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


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. (

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 = 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

“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

Coronaviruses: An Overview of Their Replication and Pathogenesis
12 February 2015

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).

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,”, (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.

(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.



1 thought on “Asymptomatic COVID-19, a Long Latency Period to Evade the Immune System?

  1. 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.

    Coronavirus clue? Most cases aboard U.S. aircraft carrier are symptom-free
    16 April 2020

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