20A.EU1, The Second COVID Wave

Has a true second wave arrived, with  the historical precedent of increased virulence? Let’s start with two points:

This combination, combined with uncertainties yet to be resolved, could define an actual second wave.

“Second Wave” does not have an exact medical meaning. It stems from historic pandemics, dating back to the first written histories. Back then, people-mobility was occasional, except for traders and soldiers. The traders  carried the news of the Silk Road, which ran between southern Europe and China.

Western forest fires are the visual. A new plague-wave started in a single place,  moving with the slow carriage of goods and people along the Road. A forest fire leaves a wake of burned-out land. As a plague moved along the Silk Road, it left a decimated population. Because mobility was so slight, ancient plague waves had sharp dates of arrival.

With the extreme mobility of the jet age,  the sharp dates-of-arrival picture is replaced by fuzzy blobs. The  U.K./Spain connection of the new strain, 20A.EU1,  is clear enough. But since constant mutation of COVID-19 is the norm, is this significant enough to justify a “second wave”?

A new strain arises by mutation in a single patient, possibly recombining in multiple patients. How a particular strain wins Darwin’s selection to become dominant is too heavy to discuss just days before Election Day. We  want to know whether 20A.EU1 follows an historical pattern of previous plagues, when the second wave was more virulent than the first. Only then does it become dire.

Increased frequency of neurological involvement may indicate a more virulent second wave. Discriminating a second wave depends on both  signs and symptoms, but  symptoms are much harder to interpret. A sign can be measured, like blood pressure, body temperature,  brain waves (EEG), or death. Symptoms can’t be measured. They are just are described by the patient.

Is this the start of a classic second wave like the 1918 Spanish flu? Or is it just a variation on a horrible theme? The clinicians will have to tabulate, palaver, and consider. It would not be wise to scoff at a “yes.”

Some time after the election, we’ll continue with the deeper discussion of COVID Second Wave; Of Hares and Foxes; Primer for Policy Makers, Part 5.

In the meantime, save your brain. Save your life.  Wear a mask.




(CNN) Johnson & Johnson pauses Covid-19 vaccine trial after ‘unexplained illness’

(CNN) Johnson & Johnson pauses Covid-19 vaccine trial after ‘unexplained illness’.

The J&J vaccine is described here: Ad26.COV2-S (JNJ-78436735) Vaccine Description. Quoting,

The JNJ-78436735 vaccine leverages Janssen’s AdVac and PER.C6® technologies. These are the same technologies Janssen used to develop and manufacture the Company’s Ebola vaccine, Ad26.ZEBOV.

AD26 is the specific strain of adenovirus. Quoting from AdVac ,


Adenoviruses are a group of viruses that cause the common cold – so they’re good for transporting things into humans.

(The “goodness” of the above has insufficient support for mass vaccination.)

Janssen’s AdVac® vectors are based on a specific type of adenovirus, which has been genetically modified so that it can no longer replicate in humans and cause disease.

While the details of manufacture are different, this shares the supposed “good idea” of the AstraZeneca and Russian vaccines, the use of a modified adenovirus to insert genetic material into cells at the injection site. The J&J vaccine now shares the distinction, with AstraZeneca, of trial halted by unexplained illness. See

With the halts of AstraZeneca and J&J trials, there is almost a pattern. An actual pattern is distinguished by one or both of:

  • Frequency of occurrence.
  • Specificity of syndrome.



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.