Thoughts on the George Floyd Riots

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Thoughts on the George Floyd Riots

Yesterday, a friend wrote me: “I really don’t know how we are going to come out of this. For a while I was okay. Over the last week I have grown more desperate with each day as the news develops.” I am trying to answer him here.

Many of my social media friends have expressed their anger, outrage, sadness and disgust at the lynching of George Floyd by a white supremacist cop in Minneapolis on May 25th (8 days ago as I write this). That lynching was carried out by an arresting cop kneeling for 8 minutes and 46 seconds on the right side of George Floyd’s neck while the handcuffed Floyd was lying face down on a city street. Floyd kept pleading for relief because he could not breathe, but the killer cop continued his kneeling choke-hold for 2 minutes and 53 seconds after Floyd had become unresponsive. Three other cops participated in the lynching: one holding Floyd’s back, another holding his legs, and the third looking on and preventing intervention by a person who stood nearby, watching in horror. (https://en.wikipedia.org/wiki/Killing_of_George_Floyd)

The country has blown up, large protests and riots now fill the streets of many cities and towns in America, and have for the last week. “A riot is the language of the unheard,” as Martin Luther King, Jr. said about the expressions of that truth in 1965 (Watts, Los Angeles CA) and 1967 (Newark NJ, Detroit MI, and 157 other places). That truth again erupted into view in over 100 cities in the United States after Martin Luther King, Jr. was assassinated on 4 April 1968, with “the greatest wave of social unrest the United States had experienced since the Civil War,” before it finally flamed out on 27 May 1968. And that truth was again acted out during 6 days of riots (29 April to 4 May) in Los Angeles CA in 1992, after the four cops who had savagely beat Rodney King in 1991 were acquitted of any crime.

“We are witnessing America as a failed social experiment,” Dr. Cornell West said on 29 May, as he preached on CNN television with crystal clarity on the massive and systemic failure of America — as a society, an economy and a tangle of governments — to protect and defend all of its people. Listen to Cornell West for yourself to unflinchingly face the reality of America (https://youtu.be/cs3jdyfx_fo), a reality that had been made plain by Malcolm X by 21 February 1965, when he was assassinated.

People are in the streets because the George Floyd murder was the last straw on their unbearably strained patience in waiting for justice in America. They blew up because they saw that justice in America will never arrive. Their many pent-up disappointments and frustrations came to a head on seeing the video of the George Floyd murder. Those disappointments and frustrations include experiences of victimization — many fatal — by racist policing, as well as economic victimization by a structurally racist and fundamentally rigged economy.

So, the victim populations of the race war against Blacks, Latinos, American Indians, and others disfavored by white supremacists; and the class war by the rich and powerful against: wage slaves, the unemployed, youth without prospects, and the 99% of Americans who are outsiders from the con games and self-aggrandizing capers of the economic insiders, just went ape-shit on seeing the Floyd murder and its obvious acceptability to the Trump-led bipartisan power structure. That is why I call it a lynching.

All this is happening during the COVID-19 pandemic, which has paralyzed society with its obvious deadliness, and that in turn has collapsed any hope of financial security for so many people who were already in the bottom tiers of the fundamentally heartless American economic system.

Many of these people are faced with sudden devastating losses: of health and life to the SARS-CoV-2 virus, and of being cast into bankrupting debt by the medical bills for having survived COVID-19; of confidence in remaining healthy while on jobs they need for economic survival; of income when their jobs disappear, and with it their health insurance if those jobs even provided it; of housing with the inability to pay rent; and even of ready access to food. The pandemic has also interfered with the most fundamental source of solace we all rely on in our times of despair: sharing the company of our families and true friends. So going out into the streets now to protest is natural for many who want relief from the unbearable suffocation of the choke-holds on them, and for some of those people who feel they have nothing left to lose, to even riot.

Unfortunately, there are rotten malevolent scumbag bigots who are taking advantage of the street protests to act violently and destructively in the hopes of provoking a much wider race war of oppression by white supremacy. And there are too many cops and government people (the cop employers) who are obsessed with control and domination instead of public and individual welfare, and they too create more hurt and provoke more reactive rioting by their heavy-handed cop-riot “law enforcement” actions.

So we get a vicious cycle of violence begetting violence. The best way to break that cycle is to quickly legislate substantive social and economic improvements that clearly address the underlying distresses of the people protesting visibly, and the people despairing silently and invisibly. The blinded-by-bigotry Trump-type people don’t want to enact those long-needed reforms because it would mean cutting back on their money-making schemes and their biased administrative actions.

I am guessing the current cycle of unrest will wind down simply because of exhaustion on the part of most of the people in the streets, coupled with heavy suppression by militarized police and federal troops. That won’t end the problem, but just make it more “invisible” to the authorities and simply delay its resolution, which if not forthcoming will simply mean another outbreak is inevitable.

