What Does COVID Do To Your Body?

What Does COVID Do To Your Body?

An illustrated look at the novel coronavirus and how it attacks the human body to cause COVID-19.

Article Contents

Anatomy of a Coronavirus

Coronaviruses are relatively simple particles. They're made up of a string of genetic material called RNA, which is stored inside a lipid membrane that's lined with protein spikes.

Anatomy of a Coronavirus: the viral RNA is protected by a lipid membrane which is lined with protein spikes

Anatomy of a coronavirus.

Viruses are not cells. They're not even considered to be alive, since they lack critical functions like growth and metabolism. But they do reproduce and evolve, by deviously hijacking our own biological equipment—our cells.

So the SARS-CoV-2 coronavirus, the parasitic particle that causes the infectious disease COVID-19, is a sort of pseudo-lifeform. One that either preceded, or spun-off from, other lifeforms during the course of evolution.

Types of Human Coronaviruses

Viruses are thought to date back billions of years, but molecular clock dating puts the coronavirus family at around 10,000 years old. Of around 50 species known to exist today, seven coronaviruses have mutated to infect humans.

The seven types of human coronaviruses (HCoV): 229E, NL63, OC43, SARS, HKU1, MERS, COVID-19

The seven types of human coronaviruses (HCoV)

The oldest living species, scientifically dubbed HCoV-229E, is likely the cause of common cold symptoms described in ancient Egyptian medical texts from 3,500 years ago. In modern times, we've seen a surge of new coronavirus species that trigger more severe symptoms than common colds.

The infectious disease known as SARS (Severe Acute Respiratory Syndrome) broke out in Guangdong in China, leading to an epidemic between 2002-2004. Although it infected around 8,000 people, 10% of whom died, the spread of the SARS-CoV-1 virus was contained with public health measures. Although no further epidemics have ensued, we can't declare SARS extinct. Specimens of the SARS virus are retained for ongoing research, and SARS has escaped from labs to infect humans on at least four occasions.

A decade after SARS emerged, MERS (Middle East Respiratory Syndrome) jumped the species barrier from bats to humans in Saudi Arabia. MERS is no common cold. Infecting around 2,500 people, it was fatal in a third of cases. Although it's widely present in bats, MERS usually spreads to humans through contact with infected camels, with human-to-human transmission often limited to within hospitals.

COVID-19 is so similar to SARS that it took on the same naming convention: SARS-CoV-2 and SARS-CoV-1, respectively. Both viruses cause a fever, dry cough, and shortness of breath, with concerning transmission and fatality rates. It took five years to detect the SARS virus in wild bats, and the base assumption is that COVID also arose from a wild bat population.

The Lab Leak Hypothesis

The genomes of SARS-CoV-1 and SARS-COV-2 are 89% similar—a fact that could lend itself to both the natural evolution of a coronavirus in bats and the Lab Leak hypothesis. But experts continue to raise questions about other lines of evidence that point to an accidental lab escape.

Early on in the pandemic, biologists like Bret Weinstein noted that COVID-19 was extremely infectious out of the gate, which seemed unlikely for a virus that had only just learned how to infect humans. He pointed to the controversial gain-of-function research performed in a handful of labs around the world, including one just 20km from the suspected origin of COVID-19. The gain-of-function research employed there involved taking existing viruses, including SARS-CoV-1, and genetically modifying them to be more pathogenic and/or more transmissible in humans.

Indeed, the Wuhan Institute of Virology had been studying SARS-CoV-1 for several years, with notable concerns raised pre-COVID about biosecurity. What's more, the Wall Street Journal reported that three WIV researchers sought hospital care for COVID-type symptoms in November 2019, a month before any cases were reported in the general population. Such red flags demand further investigation, yet a three-hour inspection of the facility was said to rule out any possibility of a lab leak.

