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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