I think things will get back to “normal” in time (within weeks?), but the “normal” that we had before late May was toxic. It carries within it the makings of more, longer and worse future riots if we let it return and continue unchanged.

A Bernie Sanders presidency aided by a helpfully supportive Congress would have been a potentially mild reform of our toxic “now,” but that reform was forbidden by the corporate-owned bipartisan power structure through its Democratic Party wing, with the full concurrence of its Republican Party wing. So now we have the George Floyd riots because people don’t feel like compromising any more, or of waiting for the Godot of American justice, or of turning the other cheek of a failed Christianity.

I don’t know and can’t really guess what’s coming next, or of how things will play out for the rest of this year.

We need a lot of wise leadership — which is obviously entirely lacking from the Trump Administration, from the U.S. Congress, and from many governors and elected politicians — and we need a lot of steady confident calmness that holds off from violent actions, by governors, mayors and police forces, who would in turn all be supported in that type of compassionately wise response by those wished-for intelligent and unbiased Federal authorities, for this national crisis to be calmed down quickly and humanely; and to then be permanently resolved by essential social and economic reform legislation, which was assiduously enforced thereafter.

The slogan “no justice, no peace” says it all. We’ve always known that, and the Kerner Commission Report spelled it all out after the riots in 1967 (https://en.wikipedia.org/wiki/Kerner_Commission), but it was ignored.

This crisis will be fixed for real when justice in America is established for real. I don’t know when or if that will ever happen. But I just wish it would soon.

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For America today: shamrock = lily; Erin = Freedom.

Most COVID-19 Contagious People Are Asymptomatic

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Most COVID-19 Contagious People Are Asymptomatic

Most COVID-19 contagious people (carriers of the SARS-CoV-2 virus) are asymptomatic: they show no symptoms.

Social distancing is essential to slow the pace of the pandemic since neither you nor anybody else will know who is a carrier that crosses your path. This has been amply shown by the exemplary and highly effective Vietnamese response to COVID-19 (https://consortiumnews.com/2020/04/16/covid-19-vietnam-winning-new-war-against-invisible-enemy/)

A Reuters news story of 16 April 2020 (Coronavirus clue? Most cases aboard U.S. aircraft carrier are symptom-free, https://www.reuters.com/article/us-health-coronavirus-usa-military-sympt/coronavirus-clue-most-cases-aboard-u-s-aircraft-carrier-are-symptom-free-idUSKCN21Y2GB) notes:

Sweeping testing of the entire crew of the coronavirus-stricken U.S. aircraft carrier Theodore Roosevelt may have revealed a clue about the pandemic: The majority of the positive cases so far are among sailors who are asymptomatic, officials say. Roughly 60 percent of the over 600 sailors who tested positive so far have not shown symptoms of COVID-19, the potentially lethal respiratory disease caused by the coronavirus, the Navy says. The service did not speculate about how many might later develop symptoms or remain asymptomatic. “With regard to COVID-19, we’re learning that stealth in the form of asymptomatic transmission is this adversary’s secret power,” said Rear Admiral Bruce Gillingham, surgeon general of the Navy. The figure is higher than the 25% to 50% range offered on April 5 by Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases and a member of President Donald Trump’s coronavirus task force.

A Boston25News story of 15 April 2020 (CDC reviewing ‘stunning’ universal testing results from Boston homeless shelter, https://www.boston25news.com/news/cdc-reviewing-stunning-universal-testing-results-boston-homeless-shelter/Z253TFBO6RG4HCUAARBO4YWO64/) reports a similar finding, that: ‘1.5 weeks ago’ (in the first days of April) testing revealed 146 positives out of a population of 397 in a Boston homeless shelter. That result indicates a rate of 36.8% positive for infection AND being asymptomatic. Those positives were then quarantined separately. ‘Now’ (15 April 2020) only one needs hospital care, while many of the other positives still show no symptoms.

If there is a ~2 week (or more?) delay between infection and outbreak of symptoms (during which time the person is invisibly infectious), then that is a long latency as compared to colds and flu (days). SARS-CoV-2 is a positive-sense single-stranded RNA virus; and by my understanding of such +single-stranded RNA viruses, they get inside infected cells, commandeer the messenger RNA manufacturing machinery and thence the protein manufacturing machinery (ribosomes) of the cell to produce the viral components (viral RNA = virions, and protein capsules to encase them) that are assembled into new viruses that exit the cell (killing it, when a large outflux), and tearing off some of outer cell lining to wrap themselves in a lipid (fat) cover.

For details about viruses and the diseases they cause I highly recommend the 1994 book, Invisible Invaders, Viruses and the Scientists Who Pursue Them, by Peter Radetsky. It is an excellent book, well-written, with a wealth of information, and fascinating reading. It spans 200+ years of viral infectious disease discovery and vaccination development history; most of it for the 20th century.

