What Does COVID Do To Your Body?

What Does COVID Do To Your Body?

Anatomy of a Coronavirus

The novel coronaviruses is fundamentally a rogue string of RNA, encased in a shell lined with spikes.

Coronaviruses contain RNA as their genetic material which is protected by a protein capsid shell. This is surrounded by a lipid envelope studded with glycoproteins.

Anatomy of the SARS-CoV-2 virus. Coronaviruses contain RNA as their genetic material which is protected by a protein capsid shell. This is surrounded by a lipid envelope studded with glycoproteins.

Viruses are not cells. They're not even technically 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.

Biologists tend to think of them as pseudo-lifeforms.

The 7 Types of Human Coronavirus

To date, there are seven coronavirus species that can infect humans, with multiple strains (subtle mutations) and variants (major mutations).

Old-school species are known as alphacoronaviruses and tend to cause common colds. The recent evolution of betacoronaviruses can cause much more severe disease.

Human coronaviruses emerge when they cross the species barrier from other animals, most recently bats and mice. Molecular clock analysis and genomic comparison allows scientists to estimate their date of origin.

A phylogenetic tree of human coronaviruses HCoV-NL63, HCoV-229E, HCoV-OC43, HCoV-HKU1, MERS-CoV, SARS-CoV-1, and SARS-CoV-2

A phylogenetic tree of human coronaviruses: HCoV-NL63, HCoV-229E, HCoV-OC43, HCoV-HKU1, MERS-CoV, SARS-CoV-1, and SARS-CoV-2.

Early life exposure to endemic coronaviruses typically leads to mild infections. As the viruses evolve, we can experience re-infection because they can appear biologically novel. Every infection takes its toll on the body, and viruses can remain in tissues for years.

"HCoV-229E RNA is detected in about 44% (40 of 90) of human brains tested, with similar frequencies in brains from multiple sclerosis patients and patients who died from other neurologic diseases or normal control subjects." - Human Coronavirus -229E, -OC43, -NL63, and -HKU1 (2021)

Betacoronaviruses are hitting us hard. First there was SARS, which jumped from wild bats in China in 2002 and caused a two-year epidemic that infected around 8,000 people with a 10% fatality rate. In people over 65, the fatality rate was 55%.

Though it's no longer endemic, SARS isn't officially extinct. The SARS-CoV-1 virus is retained in labs for research, and has escaped to infect humans on six occasions. One example is from Beijing in 2004, when two virologists were independently infected with SARS leading to a public outbreak.

MERS is another serious coronavirus that jumped from bats to humans in 2012. Originating in Saudi Arabia, it has infected 2,500 people with a 35% fatality rate. Although it jumped from bats, MERS tends to transmit to humans via contact with infected camels, or by human-to-human transmission in hospitals.

COVID-19 was first reported officially in Wuhan in November 2019. There are ongoing efforts to source a common ancestor of the virus in bats, although there's evidence to suggest it escaped from the Wuhan Institute of Virology (WIV). A 2021 GOP report on the origins of COVID-19 drew several conclusions:

  • The WIV genetically enhances bat coronaviruses in gain-of-function (GOF) research from US government funding.
  • Official biosafety concerns about GOF research were raised in 2019, both at the WIV and at labs internationally.
  • On 12 September 2019, the WIV's database of 22,000 bat and mouse pathogen samples went offline permanently.
  • Hospitals near the WIV reported unusually high rates of respiratory infections starting in September 2019.
  • International athletes at the Military World Games in Wuhan in October 2019 returned home with COVID-type symptoms which could explain the early global spread of the disease.
  • A bioweapons expert from the People's Liberation Army was made head of the WIV's Biosafety Level 4 Lab in late 2019.

The lab leak hypothesis also fits with observational data that COVID-19 was highly infectious in humans from its initial discovery. The true origins of COVID-19 will have major implications on the future of the pandemic.

How COVID Compares to Other Diseases

COVID-19 has supercharged transmission rates compared to other diseases like common colds, flu, SARS, MERS, polio, and even smallpox. While it's not as deadly as some viruses, it does have a higher overall fatality rate than flu, measles, and chickenpox.

COVID-19 Fatality and Infection Rate Comparison Graph

Fatality and Infection Rates of COVID-19 vs Other Viral Infections. Data Source: New York Times.

Compared to seasonal flu, the COVID-19 Delta variant:

  • Is ~6x more contagious than flu (R0 = 6 people)
  • Is ~5x deadlier (mortality rate = 0.5%)
  • Has a ~3.5x longer incubation period (up to 14 days)

New variants will shape the course of the pandemic.

As COVID variants evolve, those with longer incubation and higher transmission will thrive because they can replicate more. It's survival of the fittest.

The same isn't true for mortality; a dead host is no good for a virus. So there's a trade-off here. With ongoing transmission, SARS-CoV-2 will optimise for infection, unlocking adaptations to transmit the largest viral load without crossing a detrimental host-fatality threshold.

How Does SARS-CoV-2 Attack Cells?

