War on Covid-19 part 2 Coronaviral assault

A virus is a piece of bad news wrapped in protein.

Peter Medawar
Coronavirus swimming in the lung's fluid buildup.
Exhibit number 19. Coronaviral invader.

In case you missed it, here is part 1

Aliens, invaders, killers, coronavirus. All names for what ail us. Invisible forces wrecking war wantonly. An enemy that knows no sleep. A force driven by desire. “Living” between life and death. How to fight off this “zombie” apocalypse? Know your enemy coronavirus. Learn them well, and you can succeed. Deep diving into Coronavirus and the disease it causes, covid-19, will constitute part of the war plan. “speak softly and carry a big stick” in this manner, you cannot be perturbed.

Coronavirus, the poison of our times. What is it exactly? Coronavirus has spikey projections extending from it, hence the name corona. The spikes are important and play a role we will discuss later. Viruses are built in a simple manner. Our particular enemy, coronavirus, is gift wrapped neatly in what is called a lipid (fatty) layer. This thin layer of fat keeps the guts of the virus inside until the time comes to plant its seed.

There are a few Coronaviruses in the world. The more commonly known ones are SARS and MERS. Lesser known ones are HCOV, OC43, and HCOV 229E, all are responsible for the common cold. In fact, anywhere from 5-30 percent of common colds are cause by a type of coronavirus. [1][2]

Coronavirus is responsible for causing the disease COVID-19. Similar to HIV being a cause of AIDS. A virus is neither alive, nor dead. It reacts to stimuli in the body and can evade pursuit. Make it hard for the enemy to infiltrate you.

Symptoms of COVID-19

What are the signs you may have this Coronavirus? General, nonspecific symptoms are present. Fever, malaise, fatigue, a dry cough, shortness of breath (harder to breath) and a sore throat. Less common symptoms are diarrhea, nausea and vomiting. Be aware. These signs mean that you have been invaded. This Coronavirus is sneaky and tends to lie in wait for 5-11 days or longer before symptoms present. [3][4] what adds to this level of stealth is that this virus may not cause symptoms in some people. Maybe even 78% of us are walking around unknowingly aiding the enemy.[5]

How does the enemy infiltrate us?  

Viruses have wanderlust. They travel from person to person; like people travel from country to country. A virus will hitch a ride from a person actively shedding coronavirus. Once coronavirus has touch terra firma, a.k.a. your skin, it lies in wait. It either enters the territory of another or it enters your inner sanctum. Coronavirus enters by contact or droplets jettisoned out from a nose or mouth.

Being a respiratory virus, anything to do with breath has potential to form droplets. These escape pods give the virus an opportunity to enter new territory and cross borders. A cough. A sneeze. A contaminated surface caressed unknowingly by a hand. Even talking produces droplets that enter hyperspace at warp speed to reach you. Droplets may land in front of your face and be inhaled or swallowed as it mingles within you. A hand that’s been touching all over the place, does not belong in your face.

 How does Coronavirus replicate?

A virus is either RNA or DNA based. The COVID-19 causer, coronavirus, is RNA based. It will enter a cell and release its RNA into the cell. This hijacks the cell into becoming a virus creating factory. The cell will replicate viruses over and over until they overwhelm the cell and burst forth like the extraterrestrials from the movie “Aliens”. These viruses are now freely roaming and each one will infect a new cell. Imagine 1 virus creating 10000. Then each one of those creating 10000. The situation can get ugly quickly.

The infection process.

Our enemy coronavirus latches onto something called an ACE2 receptor. It reaches for this using it’s spiky projections and has a love for these receptors. [6] These receptor are located in lots of tissues in the body. Most notably in the lungs, small intestines, heart, liver and testis. [7] This in part explains why some people develop heart issues [8][9] or digestive issues[10].

Home is where the lungs are.

Coronavirus prefers the lungs over anything else. This is party central for coronavirus, like college students at the beach during spring break. The virus will congregate and replicate swiftly in this area. The virus prefers to enter lungs cells from the apical side. This apical side is in direct contact with outside air. That side of the cell also has a higher density of ACE2 receptors present. Coronavirus will exit through the same entrance it used. This virus loves to go viral. Exiting with a bang while exploding outwards. Now it further infiltrates other cells or deeper into the lungs.  

Our viral opponent strongly infects cells that are more specialized. The more specialized, the higher the count of ACE2 receptors. In this case any cell that is ciliated, meaning the cell has small hairs that assist in filtering and removing waste, are at high risk of infection. However, there is another specialized cell at risk the alveoli. Alveoli are like “balloons” inflating and filling with each invigorating breath and deflating on exhalation.

A good look at the lungs and the alveoli “balloons”.

Alveoli? is that a swear word?

These alveoli are responsible for the gas exchange that occurs in the blood. It is where oxygen enters the blood and carbon dioxide exits the blood. Funny enough, the densest concentration of ACE2 receptors in the lungs are the alveoli. [11] Coronavirus desperately prefers to be a lower respiratory infection [1]

The virus, once attached in the respiratory system, causes damage akin to a psychopath with no regard for anything but itself. The damage to the alveoli causes fluid to rush into the lungs. This reduces the oxygen exchange, leads to shortness of breath, and can lead to hospitalization or death.

lungs filling with fluid as a result of the infection winning the battle.
Healthy lung becoming more diseased as the infection overpowers the body. Notice how air cannot reach the blood as well in the bottom of the picture. ARDS is discussed below.

What makes it so deadly?

 The affinity for ACE2 receptors. ACE2 regulates something called Angiotensin II from being too high. ACE2 has been found to protect the heart against heart failure [7] lung damage and prevent what is known as Acute respiratory distress syndrome (ARDS) [12]. Worst case scenario, coronavirus, with its crushing force will cause ARDS and from there marches towards death.

 It is deduced that, due to the horrific onslaught upon the ACE2 receptors, the virus obliterates the lungs with ease. Look at this study. Mice with no ACE2 receptors succumbed to death from fluid buildup in the lungs. In contrast the mice who did have ACE2 receptors has a better survival rate. [13] The mice with no receptors showed a high level of angiotensin II associated with lung edema a.k.a. fluid buildup.

Big deal, so what?

Remember the highest density of ACE2 receptors were in the alveoli. Damaged alveoli were associated with: fluid buildup that is protein rich, inflammation, cytokines (signalers of the immune response
) and reactive oxygenation species. In other word it lead to ARDS. [14] ACE2 receptors protected against ARDS; but if more of your shield is eaten away, the higher your risk of wasting away.

How truly deadly is it? What are the outcomes and odds? What can be done to prevent an invasion into your territory? Can it be cured or killed? We will cover these answers in the next post. No need to hold your breath; you have a mask on, don’t you?

  1. https://www.tandfonline.com/doi/pdf/10.1080/17476348.2019.1555040?needAccess=true&
  2. https://jamanetwork.com/journals/jama/fullarticle/2759815
  3. https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200402-sitrep-73-covid-19.pdf
  4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7081172/
  5. https://www.bmj.com/content/369/bmj.m1375.long
  6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7119980/
  7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7110844/
  8. https://jamanetwork.com/journals/jamacardiology/fullarticle/2763524
  9. http://www.onlinejacc.org/content/early/2020/03/18/j.jacc.2020.03.031
  10. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7112380/
  11. https://thorax.bmj.com/content/71/5/462
  12. https://www.ncbi.nlm.nih.gov/pubmed/18340998
  13. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4229671/
  14. https://www.atsjournals.org/doi/full/10.1164/rccm.201903-0550UP

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