In September ’17, I wrote a series for Rex Tillerson:
- Advice for a New Secretary of State, Rex Tillerson, Part 1
- Advice for a New Secretary of State, Rex Tillerson, Part 2
- Advice for a New Secretary of State, Part 3
- Advice for a New Secretary of State, Part 4; Nikki Haley, Russia
- Advice for a New Secretary of State, Part 5; Nikki Haley, Russia
- Advice for a New Secretary of State, Part 6; How to Use a Skinner Box
Since Tillerson’s background was not that of a professional diplomat with think-tank imprinting, there seemed an opening for new ideas. Before Part 7 was published, he was replaced by equally capable Mike Pompeo, who had national security experience. So I held Part 7 back. It now follows.
The appointees of the new administration are career professionals. The experience confers both advantage and disadvantage:
- Long acquaintance with the levers of power and gears of bureaucracy promote smooth policy execution.
- Institutional and cultural biases tend to impede innovation. Some of the ideas in this series remain edgily innovative.
You might wonder why Part 7 is about Russia, and not China. It was written in the shadow of a recent hot war between Ukraine and Russia. Russia continues to complicate our approach to China for visceral reasons that elude wide understanding. In the style of good briefing material, a major point of Russian strategy comes first:
In the creation by social media of a whole new world, that world would be incomplete without war.
Advice for a New Secretary of State, Part 7
I was tempted to remark that Russian subversion of democracies is unethical, while a counter-strategy based operant conditioning is ethically beyond reproach. But there is always a chance that the Russians might open up a little, as during Perestroika. Rather than negate the possibility, I’d like to leave them with something to chew on. Vladimir Putin now seems a combination of a modern man with a nationalist in the historical mold. People who are combinations contain the possibility of change.
Let’s consider what forms the external image of the U.S., and circle back to Nikki Haley’s “…that is warfare.”
Between 1920 and 1950, reservoirs of romantic sympathy in the West for Bolshevik revolution gradually faded away, replaced by a true appreciation of the horrors. Six years later, on February 2, 1956, the first official denunciation within the Soviet Union came in Khrushchev’s secret speech. This was really the first “perestroika.” But starting from the base of an historic brutality, it was only an increment. Three generations have passed since that speech, enough time for Western Europe to abandon the nationalism of conflict dating to the Treaty of Westphalia.
With three generations, the salt of Russia’s earth still have one foot in the past. That foot threatens to drag us all back to the conflicts of centuries. This is why we are so unnerved by Russian subversion. But perhaps the Russians don’t appreciate the value of what they are trying to destroy.
Historical comparisons can be made between human rights violations in Russia, and in the West. There is the appearance of qualitative overlap, but this neglects the numbers. Russia had Stalin’s purges. The U.S. had racial lynching. Russia had extrajudicial capital punishment, via the infamous NKVD “troika.” In the U.S., capital punishment is inconsistently applied, in some cases, to innocents. Neither society is perfect, but numbers tell the story.
- While 20+ millions died in Stalin’s purges, the Tuskegee Institute documents a total of 4,733 lynchings since 1882.
- According to a study cited by Newsweek, U.S. miscarriage of justice in cases involving capital punishment since 1973 has been about 4.1%. Since 1973, 144 people on death row have been exonerated.
- Estimates that date from the 1990’s of the peak Gulag population vary, the lowest cited in Wikipedia as 4.5 million. In the U.S., people have gone to jail for political reasons, for participation in the Civil Rights Movement, the Anti-War movements, and some as almost purely as prisoners of conscience. Let the Russians come up with a list and we’ll do numbers.
- U.S. and Russian covert activities in the Third World during the Cold War have significant symmetry. Manipulation of print and broadcast media correspond to social media manipulations. A good picture of this is given in the books by C.I.A. plank owner Miles Copeland. This epoch was swept away by the Church Committee, the Pike Committee, and so forth. Since then, concerns illuminated by legislative and public scrutiny, and leaks, have alternated in importance with the exigencies of 9/11.
- The Russians may compare the former U.S. dominance in Latin America, interventions there, and the general attitude of the Monroe Doctrine, to the Iron Curtain of Eastern Europe. We don’t.
The above implies varying shades of gray, with occasional marks of black. The blackest mark on our record is the Vietnam War. Can we exonerate our fathers by saying, “We were fighting communism?” This is not to argue with you if you think we can, but the Russians, and many others, do not share the thought.
As Americans, we are free to vigorously defend the above, to be shamed, or accept them as bygone attitudes engendered by the Soviet threat. The purpose of this recapitulation is to understand Russian attitudes, particularly of the overhang of older individuals in the Russian government.
Vladimir Putin was born in the last year of Stalin’s life. His formative years were in a society of glacial change. One would have to be truly exceptional to escape the molding of Stalin’s ghost. But by comparison, he is better than any ruler the Russians have ever had. The one thing that has been lost, which gleamed so brightly under Boris Yeltsin, is the chance of further evolution of Russian society. The chance has been traded for stability.
Suppose that instead of multiple views spanning decades, we take snapshots of each society at various points in time, but in comparison mix up all the dates so that we are comparing snapshots from different periods, and leave out numbers. This kind of picture combines with personal individuality, to form the attitudes of someone who was formerly a member of the Communist Party of the Soviet Union. With the scrambling, how is that person to know that we have changed?
This hints at why the Kremlin thinks it acceptable to engage in subversion that by our social standards is (pick your adjective) unfair, dastardly, despicable, under-handed, not gentlemanly, reprehensible, evil, etc. Their possible reasons:
- It’s no better or worse than what they use for internal social control.
- Dredging from the Bolshevik past, “The capitalists want profits, and they will hang themselves with their own ropes.” It sounds ludicrous. But even after the words have lost all meaning, the sentiment remains. The Russians themselves may not be consciously aware of the origin.
- Pure Comintern habit. The Comintern was the international organ of communist subversion. It was dissolved in 1943, but the melody lingers on.
- A grudge against the West. Exclusion from EEC markets, the expansion of NATO, the loss of Ukraine, can be combined in the conspiratorial mind.
- The loss of a sphere of influence.
- Valuation of Russians above all other people. An escape clause.
- Fear for the security of Russia, which is not groundless but very misdirected.
- A new Cold war, or a sense that the old one never ended. War is the escape clause that legitimizes conduct that would otherwise be universally condemned. Perhaps Nikki Haley is right. In the creation by social media of a whole new world, that world would be incomplete without war.
- All of the above. The human mind likes to take a little bit of this, and a little bit of that.
What does this imply for our characterization of people behind the threat?
This continues from:
- 20A.EU1, The Second COVID Wave
- COVID Second Wave; Of Hares and Foxes; Primer for Policy Makers, Part 5
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.
Has a true second wave arrived, with the historical precedent of increased virulence? Let’s start with two points:
- (The Hill, 7/28) More than half of Spanish coronavirus patients suffering from neurological problems: research.
- (Guardian, 10/30) Coronavirus strain from Spain accounts for most UK cases – study.
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.
The J&J vaccine is described here: Ad26.COV2-S (JNJ-78436735) Vaccine Description. Quoting,
AD26 is the specific strain of adenovirus. Quoting from AdVac ,
ADVAC® VIRAL VECTOR TECHNOLOGY
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
- Why I Would Not Take the Russian or Oxford – AstraZeneca Vaccines – Part 2
- (CNN) AstraZeneca pauses coronavirus vaccine trial after unexplained illness in volunteer
- (CNN)NIH ‘very concerned’ about serious side effect in AstraZeneca coronavirus vaccine trial
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.
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.
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?
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.
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.
“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.