COVID 2nd Wave; How Our Behavior Influences Virulence

This continues from:

and earlier posts. Since most readers are occupied with politics, this piece is sketchier than I had planned. It has an advantage: It’s easy to pass on. It is so simplified, it could figure  in mainstream media.

We’ve seen that a virus doesn’t have brains, but it acts as though it does. Most viruses mutate constantly, with random results and no particular direction, unless a mutation confers a survival advantage. Here we consider why a virus might “choose” to  be patient, or impatient, and the advantages of each.

  • Patient virus. When people to infect are scarce, or hard to infect because they wear masks, a virus wants its host (infected person) to be walking around as long as possible, giving it the best chance of infecting more people. This means the virus can’t make the host too sick, or the host will die before Thanksgiving dinner.
  • Impatient virus. If hosts are plentiful and unprotected by masks or distancing, it’s in the interest of the virus to infect as many people as quickly  possible. This requires quick production of as many new virus particles as possible, which requires severe infection. The host  (sick person) could die, but the virus doesn’t care.  This has all the advantages of torching a restaurant to collect the insurance.

Which strategy works best influences evolution of a virus to a less or more virulent form:

  • If people are careful and vigilant, the tendency is a shift towards less virulence, milder disease.
  • If people are unguarded, as was the case in army camps in the 1918 flu epidemic, the tendency is a shift towards greater virulence, more severe diseases.

Which strategy works best for COVID-19  is determined by social distancing, and mask wearing. It’s up to us.

We’re finding out that many adult Americans think like children. This was written for a child.  It’s more transparent than adherent to the AP Style Manual, or the stilted style of academe. It loses nothing, except the pretense of sophistication, of models that can’t deliver.

Try it out on friends. Maybe you can teach them something.






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.















COVID Second Wave; Of Hares and Foxes; Primer for Policy Makers, Part 4

We continue from COVID Resurgent: Of Hares and Foxes; Primer for Policy Makers, Part 3., which poses a list of questions.  With our Houston Astrodome experiment, we explored the natural balance between the predator (virus) and the prey (host, you.) We saw that in the extreme, mutual extinction could occur.  While this may have happened unobserved, the closest known example is a transmissible cancer that affects the Tasmanian Devil, an Australian marsupial.

The first question of our list is:

  • How can a virus appear to have an intelligent strategy, when it isn’t even alive? Does Darwin’s theory of natural selection play a role?

If you think the mind has a monopoly on thinking, try to put this notion aside temporarily. When you think about a problem, you try to imagine all the ways it could turn out. At the level of atoms, molecules, viruses, and heredity, Nature tries combinations at incredible speed. The result appears thoughtful. Maybe it is.

So Nature rolls the dice constantly. The processes by which a virus or cell or any form of life reproduces has the chance of error. We call this error mutation.  The result of constantly occurring mutation is genetic diversity.

Genetic diversity is key to the survival of a species. Without it, the human species would already be extinct, killed off by something like COVID. This diversity prevents a virus from knowing its prey too well. It’s the difference between a burglar who has cased the joint, and one who hasn’t.

Genetic diversity saves us from one outcome of the Astrodome experiment. If the foxes are super-efficient at hunting rabbits, they kill off their food supply.  Both go extinct. But rabbits are wily and evasive. The foxes can’t catch all of them.

Genetic diversity is responsible for an axiom of infectious disease: No disease is 100% fatal. Rabies was thought to be. A few years ago, a young woman walked into a Texas hospital with rabies. With no specific treatment, she walked out three weeks later.

Likewise, if a virus did not mutate, the prey would develop universal immunity, so the virus would go extinct.  Mutation comes easily to RNA viruses like COVID, because RNA is fragile.  DNA is so tough you could make golf club shafts out of it. Yet mutation is so important, even DNA viruses roll the dice. (Science Daily) How poxviruses such as smallpox evolve rapidly, despite low mutation rates.

The viral mutations we see are the ones that enable one strain of COVID-19 to out-compete other strains; this is Darwin’s natural selection. Selection works on humans too, but we want to prevent it with medicine and public health policy.

We have addressed the first question of our list:  Even though they cannot think, viruses and immune systems have strategies that appear thoughtful.

The human race will survive COVID. But we want to prevent a Darwinian outcome.  And you’ve got some personal skin in the game.

Our next question: What drives virulence, and what holds it back?





Ruth Bader Ginsburg

With countless plaudits honoring the work of Ruth Bader Ginsburg, what can I add?

