To begin with, what is the difference between Coronavirus and COVID-19?

SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) is the virus that attacks your lungs. COVID-19 is the actual disease process that is caused by the virus.

SARS-CoV-2 is sometimes also called the novel coronavirus- this is just another way of saying that this is a new strain of coronavirus. Coronaviruses are actually a large class of viruses, but were not contagious to humans. But in 2019, we encountered a new strain that was the first to be contagious to humans- strain was coined the novel coronavirus. Because SARS-CoV-2 is the second new strain of coronavirus that is infective to humans, it is differentiated by the 2 in its name.  The importance of this is history-the body has not seen this strain before and therefore doesn’t have the necessary immunity against this virus. 

However, the novel coronavirus’s devastating global impact wasn’t simply because it was a new strain- it was a new kind of virus. Unlike most other viruses, it doesn’t prefer a specific demographic- NO ONE, young or old, fit or ill, was safe from the virus. It’s also unique in another way- it affects not just one organ system, but ALL organs. Perhaps most puzzlingly, its novelty extends even beyond its eradication- unlike other viruses, lasting complications can appear even well after the virus has been cleared from the body.

Initially, the virus travels through the air via exhaled respiratory droplets and is inhaled by another person, where it attaches to their nasal mucous membranes. Most of the time, the immune system is able to fight off the infection before it gets to the lower respiratory tract, preventing the virus from progressing into the actual disease process. But sometimes, the virus manages to progress to your lower respiratory tract, and targets your pneumocytes, which is simply a fancy term for lung cells. There are two types of pneumocytes- Type 1 and Type 2.

So what’s the difference?

Type 1 pneumocytes perform the actual gas exchange- they take in oxygen to diffuse into your blood, while also getting rid of carbon dioxide and waste products. When Type 1 pneumocytes aren’t able to perform gas exchange properly, the rest of your body doesn’t get the oxygen it needs. However, the surface tension in your lungs is normally too high for Type 1 pneumocytes to function- your alveoli (small sacs where the oxygen exchange actually happens) would collapse. 

To combat this, Type 2 pneumocytes create a substance called surfactant, which reduces the surface tension and allows your alveoli to stay open to continue the lung’s most vital function- gas exchange. This is the type coronavirus targets- your Type 2 pneumocytes. 

The virus infects the Type 2 pneumocytes by attaching to a receptor called ACE2, which is present on the surface of the host cell membrane. The virus then penetrates through the host cell membrane using a protruding viral protein called a spike protein, also known as the S protein. The ACE2 receptor that the virus binds to is most concentrated in lung tissue, which explains why the virus affects the lungs first. 

After penetrating the cell membrane, the virus inserts its own DNA into the pneumocyte. This viral DNA is able to command the host cell to redirect all of its resources into making more and more viral particles. Gradually, the host cell becomes completely depleted and eventually dies. Then, the viral particles burst out of the dead cell, and go on to infect other cells, continuing the cycle.

Counterintuitively, the actual death of the pneumocyte isn’t what actually causes the disease process of COVID-19- that’s caused by your own immune system. Every time a cell is injured, it releases signaling proteins called cytokines that alert your immune system to the damage, thereby essentially ringing an alarm that something has gone wrong. 

Once this alarm is raised, your immune system sends a host of inflammatory mediators to the site of infection in an attempt to kill the virus. These mediators increase blood flow to that location in order to send more white blood cells to intercept the virus before it spreads further. The increased blood flow to the affected tissues allows white blood cells to travel into the affected tissues, but it also leads to the other characteristics of inflammation- for example, redness, heat, pain, and swelling. 

It is this inflammation that actually causes the flu-like symptoms- in the process of trying to make the body’s environment hostile to the virus, your immune system’s defenses also end up damaging your own tissues. As the battle rages on between your immune system and the virus, the inflammation continues to increase. But without this response, the virus would continue to replicate and destroy your cells. Hence, your immune system will not stop at any cost, and the race becomes one of endurance- either the virus or the host will die first.  If this battle continues, the increased flow of white cell rich blood to infected tissues can become problematic. The increased blood flow can result in the overaccumulation of fluid, otherwise known as edema. If the fluid accumulates inside your lungs, it is referred to as pulmonary edema. 

Pulmonary edema essentially drowns a person from the inside. This is why patients may be gasping for air but are still unable to get enough oxygen, because there is simply too much fluid for oxygen to physically travel to the alveoli. As patients continue gasping for air, their breathing becomes labored, and they must begin to rely on accessory muscles that aren’t typically engaged to help produce the force needed to inhale and exhale. 

Eventually, this too will prove to be too laborsome, and patients will start to “tire out”. Not long after, they won’t have the strength to continue breathing- it is at this point that patients will require a ventilator to mechanically assist their breathing. If they are not mechanically assisted, there won’t be enough circulating oxygen in the body, resulting in hypoxia. 

Hypoxia simply means that the tissues in your body are not getting enough oxygen. Hypoxia can be the result of a wide range of things- in this case, your alveoli are unable to absorb the oxygen they need, and so are unable to diffuse that oxygen into your blood. This oxygen poor blood then travels to the rest of your body, but it cannot provide the amount of oxygen needed by your tissues. When your cells do not receive the oxygen they need, the mitochondria, familiar to many as “the powerhouse of the cell,” can’t make the energy (ATP) needed for cells to function properly. This is universal of every cell in the human body, in every organ system, with the exception of only red blood cells. 

While scientists don’t know exactly how the virus causes damage to so many organ systems, it’s hypothesized that both the prolonged inflammation and hypoxia play a large role. If the inflammation or hypoxia last long enough, your tissues can become permanently damaged- this is one possible hypothesis to explain the lasting organ damage that sometimes presents well after the virus has been cleared. 

Unfortunately, the lasting damage caused by COVID-19 does not get better without treatment. Generally, patients gradually become accustomed to their decreased level of functioning, and this becomes their “new normal”. Ms. Moore, a fellow survivor, confirms this- “I feel like there had to be some sort of next step because I’m not ready to accept this as my new reality.” But this doesn’t have to be the case- your body has the potential to heal with the help of therapeutics.