What’s Next…Living in a World with COVID -19 by Angela Rieck

I have been thinking about how we will live in this new world…a world where a deadly disease is lurking.  So I did what I usually do, I started researching it.  I wanted to learn about our immune system in an effort to understand my risk with COVID-19.

We live with risk.  We drive cars, we take medicines, we eat certain foods, we drink. Over time these risks have become integrated into our world and we recognize that they exist, but for most of us they do not rule our worlds.  Since a vaccine for COVID 19 is probably years away, we will have to add this virus to our risk list.

So the question that I researched: what precisely is this risk?  More about this later, first a trip down “immunity lane.”

Caveat: I have no scientific knowledge, I have been using Internet sources at NIH, CDC, Yale, Cornell, Scientific Journals and University websites for my information.  Since I don’t have the background, I could be easily misguided.  Also, I am a big, big believer in NOT using jargon or complex scientific language so I may oversimplify when I describe everything in layman’s terms.  

I have come to the conclusion that Immunology is Rocket Science.  Our immune system is unbelievably complex and variable.  We have only scratched the surface of our immune system, fantastic discoveries await.

Our immune system is filled with redundancies, complex communications, pathogen consumers, janitors, killing machines, construction crew, “generals” and soldiers…all working through our tissue, white blood cells and the limbic system.  To describe what I have learned would take volumes.  Suffice to say that there are hundreds of different cells (not including the millions of B cells with antibodies) and configurations.  So here is a VERY simple overview of the most relevant pieces of our immune system as it relates to COVID 19.

Immunologists categorize immune cells as either Innate or Adaptive.  Innate immune cells are the first to rush to an infection, they are “generalists” whose goals is to find any foreign cell and destroy it. They emerge from our tissue and the bloodstream. The second type are the Adaptive Cells, which arrive days later.  The most well-known are the T Cells and B cells, which are configured to destroy the actual villain or pathogen.  (Of course, it is not that simple, some cells are both Innate and Adaptive and our Adaptive cells also perform innate functions at the beginning of an infection…I told you this was complicated.)  There are a bunch of other types of proteins and enzymes, especially communication enzymes and proteins that notify our immune system that we have an invader and provide feedback about what is happening at the “site.”

So what happens with a rhinovirus (the common cold)?  Since viruses are small, they replicate by taking over our cells.  A rhinovirus starts invading our cells in the nose.  Our innate defenses rush to the site and start battling the pathogen: they kill, they clean dead cells, they rebuild and some consume a portion of the antigen and take it back to the T cells through limbic system. The Adaptive cells use that specific information to create T and B cells specially targeted for that pathogen.  To add to the complexity, B cells as well as dying and invaded cells may send signals to the immune system using cytokines (this is important).  Some communication is sent to the brain and other organs to help us to fight off the invader.  Then the Adaptive cells start heading to the battle.  From the beginning of the infection, T cell “generals” direct the invasion.  Based on the antigen data received, B cells with the specific antibody proteins start duplicating (antibodies are actually B cells with a certain protein configuration on their surface) and head to the site (a significant oversimplification, of course).  T cells serve as both generals and soldiers, some attacking the cells while others coordinate the immune attack.  The B cells and T cells now make a targeted attack on the specific antigen.  They “remember” this attack and store B cells (which contain the antibodies) to defend against future invaders.

Back to our rhinovirus.  During this battle, our nose swells and the cells become more porous to allow the immune cells to attack (hence the stuffy and runny nose).  That’s right, the immune response is the cause of the unpleasant symptoms (this is important for understanding COVID 19) including fever.  After the virus is eliminated, the repair crew generates new cells and gets us back to speed (another oversimplification).

Impressive, huh?  And this is only a tiny fraction of what actually happens.  But there is a problem.  First, the immune system must distinguish between our good cells and “infected” cells, which it does using mostly Toll receptors. (Auto-immune diseases occur when the immune system attack our “good” cells.) Second, the immune system must also “stand down,” or “commit suicide” when the attack is completed.  