Perhaps the most compelling evidence is the detection of the nucleotide sequence CGG-CGG at a specific location on the SARS-CoV-2 spike protein. This is a significant mutation which helps the virus gain access to host cells. In the last 30 years, at least 11 separate lab experiments have supercharged viruses with the addition of the double CGG sequence. Yet the mutation hasn't been found to exist in any natural coronaviruses of the same clade.

How would a supercharged virus behave in the real world? We may have already borne witness to it. We can't ignore the fact that COVID reached pandemic status rapidly, whereas its closest human coronavirus cousin, SARS-CoV-1, was contained to an epidemic. What's more, COVID-19 has a longer incubation period, a higher infection rate, and a higher fatality rate than other common respiratory viruses.

COVID vs Flu

Let's briefly compare COVID to another family of respiratory viruses: influenza. In a typical year, influenza infects between 400 million and 1.2 billion people, killing 290,000-650,000—a fatality rate of 0.05-0.07%.

In the twelve months to June 2021, COVID infected 160 million people despite unprecedented lockdowns—yet still killed 3.4 million people. That gives us an official fatality rate from COVID at 2.1%. Even if half of all COVID cases were not formally confirmed through testing, the fatality rate is still many multiples greater than flu.

COVID is up to 42 times deadlier than flu

Official testing and fatality data shows COVID is much deadlier than flu.

How COVID Attacks The Body

Symptomatic COVID sufferers carry trillions of virus particles in their airways. When air leaves their nose or mouth, coronavirus particles travel as an aerosol—a suspension of fine particles—that drift through the air like vapour.

Only a hundred or so particles need enter your nose, mouth, or eyes to start an infection. The coronavirus makes its way to the back of your nose and throat, where it binds to target receptors on the surfaces of cells. This lock-and-key mechanism involving the spike protein allows the virus to enter.

The virus spike binds to the cell's ACE2 receptor lock-and-key style

The virus spike binds to the cell's ACE2 receptor lock-and-key style.

The host cell engulfs the virus by surrounding it with its fatty membrane. Imagine dipping a chicken nugget into BBQ sauce until it's fully submerged. That has nothing to do with this, I just thought it would be a nice thing to imagine.

The host cell engulfs the coronavirus with its membrane

The host cell engulfs the coronavirus with its membrane.

Once the membrane-bound virus is welcomed to the party, it injects its genetic material (RNA) into the cell cytoplasm.

The coronavirus injecting its genetic material into the host cell

The coronavirus injecting its genetic material into the host cell.

When the cell workers discover the viral RNA, they mistake it for human RNA. That's because they're both made up of the same four nucleic acids: adenine, uracil, cytosine, and guanine. These four bases code for the same amino acids, which fold to become proteins—the building blocks of viruses and humans alike.

Indeed, the fact that we share a genetic code at all means that, very distantly, we're related to the coronavirus that's trying to kill us.

The host cell obligingly translates the viral RNA into new coronavirus components

The host cell obligingly translates the viral RNA into new coronavirus components.

Once the viral proteins are synthesised, chemical interactions compel them to self assemble and—BAM!—you've replicated a coronavirus. No sex required.

Chemical interactions compel the newly synthesised proteins to self-assemble into new coronaviruses

Chemical interactions compel the newly synthesised proteins to self-assemble into new coronaviruses.

No sex?! You cry, aghast.

Nope. Viruses replicate through asexual reproduction. Parent particles are simply cloned to produce offspring; there's no co-mingling of genes as we have in human reproduction.

There is just one exception to this rule. Occasionally, viruses can reproduce sexually if a host cell is infected with two related strains. During RNA replication, their genes can mingle to produce hybrid offspring, producing much greater genetic diversity in a single generation.

Soon, the host cell is brimming with an army of new viral offspring. Many are released via the cell membrane, but eventually the whole cell bursts and dies, having fulfilled its ugly destiny.

Hundreds of thousands of viral particles are produced until eventually the host cell bursts

Hundreds of thousands of viral particles are produced until eventually the host cell bursts.

