Tag Archives: respiratory diseases

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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Why Remdesivir and Hydroxychloroquine for COVID-19?

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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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Our Virally Porous Walls

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Our Virally Porous Walls

“The Invisible Invaders” is the title of Peter Radetsky’s book on “viruses and the scientists who pursue them.” It is a richly detailed, smoothly written primer on the subject for the non-biochemist. This book arcs through four topics:

first: a history from 1744 to 1930 of the development of the medical science and vaccines aimed at combatting infectious diseases (for smallpox in 1796 by Edward Jenner [1749-1823], for rabies in 1885 by Louis Pasteur [1822-1895]); the discovery of the virus in 1898 by Martinus Beijerinck (1851-1931); and the discovery in 1917 by Félix d’Hérelle (1873-1949) that viruses could attack and kill bacteria — which are living cells;

second: the science of virology, and the present understanding that viruses are parasitic forms of ribonucleic acid (RNA) or deoxyribonucleic acid (DNA) that invade living cells and hijack their functional programming, so as to reproduce and expel more viruses;

third: modern-day concerns and discoveries about viral diseases: colds, herpes, flu, hepatitis, cancer, AIDS;

fourth: gene therapy inspired by natural viral action, the intentional manipulation of biochemical dynamics to thwart viral infections and to artificially create designer proteins for desired purposes.

Radestsky states that: “[Most] of us have little idea of the impact viruses have on our lives. For they are not simply dangerous enemies, the only organisms besides ourselves that pose a threat to our survival; they’re our co-travelers in life, our most intimate fellow workers. Viruses are literally everywhere — inside us, outside us, constantly permeating the boundaries of the self… They may swap our genes around, rearrange our destinies, act as agents of the ecosystem. In their admirable simplicity and appalling efficiency, they may be the most successful life-form of all… if they can be said to be alive in the first place.”

COVID-19 is a respiratory disease caused by infection with the SARS-CoV-2 virus (Severe Acute Respiratory Syndrome Coronavirus 2). We can metaphorically visualize a viral pandemic in a manner similar to the antique and unscientific ideas that the causes of inexplicable epidemics were astrological “influenza,” and bad airs, “malaria,” wafting out of swamps; by imagining viral epidemics as very tenuous and filamentary clouds of sub-microscopic nucleic acid particles, each wrapped in fat and coated with protein, that are all coursing through our atmosphere, propelled by air currents on every scale from weather systems to human exhalations, and despite their extreme fragility have the power to penetrate through our civilization and into our very bodies and once there to penetrate into the core genetic control units of our cellular functioning — and disrupt it.

We can never perfectly wall ourselves off from viruses, to them our bodies and our patterns of living are so easily permeable. Our surest defense against viral diseases for which we have no vaccines is avoidance of infection. Such avoidance if afforded by a combination of distancing from infectious people and environments (whether visibly or invisibly contaminated), and the conscientious frequent application of personal hygienic practices and household and occupational sterilization protocols. Physically, and mindlessly behaviorally, we are an open weave to viruses, a rich meshwork of protoplasm waiting to be virally colonized and explosively exploited.

The reason we have been hit so hard by the COVID-19 pandemic, and with its still increasing force, is that the United States is a nation and society structured like a Matryoshka Doll that imprisons its people but is transparent to viruses. We each are walled in by many types of barriers intended to exclude us from the ‘tribal clubs’ of others, those barriers being: ageist, bigoted, cultural, ethnic, financial, intellectual, political, racist, religious and sexual; we humans can come up with an endless array of repulsive distinctions about ourselves.

We have a multiplicity of forms of imposed isolation, of social distancing, each tailored to the individual’s demographic characteristics, to their sociological DNA if you will. We all live within walls, within outer walls, within still outer walls, and so on for many layers of confinement away from the more favored tribes and classes, yet also shielded from the more unfortunate ones. This structure of social fragmentation and hierarchical survival is the embodiment of capitalist civilization. It is the separations and differences and conflicts and jealousies and inequalities that exist among us that create the necessary socio-political spaces and the material opportunities to prosecute individualistic capitalist schemes, those personal drives toward profits — and also for crimes and wars.

That drive towards profits — in its extreme it is pure narcissism — is impossible to even imagine in a hypothetical society of ideal socialism, a society that has been largely homogenized in the sense of eradicating all the artificial exclusionary distinctions that define the house-of-cards capitalist paradigm. That those distinctions were always illusory and only seemed intellectually sacrosanct and physically rigid was because the popular will of the nation’s many individuals had been trained over many generations by pro-capitalist anti-socialist mass indoctrination to unconsciously project the capitalist paradigm that is imprisoning them.

The COVID-19 pandemic has collapsed the illusion of that paradigmatic rigidity, of the reality of capitalism. The viral ‘cloud’ has easily penetrated through not just our bodies, but the exclusionary distinctions we previously thought of as either protective shields or barriers to our aspirations. The collapse of those illusions is experienced by the benefactors of the capitalist economy as fears of economic depression and of political revolt by the laboring masses. The collapse of those same illusions is experienced by the masses excluded from prosperity in the current paradigm, as an awakening to and anger over the unreality of the many strains of slavery we all have imagined ourselves into for so long, and an awakening to the breathtaking proximity to us of the bracingly real alternate and liberating paradigm of socialism. We can actually all live better, happier and more securely starting right away! It is solely a matter of popular will.

During this pandemic many have already stated the obvious: any successful effort to end these epidemics will necessarily be a socialist action, and the more socialist those efforts are, the greater the degree of their ultimate successes. Our exclusionary ‘walls’ and clashes of hoarding behaviors are transparent to viruses, only social solidarity can be made reasonably opaque to them. To effectively combat viral epidemics we must close up the now-gaping weave of human civilization. Such a closing up will encounter much friction and resistance, as each person seeks to preserve their private bubble of self-importance, money-making, irrational fantasy and bigoted exclusivity, which are the forces of repulsion within our atomistic social collectivity. The capitalist benefactors will actualize their resistance to the closing up of the human social weave, their economic collapse fears of the awakened and just anger of the exploited masses, by tossing bribes and police-enforced compulsion at them: the smallest, cheapest weight they can put on the lid of the bubbling cauldron of neoliberal capitalism to keep it from flying off as it boils over.

Despite the widespread and atomizing disorientation of American society in reaction to COVID-19, as if it were some impending apocalypse, it would be wise to become disciplined, rational and socialist, and to realize that this pandemic is but a skirmish in the monumental and unavoidable karmic war we now must face against our own narcissistic desecration of Nature, and which we call climate change.

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