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Status: Finished  |  Genre: Other  |  House: Booksie Classic

About the COVID-19, many articles were well written than far said but the written matter is more complicatedly composed for the considerations of ordinary people. People get scared as they hear from television and careworn as they read hearsay compositions in News Papers. The reason is simple. For COVID-19, there is no correct vaccine to prevent infection or approved medication to treat contagion within a short time or close at hand. Day by day, more surprising facts are streaming-in. But I feel the easy example to make people understand about COVID-19 is compare it to influenza rather concoct speculative layers on difficult to understand issues.

There are hundreds of viruses. Generally speaking, there are two types: Type A and B influenza viruses. The two viruses are responsible to spread for seasonal flu epidemics every year.

Another feature, influenza and COVID-19 viruses dry-gulch respiratory physiology, yet there are important differences between the two viruses and how they spread.

Firstly, COVID-19 and influenza viruses have similar disease symptoms presentation. Both cause respiratory ailment presenting wide range nascent illness from pre-symptomatic to asymptomatic or symptomatic or from mild to severe disease and eventually if not properly treated, it leads to death.

Another similarity is both viruses are spread by contact through saliva droplets and fomites. In the case of COVID-19, there are pieces of evidence of faecal-oral route.

So the best way to keep away from the viral infections is simply and strictly following public healthiness measures and awareness such as hand-hygiene habits, physical distance and good respiratory etiquettes. So far it is good and we all know this.

But we shall go a little deeper.

The new point is about the velocity of transmission and incubation and the difference between the two viruses.
We all know that the size of the viruses is important. The researchers' study reveals that the size of airborne particles determines how the influenza virus is transmitted. Large particles have limited travel distance, while smaller particles stay airborne longer and spread widely.  

Though the COVID-19 is larger than influenza coronavirus, it travels further more distance than the influenza virus. If someone who is suffering from common influenza, Infectious flu-containing particles exhaled by a sick person can travel at least 6 feet. But in case of COVID-19, Infectious COVID-19 containing particles exhaled by a sick person can transportable more than 12 feet.

Latest evidence displays a COVID-19 severely infected patient can naturally eject around 200,000,000 active viruses on every extra-optimal sneeze and paroxysmal cough based on the density loaded COVID-19. This is because of respiratory pathophysiological conditions.

We shall see how.

The interaction of the COVID-19 spike protein with its complementary cell receptor is central in determining the tissue tropism, infectivity, and species range of the released virus.  In Human Respiratory Physiology, Mucociliary clearance, mucociliary transport, or the mucociliary escalator are significant for the self-cleaning mechanism of the bronchial tree’s airways in the respiratory system. It is one of the two protective processes for the lungs in removing inhaled particles including COVID-19 before they can reach the delicate tissue of the lungs. The other clearance mechanism is provided by the cough reflex. Mucociliary clearance has a major role in pulmonary hygiene. Mucociliary clearance effectiveness relies on the correct properties of the airway surface liquid produced, both of the periciliary sol layer and the overlying mucus gel layer, and the number and quality of the cilia present in the lining of the airways.

Both in Influenza and COVID-19, the respiratory pathophysiology varies on the density of viruses present, site of infection and amount of sputum accumulation in the bronchial tree. If the infection persists in the deeper pulmonary milieu results in a stronger paroxysmal cough. More is the mucociliary irritation, speedy and forceful defence mechanism of Mucociliary clearance.

Influenza has a shorter median incubation period of 3 days that involves the time from infection appearance with symptoms. If we take COVID-19 virus, it is assessed to be weekdays longer and in many cases, it depends on one’s immunity. Here the interesting fact is common influenza spreads faster than COVID-19 but not as much lethal as the COVID-19. COVI-19 takes longer incubation with the highest multiplication. More the respiratory epithelium is irritated or hyperactivated by allergens or COVID-19 or micro-organism, there will be more respiratory expulsion force in form of cough or sneeze.

The true mortality of COVID-19 will take some time to fully understand, the data we have so far indicated that the crude mortality ratio is between 3-4%, the infection mortality rate will be lower. For seasonal influenza, mortality is usually well below 0.1%. However, mortality is to a large extent determined by access to and quality of health care.


