“Today, the greatest risk of global catastrophe isn’t nuclear war, nor is it natural disaster. Rather, it looks something like a microscopic spiky ball.” — Bill Gates
If anything kills over 10 million people in the next few decades, it’s most likely to be a highly infectious virus. Not missiles, but microbes.
Trillions up trillions of them containing the DNA to hijack the molecular machinery of a living organism’s cells, make copies of itself before trying to destroy the host, and moving on to seek more. While humans are by far the most advanced living creature on Earth, building civilizations and technology, at core we are still susceptible to these infectious agents, often times with almost no defence. No plan.
So while you got that can of fruit you have down in your basement just in case of an attack, your chances of actually eating it because of one are actually almost close to zero.
Nailing the basics 1.0
First and foremost, it’s important we understand what a virus is before I move more in depth:
“An infective agent that typically consists of a nucleic acid molecule in a protein coat, is too small to be seen by light microscopy, and is able to multiply only within the living cells of a host.” — Google Dictionary
Now some of that may sound slightly foreign, no worries, I’m here to help break it down!
After reading, this definition mentions two key points:
- The anatomy of the virus (DNA/RNA in the centre surrounded by protein).
- It’s function (To invade the property of other cells, swap the DNA and turn the cell into a virus producing factory).
Virus Anatomy 101
Most scientists accept that viruses are not living, but in fact a complex collection of organic matter that is able to self-replicate. They are much smaller and simpler than a typical single-celled organism.
In other words, they are biologically inert, and thus do not possess any biological function. Between the scale from simple molecules (biomolecules) and living organisms (bacteria) they exist more or less in a grey area in the middle of the two.
Now, if we were to slice down the middle of a single virus particle, this is what we would roughly find.
In the very centre includes the viral genome, constructed with enzymes for the replication and manipulation of their own genetic material (which is either a single or double stranded piece of DNA or RNA). This is perhaps the most vital portion of the entire virus itself, as this is the key ingredient to the creation of new viral agents. Which makes sense, as the sole reason why viruses exist is so then they can continue to make copies of themselves and thrive.
Enclosing the genetic material in a shell is the capsid, made of protein called promoters. The viral tegument surrounds the capsid as a cluster of more proteins.
Then, there’s the envelope which is the outermost layer of the virus. This is the final layer of protection which is built using derived portions of the host cell membrane.
Later on top of the envelope are envelope proteins (viral protein receptors, or viral glycoproteins), which as a matter of fact, don’t serve as an additional buffer layer, but is a crucial element which the viruses use to attack its host.
Smaller than you think
A viron is so minuscule scientists need to use an electron microscopy to magnify it 300 times or more so it can be seen and studied by the naked eye.
The average corona virus particle measures about 0.1 micrometers. To put that into perspective, it would take 1000 micrometers to fill up the space of just one millimetre, the width of your fingernail. Next to a bacteria (0.5 micrometers), it’s almost nothing.
Viral reproduction
Viruses are not able to produce life out of their own capacity. Although they can live on surfaces and objects for up to a few days, eventually they will still perish without the support of some other life form.
Cells are the smallest unit of life, manufacturing proteins, replicating DNA, and storing resources within its cytoplasm. This makes them the perfect incubator for viruses to thrive in. Ultimately, they use their encased genome, with the aid of various molecular machines to take advantage of the cell and convert it into a mindless virus producing robot.
Relentless biological vandalism
A multi-step process:
- Finding a host cell
The virus’s molecular receptors (the green spikes shown previously on the diagram) attempt to bind to the membrane of a cell. I use the word “attempt” here as most viruses can only infect certain species of hosts and only certain cells within that host. In other words, a certain viral receptor must be found on the cell’s surface for the virus to actually attach and infect.
Like how there is only one type of key that can fit into every type of lock, there is only one specific virus receptor for every type of cell-surface receptor. Thank god, because every second, we ingest and inhale millions of viral particles, and it would be terribly awful if all of them could infect us.
2. Occupying the host
Nonetheless, let’s say that a virus does manage to fasten itself onto a cell membrane without rejection. The protein receptors act as a key to the cell’s lock, and then one of two things could happen:
It uses several complicated biological pathways to either force the cell to:
- Accept its genetic material through the membrane while the virus stays binded.
- Engulf the virus as a whole directly into the cell (endocytosis).