Back to COVID-19; the first problem is that there are no B cells with the antibody proteins for a SARS virus. When the T cells and B cells are shown the antigen, the B cells must develop the antibody protein that will kill the COVID 19 antigen (takes about 7 days). For many healthy people, the Innate cells stave off the virus before it gets to the lungs until the B cells with targeted antibodies arrive.  

For those who experience mild symptoms, scientists believe is likely that their immune system is attacking it effectively before it moves to the lungs. 

But, even when it moves to the lungs, our immune cells can keep fighting it effectively.  For most of us, the system functions as it should and after the new antibodies have been developed, we are “cured.” We now have antibodies to ward off a future attack.  

But in severe cases, most scientists believe that a cytokine storm is created.  A cytokine storm occurs when the immune system gets an overwhelming signal and rushes to the site, furiously attacking all cells, even the “good cells”.  Fluid from the battle builds up and causes pneumonia.  The immune system now becomes the attacker. 

Scientists are searching for medications to prevent the storm or stop it once it starts. At Yale, scientists are searching for a bio marker to identify individuals who would be susceptible to these storms.

How bad are cytokine storms?  Very bad.  They cause sepsis. It is believed that most of the 1918 flu deaths were from these storms. 

But messing with the immune system can be dangerous.  In 2006, six healthy young men experienced a cytokine storm within 90 minutes of being injected with an experimental immune suppressant drug; five died.

So, back to risk, we need to be able to adequately assess our risk, what are the chances that we will get a cytokine storm from the COVID-19 virus?  

Now we are back in my wheelhouse.  

CDC guidelines and other guidelines are designed to prevent infection. Obviously, that is most important.  But we also need to know our risk of hospitalization and death if we get infected.

Let me repeat, most people do not develop a severe reaction from this virus.  But for those who do, it can be deadly.  So, the risk question is, “what is the likelihood that if I get a COVID-19 infection that it will become deadly?”

Cornell identified the following risk factors:  age, gender (more men die than women), underlying health conditions (kidneys, diabetes, hypertension, obesity, asthma, or COPD), immune suppression medications (including cancer treatments), race (but this may have more to do with access to health care than genetics), smoking (duh!) and viral dose (amount of exposure). In addition, stress has been found to be a significant immune suppressant.

Given the number of people infected, hospitalized and deceased from COVID 19, there is enough data to build a model that will allow us to assess our individual risk assessment for COVID 19.  We need to know our individual actual risk, especially if we have comorbidities.  (A comorbidity is the simultaneous presence of two chronic conditions, e.g., age & diabetes.) 

Epidemiologists need to create a model from which they can create a “risk assessment app” to give us a risk factor.  For example, I have asthma and I am over 65, so I have 2 comorbidities. A risk assessment app would allow me to enter my risk factors including chronic conditions, relevant medications, treatments, number of “colds or flus” per year, and psychological factors. The result would be the probability of getting the deadly reaction if I become infected with the COVID 19 virus. 

This is especially helpful for people who are healthy but have underlying illnesses. For example, diabetes is recognized as a risk, but diabetics frequently present other comorbidities (e.g., obesity, poor circulation).  What is the risk for someone who has diabetes, but keeps her A1C down, exercises and maintains a healthy weight?

The work that is being done for treatments and vaccines is most important, obviously.  But in the interim, we need to live and work in a COVID-19 world.  

To do so, we need: (a) a reliable antibody test to allow us to know if we have immunity and (b) an individual risk assessment.

Until then, we are walking in this new world without a map.

Angela Rieck, a Caroline County native, received her PhD in Mathematical Psychology from the University of Maryland and worked as a scientist at Bell Labs, and other high-tech companies in New Jersey before retiring as a corporate executive. Angela and her dogs divide their time between St Michaels and Key West Florida. Her daughter lives and works in New York City.