Viruses set in small chunks of their genetic material in human DNA and successfully make copies of itself inside a host cell. These viruses have molecular tools similar to the ones its host normally uses to translate genes into proteins. As a result, viruses have tools meticulously shaped by evolution to commandeer the protein-producing machinery of human cells. This chunks incorporation process has been occurring for millions of years. The research in this regard has established that human DNA contains viral genetic material nearly 10 per cent of the modern human genome. Over these millions of years, the incorporated DNA genome has mutated to the point that they no longer lead to active infections, but there is a mild warning: which does not mean mutants are not entirely dormant. These runaway arrangements of viral genes are called "endogenous retroviruses".

There are advantages and disadvantages to ERVs.

Occasionally, there are some built-in advantages with ERVs. Scientists have recognized many cases of viral hitchhikers bequeathing vital benefits to human hosts from protection against disease and shaping through incorporated genome is an important aspect of human evolution. Also, we can rule out that these EVRs can underwrite to the onset of diseases such as cancer or make hosts susceptible to infections from other viruses.

Still, research is going on about the possibility that COVID-19 has this ability to strive on the host’s susceptibility.

This Herd Immunity blindly starts with some old unfinished research studies. It is documented that viruses tend to attack the Human immune system. They may be particularly adept at manipulating immune system genes. Ancient human genomes may have evolved in response. Old research papers said that the genomes of humans might have repurposed viral DNA for their defence, using it to spur the immune system into action against viruses and other foreign invaders.

But, if we carefully look into the latest research observations in the above-said pathophysiology, there are more disadvantages with herd immunity. We can daresay that in the absence of a vaccine or drug, and without a clear understanding of the disease pathology, particularly in the COVID-19 cases, it would be dangerous to seek to achieve herd immunity through infection. Moreover and more often, it is fatal. So the best way is through preventive measures.

To establish an elaborative understanding of Herd Immunity, we can compare with an example of other complicated smallpox causing virus: Variola virus belongs to the family Poxviridae, subfamily Chordopoxvirinae, and genus Orthopoxvirus. We can statistically measure how smallpox can be gauged. It goes like this: On a normal, each infected person spread the disease to 5-7 more people, and this happened at some point during an 18-day period, which led to 30% deaths on average. Taking this to its extreme, 1 “typical” infection causes 7 in the first stage and then escalates to 1.17 lakh in merely 6 unfettered iterations. So much so, many readers on COVID-19 might have seen such exponential models being used in the model of COVID-19 infections. And since COVID-19 is new, many of these parameters are yet to be reliably estimated due to different factors.

So Herd Immunity is not suggestible.

Can we predict “an Ending”?

For time being, this will be continued indeterminately.

Either we must find the treatable medication or vaccine, which is on a distant horizon. My best guess is the vaccine, which is better like BCG and Polio vaccination.

And certainly “herd Immunity” is not a suggestion. It is a piece of desperate and frustrated advice by unsuccessful politicians to evade the responsibility of serving people and hide behind ridiculous façade by advising to take Acetaminophen. The disease spreads to the pool of infectible humans on Planet Earth for many years to come.

If we follow Herd Immunity in the absence of a vaccine or drug, and without a clear understanding of the disease pathology, seeking to achieve herd immunity through infection is a dangerous strategy.

If we follow Herd immunity and allow the disease to spread too quickly without ensuing preventive norms, it overwhelms the health system and causes many people to die “unnecessarily”.

Therefore, for almost all countries, at this juncture, it is a cruel choice between saving lives and saving livelihoods.

After some years, what happens?

Then COVID-19 decreases as it runs out of uninfected humans. COVID-19 bumps into people who have already developed immunity to the disease, thus reducing its spread. This is the point at which individual immunity acts synergistically at the societal level when herd immunity is achieved, it means that the pathogen can no longer infect in large numbers. And this is how the endgame can be achieved.

Submitted: June 13, 2020

© Copyright 2021 thai prasad. All rights reserved.

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