Regardless, its sole purpose is for the viral genome to make it into wanted territory.
3. Unleashing the DNA/RNA
Once the genetic material has successfully made itself into the cell’s cytoplasm, it will begin to use its molecular arsenal to hijack the cell’s protein manufacturing systems and DNA replication mechanism.
Rather than the cell performing out its normal cell functions, the viral infection will force it to instead follow its genetic code, gaining indoctrination over the host. This will cause the cell to halt on its own DNA replication and copy the genetic material of the virus, which later impacts how the proteins are manufactured.
In no time, the infection gains full control over the cell’s abilities and forces the cell to produce and assemble more viral protein shells filled with virus DNA/RNA. The scary part is the cell being in complete oblivion.
4. Exiting the cell
At the end of the day, the virus making machine begins to take over an increasing amount of the cells protein construction ribosomes, causing the interior of the cell to be soon packed with virus particles. Obviously, these particles need to find a way to exit the cell, and often the process can destroy/damage the host cell.
The Lytic Cycle:
This is when the host cell is terminated at the end of replicative cycle. Due to the extreme tension, the cell bursts open (lyses) which allows the new viruses to go on and seek other cells to infect.
“The process is exponential in nature; just a few lytic cycles has the potential to destroy an entire bacterial population.”
The Lysogenic Cycle:
This involves a process where the host is not destroyed. Instead of immediately using the cell to produce more viruses, the viral DNA is swapped with the cell’s genome (prophage). The DNA will remain largely silent, while the cell divides itself many times into daughter cells containing the same prophage.
After a certain point, some environmental signal will trigger a switch from the lysogenic cycle to the lytic mode and all the infected cells could rupture at once!
How viruses spread 1.1
Infectious Diseases — An Introduction
As the name suggest, they’re diseases caused by an infectious agent. This does not only include viruses, but other invaders such as certain types of bacteria, parasites, fungi, etc.
There are four ways which infectious diseases are classified:
- Zoonotic disease (animals → humans, over 60% of human diseases are zoonotic)
- Emerging infectious disease (are new and increase in incidence and range quickly)
- Neglected tropical disease (affects underdeveloped countries as there is a lack of treatment)
- Vector-borne diseases (infected organisms → vector (mosquitoes, ticks, etc.) → another organism, responsible for over 17% of all infectious diseases)
Droplet vs Airborne Transmission
These terms might be familiar; however, many people often don’t exactly know how to draw the line between the two. Especially during a pandemic, it’s extremely important we understand the differences.
Droplet
These infected particles are rather large. They’re released as droplets as they pick up moisture from our respiratory system along with the infectious disease. Even though they’re let out into the air, because of their heavier mass, they soon land on surfaces which then can be picked up by someone else after touching.
“It’s important to stay at least 6 feet away from others when possible” — Centers for Disease Control and Prevention (CDC)
Everywhere due to COVID, I’m assuming you’ve heard this phrase. Government officials, friends, family, work, etc. The corona virus is spread via droplets, so transmission can only happen within two meters. Any closer, the particles can go directly into the body of someone else from your face to theirs.
Aerosol
Any particle less than 5 micrometers in diameter is considered airborne. Because of their minuscule size, they can easily travel through the air, too light to sink to a surface. Areas with wind or even slight air movement can blow infected particles from someone into another person even over a long distance. They can sneak through ventilation systems and be spread simply by talking or exhaling.
To give a bit of perspective, the width of a human hair strand measures 50 micrometers, so imagine the diameter of an airborne particle as more than 10 times smaller than that, which is so, very, small.
Certain infamous diseases which are considered airborne include:
- Influenza
- Measles
- Mumps
- Diphtheria
Fortunately, vaccines have been developed and some of these dangerous infections have been eradicated in certain areas of the world by the WHO!
The Immune System Explained 1.2
Every second your body is under attack. Billions of bacteria, viruses, fungi, etc., are trying to make themselves at home within your body. The term “immune system” is one that most people have heard of and they know that it’s thanks to this system that our bodies can remain healthy, but that’s the end of the story. Furthermore, knowing the workings behind on how our immune system obstructs invaders can become an intricate process to understand.
In a nutshell, the immune system is super complex mini army, consisting of guards, soldiers, intelligence, coders, weapon factories, and communicators all to protect you from well…dying.