Coronaviruses in general seem to have a very complex chemical process for coursing through their human hosts. A very technical summary of all this is given in a 2015 National Institutes of Health (NIH) paper, conveniently posted online (Coronaviruses: An Overview of Their Replication and Pathogenesis, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369385/). The relative lengthiness of this process will account for some of the ‘delay’ or ‘latency period’ between initial infection and outbreak of symptoms.

Another and more insidious factor that could contribute to that delay is this, as described (in one sentence) in the NIH paper just noted (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369385/):

“In several coronaviruses, S protein that does not get assembled into virions transits to the cell surface where it mediates cell–cell fusion between infected cells and adjacent, uninfected cells. This leads to the formation of giant, multinucleated cells, which allows the virus to spread within an infected organism without being detected or neutralized by virus-specific antibodies.”

In other words, some of the viral goop inside an infected cell bonds it to adjacent healthy cells into which the virus can then penetrate stealthily, out of “sight” of the antibodies of the immune system floating in our bloodstream. In that way many cells can become invisibly infected, as regards our immune system’s “radar,” — thus our asymptomatic latency period — before all viral hell breaks loose from all those “sleeper cells,” and the victim is obviously in full-blown disease.

The SARS-CoV-2 virus initially causes an upper tract respiratory disease in its infected human hosts, but it can migrate deeper down the airway, then into the lungs, and down very deep to lodge in and damage the alveoli, the ‘air sacs’ where air/oxygen enters the bloodstream through capillaries. From there it can drift along with the blood to arrive at (and possibly infect) the heart and the kidneys, these latter being another type of “spongy” organ for osmotic-type transfers (of oxygen into the blood with the alveoli, of liquid wastes out of the blood for the kidneys).

Several reports, one from 12 March 2020 is cited and quoted here (Are Kidneys Targeted by the Novel Coronavirus?, https://www.cathlabdigest.com/content/are-kidneys-targeted-novel-coronavirus), show that kidneys have been infected by SARS-CoV-2, and a significant fraction of survivors have lasting kidney damage requiring dialysis thereafter. This paper notes (in the following consolidated paragraph):

New data on coronavirus disease include some startling revelations: Kidney involvement seems to be frequent in people who have been tested positive and have developed symptoms. Two studies showed a high rate of renal abnormalities in corona-positive patients: Admitted to hospital, 34% of the 59 patients developed massively elevated levels of albumin in urine (=proteinuria), a symptom of kidney damage 63% of the study patients developed proteinuria while in hospital, and many of them also had blood loss in their urine (hematuria). Kidney function was impaired in 27% of the study population and in 66% of the patients who died from the coronavirus infection. These findings are supported by a second study involving 710 hospitalized patients: On admission, 44% had hematuria and proteinuria (26.7% had hematuria only), and kidney function decreased in nearly 15%. “This shows that COVID-19 also attacks the kidneys, not just the lungs”, explains Professor Carmine Zoccali, President of the ERA-EDTA. [ERA-EDTA is one of the biggest nephrology associations worldwide leading European nephrology and one of the most important European Medical Associations.]

Some recent news stories voice concerns that, after ventilators, kidney dialysis machinery may be the next area of medical equipment shortages caused by the COVID-19 pandemic.

People who died of “complications of COVID-19” might have succumbed to pneumonia (drowning because of fluid filled lungs); or hypertension heart attacks, exacerbated by obesity, where the heart was pumping furiously to try to capture and circulate oxygen from lungs that were clogging up and choking off that gas flow; or kidney failures; or any combination of these. “Old people” are more susceptible because they generally have weaker immune systems and more underlying conditions (e.g., hypertension and heart diseases, diabetes, airway constrictions/emphysema, obesity).

Many people are curious as to how COVID-19 might be similar to, or different from, the H1N1 avian flu that caused the 1918 pandemic. In particular, some observe and ask: ‘the 1918 flu targeted its fatalities in a far younger population, why?’ The culprit was “a cytokine storm in the body,” an effect that also certainly occurs to some COVID-19 unfortunates. This article on H1N1 (Influenza A virus subtype H1N1, https://en.wikipedia.org/wiki/Influenza_A_virus_subtype_H1N1) notes (in the following paragraph) that:

The 1918 flu caused an unusual number of deaths, possibly due to it causing a cytokine storm in the body. (The current H5N1 bird flu, also an Influenza A virus, has a similar effect.) The Spanish flu virus infected lung cells, leading to overstimulation of the immune system via release of cytokines into the lung tissue. This leads to extensive leukocyte migration towards the lungs, causing destruction of lung tissue and secretion of liquid into the organ. This makes it difficult for the patient to breathe. In contrast to other pandemics, which mostly kill the old and the very young, the 1918 pandemic killed unusual numbers of young adults, which may have been due to their healthy immune systems mounting a too-strong and damaging response to the infection.