A person with COVID symptoms carries trillions of virus particles in their airways. Coughing can produce up to 3,000 respiratory droplets, as can talking for five minutes. A COVID patient with a high viral load can transmit 2.35 billion viral particles per ml of respiratory fluid, which drifts through the air as an aerosol, a bit like vapour.

Only a hundred or so viral particles need enter your nose, mouth, or eyes to trigger an infection. The viral pathogen hones in on your cells.

SARS-CoV-2 is engulfed by the cell to release its RNA, which is translated to proteins for viral replication

The pathway of SARS-CoV-2 in cells.

The coronavirus makes its way to the back of your nose and throat, where it binds to ACE2 receptors on the surfaces of cells. This lock-and-key mechanism involving the spike protein allows the virus to enter.

SARS-CoV-2 is 20 times better at binding to our cells' ACE2 receptors than SARS-CoV-1. What's more, new research suggests SARS-CoV-2 may use multiple different receptors to enter cells. This may factor in to the immense human-to-human transmission of the disease.

On binding to a receptor, the host cell engulfs the virus by surrounding it with its fatty membrane. This is endocytosis. 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.

Now the virus must escape the fat bubble, in what's known as endosomal escape, to release its RNA into the cytoplasm.

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

The fact that we share a genetic code is evidence that, very distantly, we're related to the viruses that infect us.
Ribosomes translate the viral RNA into amino acid chains, which fold to make viral proteins

Ribosomes translate the viral RNA into amino acid chains, which fold to make viral proteins.

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 SARS-CoV-2 components to self-assemble

Chemical interactions compel the newly synthesised SARS-CoV-2 components to self-assemble.

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 an exception to this rule. If a host cell is infected with two related strains, the viruses can reproduce sexually, allowing their genes to mingle to produce hybrid offspring.

Now the viral particles are carried out of the cell to go on and infect others. Eventually, the host cell brims with hundreds of thousands of viral offspring, causing it to burst and die. 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 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 Does The Immune System Fight COVID?

After a few days of covert infiltration, the growing viral load triggers an immune response.

How the adaptive immune system works

How the adaptive immune system works.

Antigen Presenting Cells (APCs) pick up viral antigens and display them to activate the troops. Helper T cells mediate the activation of Cytotoxic T cells which head out to destroy infected cells.

Meanwhile, B cells which produce neutralising antibodies based on the specific structure of the viral antigen. Once the virus is neutralised, some of these B cells stick around in case the virus returns in future.

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.

This adaptive immune response allows us to remember viruses we've encountered before, and release tailored antibodies much faster on subsequent encounters. Memory B cells perform like a personal pathogenic library.

Adaptive immunity evolved 500 million years ago, allowing vertebrates to build up a personal pathogenic library

Adaptive immunity emerged in vertebrates around 500 million years ago in our co-evolution with viruses.

But since COVID is a novel disease, we're all in need of SARS-CoV-2 antibodies for the first time. It takes the immune system 2-14 days to produce new antibodies, and this latency allows the novel coronavirus to make a real mess of your insides.

What Does COVID Do To Your Body?

Many early symptoms of COVID can actually be blamed on your immune system as it fights off the invader.

First, your body attempts to flush the viral particles from the upper airways, preventing infection of the lungs while nipping viral replication in the bud. This means:

  • Coughing
  • Congestion
  • Mucus
  • Sneezing

But your body has several orifices from which it can evacuate the virus, and by Jove she's going to use them.

  • Nausea
  • Vomiting
  • Diarrhoea

You also have inflammation in your tool box. Viruses activate many different cells in the nose and throat to produce proinflammatory cytokines and chemokines. The result is lots of swelling.

  • Sore throat
  • Hoarse voice

It's also useful to crank up body temperature when infection looms. This helps immune cells to recognise invaders.

  • Fever
  • Chills

Alas, all of these measures take energy and resources away from normal bodily functions, leaving you with yet more crappy COVID symptoms.

  • Fatigue
  • Muscle aches
  • Headaches

Generally, in mild to moderate COVID infections, the main symptoms triggered directly by the disease are:

  • Shortness of breath
  • Loss of smell
  • Small blood clots

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 virus in time, leading to a serious case of COVID. Now you feel the full force of the virus directly:

  • Trouble breathing
  • Chest pain or pressure
  • Confusion
  • Drowsiness
  • Pale skin and lips

This usually occurs after 5-8 days of symptoms, indicating the virus has reached 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.

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, leading to pneumonia.

Pneumonia is the inflammation of the lungs, triggered by the presence of the virus. The cells that make up the tiny air sacs degrade and fill up with fluid and pus from the surrounding blood vessels. This disrupts vital oxygen supply.
Illustrated comparison of healthy alveoli vs COVID pneumonia infected alveoli

Comparison of healthy alveoli vs COVID pneumonia infected alveoli

While you can make a full recovery from pneumonia, COVID-induced pneumonia is different. It can cause severe injury to both lungs, affecting breathing for months afterwards while you slowly heal.

If you can't fight off the pneumonia, you'll likely succumb to Acute Respiratory Distress Syndrome (ARDS). This causes a life-threatening lack of oxygen, affecting 33% of all hospitalised COVID patients.