A visual representation of the human immune system
Patrolling
Before attack, an immune system must first find if there is an infection , or else a defence plan would be plainly superfluous.
Leukocytes, otherwise known as white blood cells, migrate into the bloodstream and act as security patrols. Like how detectives looks for clues of the presence of their target, leukocytes search for molecular traces such as antigens, which are weird substances left behind from invaders. Once spotted, they trigger the immune response.
Lights, Camera, Action.
Let’s go through a quick mock test to see what would happen right when your body has discovered an invaded virus particle and indicated a warning to the rest of the system.
Fighter #1: Macrophages
This is the first type of cell to enter the scene. You can visualize them as massive bodyguards that stand by the entrance of a palace, the palace being more vulnerable parts of your interior body.
Their main duty is to swallow intruders and trap them inside their membrane where they are killed by toxic enzymes. Usually, they call the blood vessels to release fluids, making trapping easier. On the surface, this converts to a common side effect known as swelling: I’m sure all of us have experienced this before.
Macrophages are so strong often they alone can suffocate an attack on their own, devouring up to 100 intruders each. Nonetheless, sometimes their opponent is tricky, so they need to call for backup and do so by releasing messenger proteins that communicate location and urgency.
Fighter #2: Neutrophils
When macrophages are not enough, neutrophils leave their routine patrol routes in the blood and give a hand in the fight. They begin to generate barriers which trap and kill the foreign raiders. Because they attack so furiously, they end up killing healthy cells and so they are programmed to commit suicide after five days of battling to prevent causing too much damage. If not enough, the macrophages call in contestant #3.
Fighter #3: Dendritic Cells
These are considered the “brain of the immune system,” in other words, the component which is most intelligent. When the neutrophils must surrender, these cells take place on stage and being to collect samples of pathogens, ripping them into pieces and presenting their parts on their outer layer. This is crucial to the activation of B-cells (will be explored soon!).
From there they must make a decision based on the current situation of the battle:
- Call anti-virus forces which eradicate all infected body cells?
- Or call an army of bacteria killers?
Let’s say in this scenario, the dendritic cells decide to progress with the second option. Then, the producer of the show calls in contestant #4.
Fighter #4: Anti-Bacterial Forces
In the span of 24 hours, these forces travel to the nearest lymph nodes, where billions of helper B and T cells are waiting to be activated. They attempt to activate as many as possible as ultimately, only about a quarter of them will make it through, the training process being extremely brutal.
They return to the battlefield, where the dendritic cells locate them and ask them to bind onto the viral bits it has previously collected and presented on its membrane. If the helper T cell’s setup matches perfectly, that specific type of T-cell is activated again, duplicating thousands of times at an exponential rate.
From there, these duplicated T cells branch off into 3 different groups:
- Some transform into “memory helper T-cells” which essentially make you immune against the enemy should they return.
- Some contribute their energy to the battlefield.
- The last handful travel to the centre of the lymph node to activate a very powerful weapons factory: B cells
Every B cell is constructed with a different setup, but when a helper T cell of the same setup meets with it, The B cell automatically begins to duplicate rapidly (like the activated helper T-cells). Not only do they replicate themselves, but they begin to assemble billions of tiny weapons (why I used the term “weapons factory”). Due to this, their lifespans are greatly reduce because of extreme exhaustion. Nonetheless, helper T-cells being the great helpers they are, provide motivation to the B cells to persevere. At the battlefield sight, the helper T cells there do the same for their fellow guard and attacker cells.
These weapons are a term you’ve heard of course: Antibodies! Tiny, but powerful weapons made of proteins which are designed to bind onto the surfaces of their intruder.
A selection of different antibodies are produced, and the helper T cells signal which type is needed the most in the invasion.
Once the choice is clear, millions more antibodies are produced which quickly fill the body and saturate the blood. They flood themselves over the raiders, rendering them paralyzed or dead. The macrophages return and engulf these cells much more easily and at last, the infection is wiped out!
At the end of their victory, many healthy cells have been killed off, but the body quickly replenishes them. As for the army itself, many of them commit suicide, as they are now useless and don’t want to consume any more resources.
All except for the memory T helpers and B cells, which stay behind with the “memory” of the intruder and antibodies to knock them out should the same invaders visit again.