The article Cytokine Release Syndrome (https://en.wikipedia.org/wiki/Cytokine_release_syndrome) describes cytokine storms in greater detail (the next 2 paragraphs):

Cytokine release syndrome (CRS) or cytokine storm syndrome (CSS) is a form of systemic inflammatory response syndrome (SIRS) that can be triggered by a variety of factors such as infections and certain drugs. It occurs when large numbers of white blood cells are activated and release inflammatory cytokines, which in turn activate yet more white blood cells. CRS is also an adverse effect of some monoclonal antibody drugs, as well as adoptive T-cell therapies. Severe cases have been called cytokine storms. When occurring as a result of drug administration, it is also known as an infusion reaction.

CRS occurs when large numbers of white blood cells, including B cells, T cells, natural killer cells, macrophages, dendritic cells, and monocytes are activated and release inflammatory cytokines, which activate more white blood cells in a positive feedback loop of pathogenic inflammation. Immune cells are activated by stressed or infected cells through receptor-ligand interactions. This can occur when the immune system is fighting pathogens, as cytokines produced by immune cells recruit more effector immune cells such as T-cells and inflammatory monocytes (which differentiate into macrophages) to the site of inflammation or infection. In addition, pro-inflammatory cytokines binding their cognate receptor on immune cells results in activation and stimulation of further cytokine production. This process, when dysregulated, can be life-threatening due to systemic hyper-inflammation, hypotensive shock, and multi-organ failure.

So, some COVID-19 fatalities may be due to over-acting immune systems that cause massive inflammation in response to the infection, and consequently excessive cell damage to the unfortunate human victims. As auto-immune diseases demonstrate, it is possible for people of any age to have a trigger-happy immune system.

Viral particles ride on tiny droplets (aerosols) released as part of infected breath. Given the uncertainty on the scope of infection in the population you live among, and their degree of contagiousness, both because of the asymptomatic latency and the limited extent of testing (especially in the USA), your best tack is to stay away from other people’s “breath plumes,” the clouds of vapor and water droplets that expand from their mouths and noses as coughs, sneezes and exhalations (which are stronger and of longer range when exercising or under physical strain). Eventually such droplets fall to the ground. Face masks are helpful for limiting the outward range of plumes expelled by an emitter, and also for shielding impacted passers-by, by filtering the wafts of an emitter’s infected breath (hopefully attenuated by an emitter’s mask) before it reaches their own noses and mouthes.

Over time, aerosolized virus is eliminated and destroyed by the combination of sunlight, heat and humidity. These three weather-related virus-destroying factors are noted in an 11 February 2020 report, which otherwise seems overly optimistic about when SARS-CoV-2 will “go away.” (https://www.accuweather.com/en/health-wellness/coronavirus-expert-says-the-virus-will-burn-itself-out-in-about-6-months/679415)

Sunlight, as ultraviolet (UV) radiation, ‘bleaches’ or ‘oxidizes’ the virus particles; heat can cook them to death (breaking them apart; heating is a technique that has been used to make weak-germ and killed-germ vaccines); and humidity can “rain out” virus particles from the atmosphere, washing them away in ground runoff, eventually to break apart. Flu is seasonal because of these effects: it expands through its human hosts in the fall and winter (in the northern hemisphere), and dissipates when sunnier warmer weather arrives (by retreating into asymptomatic wildlife hosts, usually migratory birds and also bats).

So to recapitulate, most people infected with COVID-19 are asymptomatic at a rate of 60%. (The two ‘full population testing’ studies cited here reported rates of 60% from over 600 infected on a US Navy aircraft carrier ship, and nearly 37% from 146 infected in a homeless Bostonian population housed in a single shelter.) For the SARS-CoV-2 virus, “stealth in the form of asymptomatic transmission is this adversary’s secret power.” That stealth, in the form of its asymptomatic latency period, seems to be due to its lengthier chemical process for reproducing itself in human host cells and then expelling itself from them, and probably also with the added subterfuge of ‘glueing’ infected cells to adjacent healthy ones, which the virus then penetrates and infects without going outside the cells so as to not alert the human immune system antibodies coursing through the bloodstream.

Social distancing and face masks — inconvenient, uncomfortable and unpopular — are essential behaviors to limit the expansive speed and range of this SARS-CoV-2 pandemic. This disease can be fatal, and it has been shown to leave lasting damage to the hearts and/or kidneys of a portion of its survivors. People most susceptible to succumbing fatally to COVID-19 are older, and/or have underlying medical conditions that weaken the operations of the lungs, and/or heart, and/or kidneys, and/or the immune system. Another morbidity factor, which can occur in people of all ages, is having a overly aggressive immune system that would unleash a cytokine storm in response to this viral infection.

The appropriate political response by the survivors of this pandemic is to support national universal healthcare, and to support the just and generous remuneration, job security and workplace safety of the frontline medical personnel attending to the sick and dying, not just during this pandemic but thereafter. Also, we must support the robust financial support of epidemic and pandemic response planning agencies, beyond the cheapskate, ‘just in time’ high-profit business-wise lower levels of support reluctantly agreed to by reactionary neoliberal privatization freaks like Donald Trump.