The viral swarm goes on to infect more cells, causing the rate of infection to scale exponentially. Welcome to the incubation period of COVID-19.

If this biology has you salivating, check out my award-winning* posts Evolution Explained: From Bacteria to Humans and How Does DNA Work?

*Awards issued by myself—to myself.

**The after party was amazing.

***The after party went on to win dozens of after party awards.

****These after party awards were also issued by me.

How The Immune System Fights COVID

After a few days of covert infiltration, the growing viral load finally triggers an immune response. Two types of white blood cells, called lymphocytes, make their coordinated attack against COVID:

T-cells circulate the body to seek and destroy infected cells. The tell-tale markers are viral antigens left behind on the cell membrane where the viruses entered. T-cells bind to these antigens and release cytotoxins to destroy the infected cells.

A killer T-cell binding to an infected cell and releasing cytotoxins to destroy it

A killer T-cell binding to an infected cell and releasing cytotoxins to destroy it.

B-cells produce pathogen-specific antibodies which circulate and lock on to the viral particles to neutralise them.

A plasma B-cell producing pathogen-specific antibodies to neutralise the viral particle

A plasma B-cell producing pathogen-specific antibodies to neutralise the viral particle.

At the same time, the immune system releases inflammatory chemicals called cytokines. They make their way to the brain to trigger a fever. Cranking up your body temperature helps lymphocytes recognise cells infected with viral particles.

But it takes your body 2-14 days days to detect SARS-CoV-2 and produce B-cells and T-cells tailored to destroy it. This latency gives the coronavirus the opportunity to make a real mess of your insides.

What Does COVID Do To Your Body?

The early symptoms of COVID can be blamed on your immune system. Coughing and mucus are your body's attempt to flush the virus from the upper airways, preventing infection to the lungs while nipping viral replication in the bud. A strong immune system means you can get ahead of the viral load, which is essential given its capacity for exponential replication.

Similarly, other symptoms of COVID—like vomiting and diarrhoea—are your immune system's attempt to evacuate viral particles from the body. All of these measures take energy and resources away from normal bodily functions, resulting in fatigue, muscle aches, and headaches.

So you've got a fever, you're coughing, and you're fatigued. Life's not fair. But your immune system is fighting trillions of viral particles right now. In a week or so, the coronavirus will be eradicated from your body and you'll feel much better.

Or not. In 20% of COVID infections, the immune system can't get on top of the invasion in time, leading to a serious case of COVID. After 5-8 days of symptoms, the virus reaches the lower respiratory tract—known to you and I as the lungs.

The coronavirus must clear the upper airways before reaching the lungs

The coronavirus must clear the upper airways before reaching the lungs.

COVID Pneumonia

Your lower airways have many more ACE2 receptors than your upper airways, which is a tantalising prospect for the virus. This is why COVID is more likely to go deeper than the common cold, and why it's so much more deadly.

Coronavirus in the lungs triggers inflammation, which creates shortness of breath and a persistent pain or pressure in the chest. The shortfall of oxygen in the blood also produces confusion and drowsiness. These are all signs that you have a more serious case of COVID and need urgent medical help.

During this time, the cells that make up the tiny air sacs in your lungs are under attack. As they degrade, they fill up with fluid from the surrounding blood vessels. This is very bad news.

Illustrated comparison of healthy alveoli vs COVID pneumonia infected alveoli

Comparison of healthy alveoli vs COVID pneumonia infected alveoli

Pneumonia is the inflammation of the lungs, where the air sacs fill with pus and can even become solid. It can be caused by viruses, bacteria, and fungi. While you can make a full recovery from other types of pneumonia, COVID pneumonia causes severe injury to both lungs and can affect breathing for months afterwards. Assuming you survive COVID, that is.

COVID ARDS

The most severe COVID cases result in Acute Respiratory Distress Syndrome (ARDS), often in correlation with pneumonia. ARDS is life-threatening and occurs in 33% of hospitalised COVID patients. It's characterised by shortness of breath, rapid breathing, and a lack of oxygen to the blood.