Discovering Viruses
Viruses can be incredibly sneaky, so the body is smart enough to manufacture cytotoxic T-cells, another type of T-cell specifically for the detection of viral invasion.
When not under attack, they patrol the body, checking to see if the proteins on the MHC receptors of a cell are the right ones. Proteins that do not belong to those of the cells found on the surface of one can indicate that the virus is infected, as viruses hijack the protein manufacturing cell system and create their own, which end up being displayed on these receptors.
So, essentially, cytotoxic T-cells act as security guards that look for different footprints in the snow.
Nevertheless, let’s say that they do find unusual proteins on the surface of a cell. They being to release cytotoxic factors which degrade the cell, once example being perforin. Perforin is a substance which makes holes in the cell’s membrane and let’s out granzymes into the cell via these holes, which initiate a process called apoptosis (aka. cell self-destruction). Then the macrophages enter and clean them up.
However, viruses know about the presence of the cytotoxic T-cells and their anti-virus loathing, so they perform a trick: they stop the MHC receptors from showing any proteins. Thus, these T-cells will simply pass by, unaware that a certain cell has been hacked.
But, then there are the natural killers (immune cells). They know viruses are witty and expected this stratagem. What the viruses weren’t too cautious about was that after taking back the proteins, there would be no proteins shown on the surface. Healthy cells don’t show this behavior; they will still have proteins on their receptors, just the right ones. These natural killers police the area, and when they recognize that a particular cell isn’t displaying as many surface proteins as it should be, they release toxins in the cell to finish it off.
Of course, cells weren’t left with absolutely no defence plot of their own. In fact, all cells possess interferons, which are solely for the purpose of detecting viruses. When a viral agent has entered and manipulated a cell, the host cell will realize this and release signalling proteins in response. It directly affects the ability of the virus to replicate itself and indicates to neighbouring cells that it is infected. Nearby healthy cells to heighten their anti-viral defences, increasing their amounts of MHC class 1 receptors and proteins. This is a strategy to help make the infected cells more recognizable by the natural killer cells, since these sick cells aren’t presenting as many as the others.
From there, the immune response is triggered, along with the production of antibodies.
The Workings of Vaccination 1.3
Vaccines x Immune System
Vaccines take advantage of the immune system response and their side effect of producing antibodies to build immunity to a specific intruder.
Vaccines don’t act as typical medicine, instead they directly contain weakened or dead bacteria/viruses (or even a few proteins/sugars from the surface of the specific invader). They don’t have enough power to actually make you ill and hijack your body’s cells, so they’re basically futile. However, it’s enough to convince the immune system a real invader has broken in. Remember antibodies? Well, this is how vaccines work to make you immune to a specific attacker.
Essentially vaccines trigger a “mock immune system reaction.” For an antibody to work, their receptor needs to be exact, and often although you may have antibodies, they may not have the right “shape” so your body has to figure it out during the invasion…which takes time. Using vaccines and exposing your body to this virus earlier allows the production and storage of the right antibody before a legit invasion. Thus, days can be saved as your immune system has the correct weapons beforehand and can whip them out during the initial attack, quickly destroying invaders by attaching the right antibodies onto their surface receptors and sugars.
I’ve Heard the Vaccine Development Process is Tough. Is that true?
Yes, it’s certainly not an easy challenge, but a process that can take years to achieve widespread success. The vaccine industry holds even tougher standards in comparison to medicine development, testing being unbelievably rigorous and many safety measures being held accountable.
A step-by-step run-down: testing edition
- First group of testers: Small group
Once the vaccine formula has been developed and is ready for the first round, a small group of people who volunteer are gathered. During this testing process, experts work out the right dose and observe for any major complications.
2. Runners up: 100 people
Gradually, they increase their quantity of testers and continue to monitor if the vaccine is working consistently and/or presenting any unwanted side effects.
3. A crowd: 10s of thousands
After stage 2 has been deemed successful, the teams move to test on thousands more willing volunteers. Now, there are enough people to be able to get an accurate test to see if the vaccine can protect against natural infection. The most failures are spotted in this stage, as given the wide-reaching population, it gives a better chance of discovering rare problems not discerned in smaller studies.
4. Official distribution
If the vaccine test manages to pass stage 3, then it’s a green light that it can now be delivered to vulnerable people, and later on the general population. Nonetheless, the process doesn’t stop here; the vaccine and its effectiveness is still continuously monitored even after they’ve proceeded through all the steps.