While several prototype vaccines and cures for COVID-19 are currently in clinical trials, it is not yet known if the SARS-CoV-19 virus will be able to be warded off once and for all with one or two antiviral vaccine “shots,” or if it will become another of the seasonally recurrent viruses, like the cold and flu viruses, that mutate (by viral “drift,” a small change in the surface H gene; or “shift,” by forming a new strand of RNA) too quickly for our medical science to ever devise an unchanging vaccine that affords us a permanent immunity.

Given this COVID-19 global experience, will humanity now find common cause to alter its various regional behaviors that in aggregate give rise to such insidious viral pandemics? We’ll see. I suppose that a science-fiction writer could craft a dystopian tale from the individual human and societal failures that we are yet likely to witness, in which our atmosphere is routinely contaminated with disease-causing viruses like SARS-CoV-2, along with our usual copious greenhouse gas and fossil fuel carbon particulate pollution, so that the human denizens of Planet Earth would then have to move about clothed in hazmat space suites with oxygen tanks, and with their livestock housed in large controlled atmosphere feedlot bubbles; and tough luck on the wildlife.

On the prospects of humanity changing its ways after this round of COVID-19, I am reminded of the last scene in the 1959 movie On The Beach, of the empty windblown streets of post-human Melbourne, Australia, with a slowly fluttering Salvation Army street banner that reads: “There is still time…Brother.”

I am grateful to Katje Erickson for pointing me to the two ‘full population testing’ studies cited here.

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Drawing by Babak Kateb, MD

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Asymptomatic COVID-19, a Long Latency Period to Evade the Immune System?

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Asymptomatic COVID-19, a Long Latency Period to Evade the Immune System?

1.5 WEEKS AGO: testing revealed 146 positives out of 397 population (in a homeless shelter in Boston) = 36.8% positive AND asymptomatic. Those positives were then quarantined separately.

NOW: only 1 needs hospital care, while many still show no symptoms.

CONCERN RAISED: very possibly many infectious asymptomatics out and about in the general population. (https://www.boston25news.com/news/cdc-reviewing-stunning-universal-testing-results-boston-homeless-shelter/Z253TFBO6RG4HCUAARBO4YWO64/)

If there is a ~2 week (or more?) delay between infection and outbreak of symptoms (during which time the person is invisibly infectious), then that is a long latency as compared to colds and flu (days). SARS-CoV-2 is a positive-sense single-stranded RNA virus; and by my understanding of such +single-strand RNA viruses, they get inside infected cells, commandeer the messenger RNA manufacturing machinery and thence the protein manufacturing machinery (ribosomes) of the cell to produce the viral components (viral RNA = virions?, and protein capsules) that are assembled into new viruses that exit the cell (killing it, when a large outflux), and tear off outer cell lining to wrap themselves in a lipid (fat) cover.

Coronaviruses seem to have a very complex chemical process for doing all this (according to the 2015 NCBI paper PMC4369385 = https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369385/) and my surmise is that that may account for a relatively long latency period between initial infection and outbreak of symptoms.

Another factor for such a delay could be this (from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369385/):

“In several coronaviruses, S protein that does not get assembled into virions transits to the cell surface where it mediates cell–cell fusion between infected cells and adjacent, uninfected cells. This leads to the formation of giant, multinucleated cells, which allows the virus to spread within an infected organism without being detected or neutralized by virus-specific antibodies.”

In other words, some of the viral goop bonds the infected cell to adjacent healthy cells into which the virus then penetrates stealthily, out of “sight” of the antibodies of the immune system. In that way many cells can become invisibly infected as regards our immune system “radar,” – our asymptomatic latency period – before all hell breaks loose from all those “sleeper cells” and the victim is evidently in full-blown disease.

These articles are interestingly suggestive; but beware that I have injected my own speculations here.

CDC reviewing ‘stunning’ universal testing results from Boston homeless shelter
15 April 2020
https://www.boston25news.com/news/cdc-reviewing-stunning-universal-testing-results-boston-homeless-shelter/Z253TFBO6RG4HCUAARBO4YWO64/

Coronaviruses: An Overview of Their Replication and Pathogenesis
12 February 2015
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4369385/

Invisible Invaders, Viruses and the Scientists Who Pursue Them, by Peter Radetsky (1994), is an excellent book, well-written, wealth of information, fascinating. Spans 200+ years of viral infectious disease discovery and vaccination development history; most of it for the 20th century.

