Covid-19

The best ally of the virus is its victim.

This article, which is intended for a curious audience rather than eminent specialists, attempts to explain the relationships between the virus and its target, the lung cell.
Cet article existe en français.

The texts braces {} are immediate explanations of the preceding word(s).

The fighters

SARS-CoV-2 is the virus that causes a serious disease, coronavirus disease 2019, Covid-19. This virus is very small, like most other viruses. But compared to other viruses, it has a diameter of 125 nanometers {one nanometer = one billionth of a meter or one millionth of a millimeter} which makes it a big virus. Its image is very well known with its spikes which form a crown; it also brings to mind sea mines.
That’s how it is, a marine mine.

His favorite target: the epithelial cells {cells lining the alveoli} of the lung. A cell measures approximately 25 µm {25 microns or micrometers; one micron = 1 millionth of a meter or one thousandth of a millimeter}

Its objective: to enter the cell and modify it (or modify its program) so that the cell manufactures replicas.

In terms of size: if the cell is an official soccer ball (22 cm in diameter), the virus would be represented by a 0.11 cm pinhead.

Click on the link to see the diagram of the virus

Click on the link to see the diagram of the epithelial cells

The battle

Driven by a flow of air or liquid or by a shift in phlegm {viscous, clear substance secreted by certain glands}, the virus comes into contact with a cell. This is where the spikes come into action; they have the ability to lie down and retract. They lengthen to feel the outer surface of the cell membrane thanks to the molecules at the tip of the spikes and the molecules that dot the surface of the membrane. The cell is deceived by the spikes of the virus masquerading as food.

When there is correspondence between the two elements, the spike attaches to the membrane, and even very securely, and contracts to bring the two membranes into contact.

The cell provides the virus with two possibilities for entering:

• an enzyme {chemical reaction accelerator} ACE2 which binds to the envelope of the virus, observed for SARS-CoV-2,
• a protease {another enzyme which cuts and puts in the trash the piece of membrane} TMPRSS2 which causes the fusion of the two envelopes.

Once a large hole has been dug in the cell membrane, the virus enters the cytoplasm {everything inside the cell envelope excluding the nucleus and, if there is one, the nucleolus} of the cell. The two membranes merge at this time, on the virus side this destroys the envelope and releases the capsid {second envelope which encloses the virus program} in the cytoplasm.

Again, it is the cell that will do the work, the viral capsid will be dissolved by the proteases of the cell. As a result, the genome {all the genetic material, the program, which is in the RNA} of the virus walks around the cell with complete freedom.

All the work that remains to replicate the virus will be accomplished by the cell which, on reading the program contained in the RNA {ribonucleic acid, long chain of 4 molecules whose combinations and sequencing form a program}, will synthesize all the elements to reconstruct a virion {an almost complete virus including the capsid and its contents}.

The capsid will move towards the surface of the cell and come into contact with the cell membrane; the process tears the membrane with enough surface to wrap the virion which is expelled outside where the assembly ends to give a virus in good working order which will hasten to conquer another cell.

And?

A lost virus, a new virus = draw, equality! Well no, the program contained in the injected RNA has an instruction for the cell: once the process of creating a virion is complete, we start over from the beginning. This allows, from a virus, to create a large number until … the cell depletes its resources and sees its membrane torn apart by lots of small holes (hence the mention at the beginning of this article of the large difference in size between virus and cell).
The cell dies and rots on the spot: Virus the Little has destroyed Big Cell.

Reflection on human intervention to defeat the SARS-CoV-2 virus

When you can no longer destroy the virus before it approaches its target – for example by attacking it with soap and apple cider vinegar which will destroy the envelope or soap and alcohol which will destroy the capsid – there is not much left to do, if we discard the possibility of destroying the target cell. It is imperative to prevent the bonding between the virus and the cell. Such a possibility is theoretically possible, as this publication proves:
Inhibition of severe acute respiratory syndrome coronavirus in vitro by chloroquine
Abstract:
We report on chloroquine, a 4-amino-quinoline, as an effective inhibitor of the replication of the severe acute respiratory syndrome coronavirus (SARS-CoV) in vitro. Chloroquine is a clinically approved drug effective against malaria. We tested chloroquine phosphate for its antiviral potential against SARS-CoV-induced cytopathicity in Vero E6 cell culture. Results indicate that the IC₅₀ of chloroquine for antiviral activity (8.8 ± 1.2 μM) was significantly lower than its cytostatic activity; CC₅₀ (261.3 ± 14.5 μM), yielding a selectivity index of 30. The IC₅₀ of chloroquine for inhibition of SARS-CoV in vitro approximates the plasma concentrations of chloroquine reached during treatment of acute malaria. Addition of chloroquine to infected cultures could be delayed for up to 5 h postinfection, without an important drop in antiviral activity. Chloroquine, an old antimalarial drug, may be considered for immediate use in the prevention and treatment of SARS-CoV infections.
Copyright © 2004 Elsevier Inc. All rights reserved.

Come on, yet another:
Chloroquine is a potent inhibitor of SARS coronavirus infection and spread
Abstract:
Background:
Severe acute respiratory syndrome (SARS) is caused by a newly discovered coronavirus (SARS-CoV). No effective prophylactic or post-exposure therapy is currently available.
Results:
We report, however, that chloroquine has strong antiviral effects on SARS-CoV infection of primate cells. These inhibitory effects are observed when the cells are treated with the drug either before or after exposure to the virus, suggesting both prophylactic and therapeutic advantage. In addition to the well-known functions of chloroquine such as elevations of endosomal pH, the drug appears to interfere with terminal glycosylation of the cellular receptor, angiotensin-converting enzyme 2. This may negatively influence the virus-receptor binding and abrogate the infection, with further ramifications by the elevation of vesicular pH, resulting in the inhibition of infection and spread of SARS CoV at clinically admissible concentrations.
Conclusion:
Chloroquine is effective in preventing the spread of SARS CoV in cell culture. Favorable inhibition of virus spread was observed when the cells were either treated with chloroquine prior to or after SARS CoV infection.
© 2005 Vincent and al; licensee BioMed Central Ltd.

The other possibilities are immunization acquired after a primary infection (viruses are so unpredictable that the effect may or may not exist, occur immediately or late, last a long time or fade quickly) and the vaccine (a few months or more years, see the history of the always awaited HIV vaccine). Studies and research are underway on this subject.

Notes:

For the brave: Apical Entry and Release of Severe Acute Respiratory Syndrome-Associated Coronavirus in Polarized Calu-3 Lung Epithelial Cells ePub or PDF version at the top right.

For virion fans: a photo (without dedication) of the virion

For those who need a graphic diagram: The life cycle of SARS-CoV