What about Antibiotics? Are they a type of antibody?
Antibiotics are not antibodies, but medicine that helps to stop infection caused by bacteria. They are not produced by your immune system, but rather ingested through prescription or foods. If you’re looking for a food high in natural antibiotics, there are tons on google including garlic, honey, and ginger.
Its purpose is to kill/damage bacteria walls or block the production of crucial proteins, hence the name “anti-bio” which means “against-life.” Similar to antibodies they attach themselves onto the pathogen, making them unable to function correctly. Then they pin them down, and call the macrophages which enter and clean up the mess.
Antivirals vs Antibiotics
Antivirals are also another drug which help to battle against invaders, however they only target viruses, unlike antibiotics. Often they’re taken as protection against flu viruses, however they can only be given in a specific time frame.
In a nutshell, they unleash their power by affecting virus replication; they have the ability to stop virus production without negatively affecting nearby healthy cells. However, viruses are sneaky and learn to mutate, so an anti-viral that may be successful now may be ineffectual the year after.
The fight of the corona virus depends on you
It’s quite interesting how I’m sitting in my dark room and writing this article in the midst of a global pandemic. I mean even though it really does suck, there hasn’t been an event similar to this since the Spanish Flu ended in 1920, an entire century ago.
Nonetheless, 100 years later, this time we have technology humanity can use to it’s advantage both in detection (check out my last article on how MIT is using an AI voice-recording tool to detect COVID in asymptomatic patients!) and treatment development.
Over the two years when the Spanish Flu seized power, there were roughly 500 million infections total, a staggering one-third of the world’s population. So far, we’re just over one year since the initial covid case, and worldwide cases have amounted to roughly 90 million, less than 1/5 of the total infections from the Spanish Flu.
Say if covid were to end within the next year, and infection rates remained the same. There would only be a sum of 180 million cases, 36% of the total from the 1920s. That’s a massive improvement, especially considering that the average person has better access to transportation, increasing mobility and thus the risk of transmission.
But, we can’t rely on government officials and big tech companies to expect to play the bigger part in finally putting an end to this nightmare. The virus doesn’t solely affect these groups, but mainly rather through normal citizens like me and you. Ultimately, the situation still depends on us.
For instance, with COVID-19 you may be asymptomatic but still spread the virus to the more vulnerable and/or others who will continue to carry the virus and show no symptoms. Due to asymptomatic numbers, we see so many people overheat the healthcare system in such a short period of time.
How Fast Can the Corona Virus Spread?
The corona virus is infectious. This is definitely not brand new information, however many people don’t have perspective on just how fast transmission can occur.
Let me give you a quick explanation:
Over the span of 14 days, 1 infected person can grow into 32,000 more. The horrible part is that up to 80% of those contaminated will experience mild to no symptoms, essentially meaning the case numbers grow exponentially. At the end of the day, an area could have up to twice as much infection, with more than three quarters of its citizens unaware of their illness and continuing to spread the virus.
“The corona virus can be 10 times more lethal than seasonal flu without any sort of containment. “— CNBC, Health and Science
In the Long Run
In the absence of herd immunity, the best way to reduce unnecessary death is to act as though you already have the virus. This means avoiding transportation, small gatherings, going in person to work/school, etc., unless if absolutely mandatory. And social distancing! But, people can only tell us what to do for our own and other’s well beings up to a certain extent.
Sooner or later, it’s up to our own choices that determine the day when the corona virus is officially called over.
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Sources
- https://www.youtube.com/watch?v=PSRJfaAYkW4
- https://www.youtube.com/watch?v=zQGOcOUBi6s
- https://www.youtube.com/watch?v=7KXHwhTghWI
- https://www.youtube.com/watch?v=wUgEhfo_qxU
- https://www.youtube.com/watch?v=-muIoWofsCE
- https://www.youtube.com/watch?v=xg-Afd7ytJs
- https://www.youtube.com/watch?v=uVUf_pt7Sh0
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Hi, it’s Ashley thanks so much for taking the time to read this article! If you enjoy this content, make sure to follow so you don’t miss any new great stories!
In the meantime I would love to connect with you! Always trying to meet new people and learn more!
Email: moas@utschools.ca
Linkedin: www.linkedin.com/in/ashley-mo-a044781b5