Viruses are ever changing to evade immune systems, and reliably persistent at seeking to infect animal and human hosts. Humans can be amazingly clever in deciphering viral codes and schemes — giving us the cures and vaccines we have gotten so far — but for the most part are unchanging as regards being petty and conniving in the extreme, all for the sake of seeking approval, recognition, and to profit financially from their otherwise humanitarian efforts. Behaviorally, on average we are a monoculture, and monocultures are much more easily penetrated by viral diseases, whether physical (like COVID-19), or mental (like money-making one-upmanship, a.k.a. capitalism, neoliberalism).

While I have explicitly speculated here, please note that I defer to the medical experts, like Dr. Fauci, on “what it is,” and “what we should do.” My own best estimates are informed by the articles noted above, and the following, particularly Radetsky’s book (described above and in the pictures).

Three questions by Henry Coulter, and my “answers” follow.

1. “Is this virus compatible to the one of Spanish Flu fame?”

It is somewhat similar (a positive sense single strand RNA virus for SARS-CoV-2, and maybe also for H1N1 1918 Flu), both causing (initially) respiratory diseases. SARS-CoV-2 can migrate deeper into the airway, then lungs, and down deep there in severe (life threatening) cases. Now reports (mainly from China) have emerged that for severe cases (survivors) something like 30% (??) of them develop heart damage and permanent kidney damage thereafter requiring dialysis.

MY SPECULATION: is that once the virus is deep deep in the lungs, and damaging the alveoli (where air/oxygen enters the bloodstream through capillaries), that it may drift along with the blood to arrive at the heart and the kidneys (another “spongy” organ for osmotic-type transfers), and in that way infect and damage them. People who have died from “complications of COVID-19” MIGHT then have gone because of pneumonia (drowning), or hypertension heart attacks where the heart was pumping furiously to try to capture and circulate oxygen from lungs that were clogging up and choking off that gas flow, or kidney failures.

The “old” are more susceptible because they generally have weaker immune systems, and more underlying conditions (e.g., heart diseases, diabetes, airway constrictions/emphysema, obesity).

2. “If we simply have much better communication channels to mitigate the spread.. thus lower the impact on the population.”

See the story about Vietnam’s response to the pandemic. It shows exactly that, and much more (important story).
https://consortiumnews.com/2020/04/16/covid-19-vietnam-winning-new-war-against-invisible-enemy/

3. “The Spanish flu targetted a far younger population.”

There is an extreme immune system response called a “cytokinetic storm,” and is POSSIBLY (MY SPECULATION) more likely to occur with strong young adult (not child) immune systems:

From “Cytokine Release Syndrome,” https://en.wikipedia.org/wiki/Cytokine_release_syndrome, (next 2 paragraphs):

Cytokine release syndrome (CRS) or cytokine storm syndrome (CSS) is a form of systemic inflammatory response syndrome (SIRS) that can be triggered by a variety of factors such as infections and certain drugs. It occurs when large numbers of white blood cells are activated and release inflammatory cytokines, which in turn activate yet more white blood cells. CRS is also an adverse effect of some monoclonal antibody drugs, as well as adoptive T-cell therapies. Severe cases have been called cytokine storms. When occurring as a result of drug administration, it is also known as an infusion reaction.

CRS occurs when large numbers of white blood cells, including B cells, T cells, natural killer cells, macrophages, dendritic cells, and monocytes are activated and release inflammatory cytokines, which activate more white blood cells in a positive feedback loop of pathogenic inflammation. Immune cells are activated by stressed or infected cells through receptor-ligand interactions. This can occur when the immune system is fighting pathogens, as cytokines produced by immune cells recruit more effector immune cells such as T-cells and inflammatory monocytes (which differentiate into macrophages) to the site of inflammation or infection. In addition, pro-inflammatory cytokines binding their cognate receptor on immune cells results in activation and stimulation of further cytokine production. This process, when dysregulated, can be life-threatening due to systemic hyper-inflammation, hypotensive shock, and multi-organ failure.

4. Henry: Stay away from other people’s “breath plumes,” the clouds of vapor and water droplets that expand from their mouths and noses on exhalations (stronger and of longer range when exercising/under physical strain), coughs and sneezes. Eventually such droplets fall to the ground.

The aerosolized virus is eliminated and destroyed by the combination of sunlight, heat and humidity.
https://www.accuweather.com/en/health-wellness/coronavirus-expert-says-the-virus-will-burn-itself-out-in-about-6-months/679415

(But that report from February 2020 may be too optimistic about when SARS-CoV-2 will “go away.” We’ll see.)

Sunlight, as UV radiation, ‘bleaches’ or ‘oxidizes’ the virus particles [MY CHARACTERIZATION]; heat can cook it to death (breaks it apart, a technique often used when making weak-germ and killed-germ vaccines), and humidity can “rain it out” of the atmosphere (on to the ground, and washed away in runoff).

FINALLY: I AM NO MEDICAL NOR VIROLOGY NOR EPIDEMIOLOGY EXPERT!! But (since I’ve been explicit with my caveats), you can share this commentary as/if you like.