There is a folk expression to the effect that with every passing year, the personality is more deeply etched upon the face. By age 87, her personality was in clear display.

She was kindly, yet fiercely determined.

So many strivers are driven by  ambition. Hers was a calling, a vision of principles.

Like cellist Pablo Casals, who improved every year before he died,  Ruth Bader Ginsburg was born a mortal, and died a giant.

We need her still. Who will champion “Be all you can be”?

Although the opinions of a Supreme Court justice, even in dissent, tend to be monumental, I can’t think of her by other than her first name.

Thank you, Ruth.

(CNN)NIH ‘very concerned’ about serious side effect in AstraZeneca coronavirus vaccine trial

Let’s see if we can find a smoking gun. To follow this, you need to read (CNN) AstraZeneca pauses coronavirus vaccine trial after unexplained illness in volunteer. Follow the links back.

(CNN) NIH ‘very concerned’ about serious side effect in AstraZeneca coronavirus vaccine trial. Quoting,

“The highest levels of NIH are very concerned,” said Dr. Avindra Nath, intramural clinical director and a leader of viral research at the National Institute for Neurological Disorders and Stroke, an NIH division. “Everyone’s hopes are on a vaccine, and if you have a major complication the whole thing could get derailed.”

The Oxford- Astrazeneca vaccine belongs to the most aggressively novel class of new vaccines: It transfects cells in the recipient with a vector, a carrier virus, to cause them to make COVID spike protein. For a COVID vaccine, transfection  means:

  • Deliberate infection of cells near the injection site with an engineered virus, the vector.
  • Transport of spike protein DNA into the cell.
  • Modification of the cell machinery to make COVID spike protein.

The virus particles of the Astrazeneca vaccine are active micro-machines. This is not as radical as it sounds. Live-virus vaccines were the first devised. They are still used today. Some, such as the live virus polio vaccine, or yellow fever 17D, have known hazards. But in comparing with live virus vaccines of the past, there are meaningful differences:

  • Trials were over a much longer period.
  • Trials defined age groups, typically juvenile, when the immune system seems to handle well challenge with live virus.
  • These vaccines contain large amounts of virus, easy for the immune system to spot, and weakened by multiple passages through nonhuman tissue, cold adaptation, or chemical degradation. This goes back to Pasteur.

There is no rigorous argument for why weakened live virus is usually safe, but it has 150 years behind it. AstraZeneca’s argument is weak, and they have about 3 months behind it.

Is the Astrazeneca event a random event or a smoking gun? Let’s see if we can smell smoke. Details of the event are important, not to establish fact, but possibly requiring the trial be halted.  Let’s begin with rabies, a virus with a stealth trick:

  • Somebody gets bit in the deltoid muscle, where you would get the shot. Most immunizations inject into the deltoid muscle of the upper arm.
  • Virus in the animal’s saliva incubates silently in muscle for weeks, months, or years. In perhaps 1/3 of bites, it evades the immune system.
  • The deltoid muscle is served by the axillary nerve, which, combined with other nerves, exits the spine at the base of the neck. In the deltoid, the nerve has little bulbs, neuromuscular junctions.
  • If the rabies virus has evaded the immune system, it breaks into the junctions. It then travels up the nerve, the spinal cord, and finally the brain, where it causes rapid death.

Besides rabies, any virus which incidentally penetrates a neuromuscular junction, or penetrates the brain in some other way, has a chance of infecting the nervous system. Once inside the nervous system, a virus is partly shielded from the immune system, which is why a virus like West Nile can be innocuous or fatal.

So a virus  that does not normally cause encephalitis can be big trouble if it gets into the brain. In a child who has not been vaccinated, measles can cause subacute sclerosing panencephalitis, invariably fatal, with a timeline unaddressed by COVID clinical trials.

Suppose somebody gets the Astrazeneca shot, and the tip of the needle nicks a neuromuscular junction, and virus gets into the junction. The vaccine contains two viruses. One is the Kamikaze, which carries the payload, spike protein, into the muscle cell target. Traces of the helper virus are also present.  But how does a virus which has no experience with nerves know how to climb the axillary nerve all the way to the cervical vertebrae, where it might cause transverse myelitis?

A virus doesn’t have to know a thing. The axillary nerve contains a conveyor belt, reverse axonal transport. Hooked onto the conveyor, even completely inert particles will reach the brain. This was shown years ago by an experiment with patients who had a few days to live. Colloidal gold was sprayed into their noses. When the patients died three days later,  their brains were sectioned, and the gold was found.