Patients with moderate to severe COVID ARDS require ventilation to supply their vital organs with oxygen. Without this support, essential organs like the kidneys, lungs, and liver can shut down completely. Even with ventilation, only half of people with COVID ARDS survive.

Blood Clots

Although it's not yet understood why, COVID-19 makes your blood cells more likely to clump together, forming clots. These blood clots can travel through the bloodstream and lodge in the brain, heart, lungs, legs, liver, and kidneys, depriving the organs of oxygen.

"COVID toes" is the name given to red, swollen toes likely due to small blood clots. No-one knows how common clots are in mild cases of COVID, but around one-third of hospitalised patients suffer from COVID blood clots. Small such clots may pose no threat, but larger clots can be life-threatening. If you have COVID, watch for symptoms of a blood clot such as swelling in one leg.

Long COVID

While the major common symptoms of COVID concentrate on the lungs, SARS-CoV-2 attacks the body in a number of ways, leading to post-COVID syndrome. The heart, nervous system, kidneys, and liver can all be affected, with damage lasting for many months after the original infection has disappeared.

Mild to moderate cases of coronavirus last about two weeks. Yet long haulers report fatigue, shortness of breath, persistent coughing, joint pain, and chest pain for extended periods after COVID. Some symptoms may last for years in some people—only time will tell.

Long COVID has been reported after both mild and severe infections. It's likely a result of organ damage, or a persistent inflammatory or autoimmune response. For instance, one study found that 60% of COVID survivors had long term heart inflammation, causing persistent shortness of breath, rapid heartrate, and palpitations.

What Does COVID Do To Your Brain?

Around 40% of people self-report losing their sense of smell during COVID, while more rigorous smell-identification tests find partial or total olfactory dysfunction in 96% of patients. Is this a sign that COVID gets into the brain?

It may be that SARS-CoV-2 simply attacks cells in the nose responsible for sending scent signals. However, doctors in Maryland have reported COVID post mortems where the olfactory bulb, located in the forebrain, had suffered clear signs of inflammation such as leaky blood vessels.

The current hypothesis is that coronavirus doesn't infect the brain directly, but it can still do significant damage. In one COVID autopsy study, researchers found brain damage linked to oxygen deprivation, likely caused by blood clots that temporarily blocked the flow of blood. Numerous immune cells in the brain (microglia) were also activated, causing them to attack neurons.

Because no viral particles were found in the brain, it's likely that cytokines trigger the microglia into action. At the same time, neurons deprived of oxygen send "kill me now" signals to the microglia, which happily oblige. This happens most frequently in the lower brain stem, in charge of heartrate and breathing, as well as the hippocampus, involved in learning and memory.

The developing brain may be even more vulnerable to COVID. This study by US doctors found that 8% of previously healthy children hospitalised for COVID also suffered neurological symptoms. Complications rose to 22% including children with underlying brain conditions. Neurological problems triggered by COVID included severe encephalopathy, stroke, central nervous system infection, Guillain-Barre syndrome, and cerebral oedema. Of the patients studied, 26% died and 40% still had COVID brain injury at hospital discharge.

Final Thoughts

The science of COVID will unravel for years to come, as research hones in on the precise effects of the spike protein and the body's immune response to it. Scientists are familiar with many of the individual symptoms of COVID, from inflammation, to blood clots, to pneumonia. And yet the novel disease mechanisms pose entirely new riddles.

Why is COVID pneumonia worse than other types of pneumonia? Why do so many COVID patients die on ventilators? How does COVID cause brain injury without the SARS-CoV-2 virus present? Why is COVID so damaging to the developing brain? Are the effects of long COVID temporary or permanent? There's a lot more we need to investigate before we can fully understand what COVID does to your body.

Becky Casale Bio

Becky Casale is the creator of Science Me. She's studying for a BSc and raising two small humans so parts of her DNA can live a bit longer.