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Why Remdesivir and Hydroxychloroquine for COVID-19?

Louis Proyect writes: “I understand the reluctance to put a plus where Trump does, but this article [“How New Jersey’s First Coronavirus Patient Survived,” in the New York Times, ~3 April 2020] indicates that a doctor who was close to death had a miraculous recovery after receiving Remdesivir and Hydroxychloroquine.”

Remdesivir (https://en.wikipedia.org/wiki/Remdesivir): “Remdesivir (development code GS-5734) is a novel antiviral drug in the class of nucleotide analogs. Remdesivir is an adenosine analogue, which incorporates into nascent viral RNA chains and causes their pre-mature termination. It was developed by Gilead Sciences as a treatment for Ebola virus disease and Marburg virus infections, though it subsequently was found to show antiviral activity against other single stranded RNA viruses such as respiratory syncytial virus, Junin virus, Lassa fever virus, Nipah virus, Hendra virus, and the coronaviruses (including MERS and SARS viruses). It is being studied for SARS-CoV-2 and Henipavirus infections. Based on success against other coronavirus infections, Gilead provided remdesivir to physicians who treated an American patient in Snohomish County, Washington in 2020, who was infected with SARS-CoV-2, and is providing the compound to China to conduct a pair of trials in infected individuals with and without severe symptoms.”

Hydroxychloroquine (https://en.wikipedia.org/wiki/Hydroxychloroquine): “Hydroxychloroquine (HCQ), sold under the brand name Plaquenil among others, is a medication used to prevent and treat malaria in areas where malaria remains sensitive to chloroquine. Other uses include treatment of rheumatoid arthritis, lupus, and porphyria cutanea tarda. It is taken by mouth. It is also being studied as an experimental treatment for coronavirus disease 2019 (COVID-19). Common side effects include vomiting, headache, changes in vision, and muscle weakness. Severe side effects may include allergic reactions. Although all risk cannot be excluded, it remains a treatment for rheumatic disease during pregnancy. Hydroxychloroquine is in the antimalarial and 4-aminoquinoline families of medication. Hydroxychloroquine was approved for medical use in the United States in 1955. It is on the World Health Organization’s List of Essential Medicines, the safest and most effective medicines needed in a health system. In 2017, it was the 128th-most-prescribed medication in the United States, with more than five million prescriptions.”

My CONJECTURE (a non-medical person’s hypothesis) is that the SARS-CoV-2 virus (causing COVID-19) may act in a somewhat similar manner to the Epstein-Barr Virus (EBV). If so, this hypothetical (and likely only partial) similarity might lead some doctors treating critically ill COVID-19 patients to administer the drug combination of: the antiviral drug Remdesivir to reduce the viral load, and the anti-malarial drug Hydroxychloroquine to buttress the patient’s immune system, which is assumed to be in a pre-existing weakened condition.

My following description of the Epstein-Barr Virus (EBV) and its several disease-causing effects are drawn from the book The Invisible Invaders, Viruses And The Scientists Who Pursue Them, by Peter Radetsky, (published by Little, Brown and Company, 1991, 1994). Passages quoted from that book are woven into my interpretive discussion, below.

Bone marrow produces a number of kinds of blood cells, including “the B and T lymphocytes, which comprise an essential part of the immune system. Without these disease-fighting cells [we] couldn’t fend off the mildest infection; something as insignificant as the common cold could kill [us].”

The Epstein-Barr Virus is ubiquitous in people (~95%), it invades B lymphocyte cells, but is usually held in check by the human immune system, which produce antibodies to eliminate EBV-infected B lymphocyte cells.

In poor regions with primitive and/or inadequate hygiene (e.g., parts of Africa) children are exposed to EBV early in life (3-4 years) and may only get a mild ‘childhood’ disease of sore throat, cough and flu-like symptoms for a few days, and that’s all. “For some reason, whether because of the immaturity of their B lymphocytes (the cells the Epstein-Barr virus invades) or the immaturity of their immune system as a whole, [most of these] children infected with EBV rarely come down with any kind of obvious illness.” (The EXCEPTION to this will be described further below.) Thereafter, these minimally affected and now recovered children have antibodies to EBV.

In the developed and generally very hygienic countries, children may not be exposed to EBV until much later: adolescence and early adulthood. “But when the virus invades later, the result is usually more severe: a case of mononucleosis. In causing a more serious illness in older people, EBV acts much like other viruses, hepatitis and poliovirus among them. The reason may be that in older individuals the immune system responds inappropriately to infection. In any case, as far as EBV is concerned, at least half of the people belatedly infected with EBV experience significant illness.”

“Mononucleosis is a disease in which blood cells proliferate out of control. Here [is] a virus, EBV, that was first detected in cancer tumors [Burkitt’s lymphoma], and now [has been shown] to be intimately involved in mononucleosis, a common cancer-like disease… Mononucleosis is essentially a disease of developed countries.”