Before COVID, the most common cause of ARDS was sepsis (an infection of the bloodstream). It's also caused by the inhalation of chemical fumes, or water in a near-drowning.

In the case of pneumonia, ARDS is triggered when the lungs fill excessively with fluid, preventing many of the 500 million alveoli from performing the exchange of oxygen and carbon dioxide to the bloodstream. There's no treatment for ARDS; only support like mechanical ventilation to supply the body with oxygen.

The worst case scenario is insufficient oxygen to your vital organs including the kidneys, liver, and lungs. While the survival rate of COVID-related ARDS is 65%, up to 90% of COVID deaths are ultimately caused by ARDS.

Why Does COVID Cause Blood Clots?

COVID-19 can cause severe inflammation, which in turn triggers blood clotting. This makes sense in the context of injury: if you open up your knee, inflammation calls up immune defences, while clotting closes the open wound to bacteria.

But when you have a widespread infection like COVID, this tendency to clot can create serious problems. The virus triggers both small and large blood clots which can lodge in the brain, heart, lungs, and legs. And when a clot cuts off blood supply to a vital organ, the result can be fatal.

Your behaviour can exacerbate the clotting problem. Whether you're stuck at home on the couch, or holed up in a hospital bed, you're not moving around. And this is a huge risk factor for blood clots.

"COVID toes" is the name given to red, swollen toes due to small blood clots. Around one-third of hospitalised COVID patients have them. If you have COVID, watch for symptoms of a blood clot such as pain or swelling in one leg.

The Symptoms of Long COVID

What started out as a mere curiosity is finally being taken seriously as a public health problem. Long COVID describes a vast array of possible symptoms that occur all around the body for months after a COVID infection.

You may have long COVID if you have any of these common symptoms for more than 12 weeks:

  • Extreme fatigue
  • Shortness of breath
  • Heart palpitations
  • Chest pain or tightness
  • Joint pain
  • Loss of smell or taste
  • Brain fog
  • Tremors

That's just the short list. This study identified 200 different long COVID symptoms, affecting 10 different organ systems. Also known as Post-COVID Syndrome, it can occur after mild, moderate, and severe COVID infections alike.

Long COVID is likely the result of organ damage, or a persistent inflammatory or autoimmune response. For instance, 60% of COVID survivors have heart inflammation, which can cause shortness of breath, rapid heart rate, and palpitations.

Around 15% of people who've had COVID go on to develop long term neurological symptoms. Unlike its coronavirus cousins HCoV-229E and HCoV-OC43, there's insufficient evidence to determine if the SARS-CoV-2 virus crosses the blood brain barrier in humans. However, we do know that the spike protein enters the brain in mice.

"Coronavirus spike proteins are often cleaved from the virus by host cell proteases... It is possible that during infection by SARS-CoV-2, shed S1 is available to cross the BBB, triggering responses in the brain itself..." - The S1 Protein of SARS-CoV-2 Crosses The Blood–Brain Barrier in Mice (2020)

But we also know that the immune response itself may backfire, with the potential to cause blood clots, inflammation, and cell death within the brain. Directly or indirectly, COVID does attack your brain.

What Does COVID Do To Your Brain?

Losing your sense of smell is a common symptom of both acute and long COVID. Research suggests the virus aggressively attacks cells in the nose responsible for sending scent signals. But at the same time, autopsies of COVID victims have found brain inflammation in the olfactory bulb. Both are potential causes of COVID anosmia.

A third potential cause is from the entire virus, or just its spike proteins, entering the brain. And a potential entry door has been identified. The cells at the top of your nasal chambers are loaded with ACE2 receptors which give SARS-CoV-2 access to cells. The abundance of ACE2 receptors offers an uninterrupted path from the sustentacular (supporter) cells of the olfactory neuroepithelium, directly to brain cells.

Through direct access or an inflammatory response, COVID has demonstrated a number of effects on the brain, including:

  • Stroke
  • Encephalitis
  • Haemorrhage
  • Memory loss
  • Confusion
  • Psychosis

COVID autopsies have found blood clots and severe damage to tissues in the lower brain stem, in charge of heart rate and breathing, as well as the hippocampus, involved in learning and memory.

The developing brain may be especially vulnerable to COVID. Although children are far less likely to suffer from severe infection, a study of 1,700 hospitalised children succumbed to neurological symptoms at a rate of 8%, rising to 22% in children with underlying brain conditions. These included:

  • Encephalopathy
  • Stroke
  • CNS infection
  • Guillain-Barre syndrome
  • Cerebral oedema

While most had transient symptoms and survived, a minority still suffered life-threatening conditions from COVID.

Final Thoughts

The science of COVID will unravel for years to come, as research hones in on the precise mechanisms 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 so aggressive? Why is the mortality rate so high on ventilators? How does COVID cause brain injury? Are the symptoms of long COVID permanent? There's a great deal to investigate before we fully understand what COVID does to your body.

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Becky Casale Author Bio

Becky Casale is the founder, keyboard smasher, and drinks lady at Science Me. If you like her content, please take a hot second to share it with your favourite people. If you don't like it, why not punish your enemies by sharing it with them?