The rumored  adverse event is transverse myelitis. Instead of a lesion extending up, down, and sideways, it mainly goes sideways. It’s like nerve block anesthesia, which affects function below the the block. The lesion extends across the whole spinal cord near a few vertebrae. With the Astrazeneca patient, we would expect to see symptoms of a spinal lesion around C5 and C6, the lower cervical vertebrae, at the base of the neck.

This is the smoking gun. If the lesion is not around C5/C6, it could still be the vaccine, but we don’t smell smoke. We would have to consider more typical causes, such as autoimmunity caused by the vaccine. This too has happened.

Are the symptoms caused by the Kamikaze virus, or the helper virus? This is hard, but important. The Kamikaze cannot reproduce, so it cannot cause a slow virus infection, like subacute sclerosing panencephalitis. The helper virus, though present only  in trace amounts, can reproduce. There is a questionable presumption of safety.

This  scenario pertains to vaccines that use a virus to  penetrate cells in the recipient. It cannot happen with:

  • Killed virus vaccines.
  • VLP (virus-like particle) vaccines.
  • RNA vaccines.
  • DNA vaccines.

These vaccines have similarity-to-safe; for what this means, see Why I Defend FDA Commissioner Stephen Hahn. A single live-virus vaccine in use today, 17D for yellow fever, can cause fatal infection. See Moderna Partial Results Part 1.

Whether a vaccination can introduce live virus into neuromuscular junctions was not formerly a troublesome question. Now it is. Rigorous safety demands an answer to: Why did this  adverse event happen? It cannot be well studied in humans, because the spinal cord of a living person is not available. It can be studied in animals in a far more detailed way. The answer will not come quick.

So do the right thing.


(CNN) AstraZeneca pauses coronavirus vaccine trial after unexplained illness in volunteer

(CNN) AstraZeneca pauses coronavirus vaccine trial after unexplained illness in volunteer. Quoting,

“In large trials, illnesses will happen by chance but must be independently reviewed to check this carefully. We are working to expedite the review of the single event to minimize any potential impact on the trial timeline. We are committed to the safety of our participants and the highest standards of conduct in our trials.”

Chance is one possibility. For another, see  Why I Defend FDA Commissioner Stephen Hahn. Quoting,

This sounds informative, but it leaves out a crucial safety question, discussed in Why I Would Not Take the Russian or Oxford – AstraZeneca Vaccines – Part 2. Quoting the nut of it,

After a while, we’re ready to harvest the culture medium for the virus we want, the Kamikaze, purifying it of the helper virus. We don’t want the helper virus in our vaccine, because it  does not contain the code for the spike protein, and it can replicate…

Very small quantities of live, helper adenovirus are present in the finished vaccine product.  Supporters of these vaccines make these claims:…

(Reuters) Putin critic Navalny was poisoned with Novichok nerve agent, Merkel says

(Reuters) Putin critic Navalny was poisoned with Novichok nerve agent, Merkel says. Quoting,

She said Berlin now expected Moscow to explain itself and that Germany would consult its NATO allies about how to respond, raising the prospect of new Western sanctions on Russia, sending Russian asset prices tumbling.

You read it here first:  Alexei Navalny, Poisoned Again? The Russian Poison Trick. Quoting,

The modern syndrome is near-death, prolonged illness, partial recovery, and prolonged or permanent disability. It is characterized by stealth and extreme precision,  a sub lethal dose of a  substance so poisonous it completely evades standard toxicology. Vil Mirzayanov revealed the existence of the Novichok family of nerve agents in 1992, but hope for a “new Russia” delayed assessment of the threat.

You read it here first, and there isn’t a subscription fee!

But you might have guessed as much if you read (NPR) Navalny Was Poisoned, But His Life Isn’t in Danger, German Hospital Says. Quoting,

Navalny is now being treated with an antidote called atropine; the medical team says there’s the possibility of long-term effects on his health and particularly his nervous system.

Treatment with atropine as the only named substance suggests a partial truth. Atropine is only part of a treatment protocol. Additional chemicals are required to reactivate cholesterinase, and scavenge loose  Novichok. According to the inventors of Novichok, the bond is much harder to break than with VX. The Russians considered Novichok exposure to be untreatable, except for supportive care.

Since Porton Down chose not to disclose the protocol that saved the Skripals, it is reasonable to suspect that Charité Hospital told a little white lie, to protect British innovation.

How did the Germans or Brits determine the poison? The Raman microscope, with the ability to perform spectroscopy on  microscopic quantities, is probably involved.



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