Now for the EXCEPTION.

Denis Burkitt, a Scottish surgeon and physician practicing in Africa during the 1950s and 1960s, first identified the cancer “Burkitt’s lymphoma” in African children, by engaging in a massive study and expedition between 1957 and 1961. In 1963, EBV was isolated by M. Anthony Epstein and Yvonne Barr from specimen tumors sent by Burkitt to London in 1961. If so many African children were exposed to EBV as toddlers with little consequence (and certainly no mononucleosis in early adulthood), why did some of those children develop the specific cancer of Burkitt’s lymphoma?

Obviously, the fundamental factor that can lead to Burkitt’s lymphoma is exposure to and infection by EBV.

The first necessary co-factor to developing Burkitt’s lymphoma is having “been exposed to an unusually heavy dose of the [EBV] virus.”

The second necessary co-factor to developing Burkitt’s lymphoma is “a weakened immune system.”

“It has been suggested…that Burkitt’s lymphoma arises as a result of immunological disorders in children exposed since early infancy to heavy malarial infection.” [Guy de Thé, 1978].

The fact that infection with EBV in an individual with a weak immune system can lead to cancer was proved by the case of David, “The Bubble Boy.” David was born with no immune system and lived in the sterile interior of a plastic bubble (a tent). In 1983, he was given a bone marrow transplant from his healthy sister, but he died in 1984 at the age of 12. The cause of death was cancer, “the B cells that David had obtained through the bone marrow transplant had run amok. He died of cancer of the B lymphocytes, with tumors similar to Burkitt’s lymphoma. All the cancer cells contained Epstein-Barr virus. [David’s] sister had at some point been exposed without harm to EBV; she passed on this otherwise harmless dose to David through her bone marrow.”

Epstein-Barr virus causes a very broad stimulation of B-cell growth. Out of that a tumor can develop if given “some kind of other agent that compromises the immune system… In the case of Burkitt’s lymphoma, that agent is almost certainly malaria.”

Guy de Thé [1984]: “We know that very early viral infection can lead to Burkitt’s lymphoma. It’s a situation exactly like [that of] cigarette smoking and lung cancer. You don’t fully understand the mechanism, but you can measure the risk. Very heavy and early exposure to EBV is as though you were smoking all your life, two packs a day. Then malaria enters at the second level, by promoting further proliferation of the B cells infected with EBV. We’re all infected by EBV, but nothing happens to most of us because our immune system controls the infected B cells. Malaria specifically depresses the part of the immune system whose job it is to control the B cells. And after that, something, possibly a chance event, induced by nobody knows what, causes a change in chromosomes that transforms the cell into a tumor cell.”

Now, recall the CONJECTURE. Hypothetically, a similarity of causes exists between:

— the cause of serious COVID-19 illness and death (by the SARS-CoV-2 virus, plus an assumed immunodeficiency co-factor), and

— the cause of Burkitt’s lymphoma, as well David “Bubble Boy’s” cancer of the B lymphocytes (by the Epstein-Barr virus, plus an immunodeficiency co-factor; which for Burkitt’s lymphoma is malaria, and for David was a complete lack of an immune system).

Some doctors working under the stress of trying to save dying people during the explosive growth of this current COVID-19 pandemic, and who may have made conjectures about causes similar to the one stated here, arrived at the drug cocktail of:

— Remdesivir, to try a direct reduction the SARS-CoV-2 viral load in the patient’s respiratory tissues; and

— Hydroxychloroquine, to buttress an assumed immunodeficiency — as with malaria — of inadequate control of B lymphocyte cells presumably infected with the virus.

So much for my amateur speculations on the Remdesivir plus Hydroxychloroquine cocktail administered to some COVID-19 patients.

What I can see clearly as fact is that doctors and virologists are in a frantic race against death (within days to a couple of weeks for the unlucky patients), to save as many COVID-19 stricken as they can, while yet having incomplete knowledge about the mechanism, and its unknown associated co-factors, by which the SARS-CoV-2 virus actually causes fatalities. Also, they are simultaneously trying to ascertain the details of both the progression of infection and the nature of all associated co-factors that aggravate the disease to the point of fatality, so as to then be able to design drugs that cure COVID-19, and vaccines that can prevent people from developing the disease if exposed to the virus.

Both as individuals and as a society we should be very grateful to the medical people working so furiously — and for many at great personal risk — on COVID-19 today, and on all the as yet little-known and untamed viruses that might infect us in the future; and we should support their work fully (politically and financially) as a matter of public health national policy. “Public” as in Medicare-For-All, and as in drug and vaccine development that is as much a publicly funded and owned service, rather than only a for-profit exploitation of human need by a mercenary pharmaceutical industry.

Acknowledgement: I want to thank Gretchen Hennig for giving me a copy of Radetsky’s book, and for explaining the concept of “viral load” to me.

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