenoviruses, used in gene therapy and in some COVID vaccines, were thought to be stable for the same reason as baculoviruses. But because stability is critical., the assumption has been studied, and found to be unjustified, and possibly false. See Why I Would Not Take the Russian or Oxford – AstraZeneca Vaccines – Part 2, and (CNN) AstraZeneca pauses coronavirus vaccine trial after unexplained illness in volunteer.
  • Rarely, radical mutation of viruses occurs. Could COVID become radically different, lose its trademark halo, become something radically different? When the measles virus infects the brain, it undergoes radical mutation. So all things are possible, but mostly rare. Our focus is on mutations that occur all the time.

SARS-CoV-2 is a single strand RNA coronavirus. The instability of RNA means it undergoes frequent mutation and recombination. Nothing in the natural history suggests coronaviruses are anywhere near as versatile as rhabdoviruses. But the way a coronavirus attacks a cell can, by rapid mutation, quickly change virulence.

The surface of a cell is studded with hormone receptors. Mimicking the angiotensin-2 hormone, COVID-19 attaches to and enters the cell via the angiotensin-2 receptor. When angiotensin-2 attaches to and/or enters some cells,  it causes blood vessels to constrict, blood volume to increase, and a bundle known as the fight-or-flight response, which may be why anomalous blood clotting is also observed.

It does not benefit COVID-19 to kill the patient. It uses the angiotensin-2 receptor without considering the consequences. But it may be found that the more strongly COVID mimics angiotensin-2, the more lethal it is. 

People with hypertension are at risk for severe COVID.  Hypertension is treated with angiotensin blockers. But as of 9/1, interrelationships of these factors is unknown:  (AJMC) Patients With COVID-19 Should Stay on ACE Inhibitors, ARBs, Study Finds.

What of infectivity, the ability to propagate from one infected person to another? It’s not a completely separate issue. Besides attachment to a cell, where it entangles with virulence, infectivity involves:

  • Concentration. How much virus is present in exhaled air.
  • Aerodynamics. how easily it forms an aerosol.
  • Durability. How long it survives outside the body.
  • Stealth. how obvious it is that a person is infectious.

These are 5 adjustments subject to random mutation. They are not likely to be independent, but the details will come in coming years.  We’ve done the groundwork for:

  • What drives virulence, and what holds it back?

With 5 knobs twisted by random mutation, and the Houston Astrodome (see COVID Resurgent: Of Hares and Foxes; Primer for Policy Makers, Part 3), we’re poised to see Darwin’s Natural Selection in action.  See if you can get a skybox.

I’ll try and dig up Howard Cosell.















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