A Guide to Understanding Our Amazing (and incredibly complicated) Immune System and Its Response to COVID-19 – What We Know and What We Don’t Know

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By Laurie Birkholz, MD

Laurie Birkholz, MD, and Associates | Ms.Medicine

Holland and Douglas, Michigan

There has been much in the media lately regarding the role of our immune system’s response to COVID-19 and how this information may be useful. Our economy has taken a huge hit, and so it is understandable that people are looking for ways that we can all get back to work. We have seen our leaders discuss things like “immunity cards” as a way to “open up the economy,” yet many questions remain unanswered regarding how our bodies respond to COVID-19 infection now – and what that means for the future. Keep reading to learn some basics about how our immune systems work in general, what we know about COVID-19 and the immune system, and maybe most importantly…what we still don’t know.

Our immune systems are always “on,” constantly watching for foreign invaders that may pose a risk to our health. In the case of the COVID-19 coronavirus, we are still trying to learn why some people’s immune systems are capable of fighting off the virus while others’ are not.

In an interview with Vox, Dr. Akiko Iwasaki, an immunologist at the Yale School of Medicine, says our body’s immune system is “like an orchestra with a huge array of cells and chemicals working in concert – each with a different part to play – to defeat the virus.”

The COVID-19 virus is mainly transmitted via respiratory droplets and thus enters our body through the nose or mouth. Infection begins when the virus attaches to a cell and makes its way inside where it begins to wreak havoc.

The virus replicates by taking over the cell’s machinery to make copies of itself which then escape that cell and spread throughout the body. This process of breaking into cells and using the cell’s own mechanisms to replicate continues as the virus grows in number (referred to as the “viral load”).

We refer to our body’s immediate immune response as the “innate immune response.” Each of our cells has its own sort of mini-immune system. Once a cell detects viral activity, it sends a warning message to neighboring cells to begin an assault on the foreign invader in an attempt to limit spread of the virus.

Unfortunately, many viruses are smart enough to evade this initial attack and continue to grow in number, causing more problems as they do. This is often the case with COVID-19 which continues to replicate in our body reaching a peak viral load around 2 days prior to the onset of symptoms. Data suggests this is when we are most contagious. It is also when the second phase of our immune response kicks in. We refer to this second, more specialized phase, as the “adaptive immune system.” In the case of COVID-19, it appears this response kicks in around 10-14 days after an individual is infected and coincides with the onset of symptoms, such as fever.

The adaptive immune system is made up of different types of cells with cool names, like “killer T-cells,” which literally track down and kill cells that have been infected by the virus. Another soldier in this army is the “helper T-cell” which recruits yet another type of cell called a “macrophage” that works to gobble up infected cells and stimulate something called “B-cells.”

It’s the B-cells that produce the antibodies we’ve been hearing all about. These antibodies work by attaching to the virus rendering it incapable of taking over our cells. They can also attach to the virus making it easier for our other immune cells to find and destroy. One of the very first antibodies to be produced is IgM which makes its way onto the scene right around the time we begin to feel ill, peaking around day 7-10, then trailing off and disappearing around a month or so later.

Another type of antibody, IgG, shows up about a week after IgM and sticks around for much longer, so that even after an infection begins to decline, IgG remains present and can prevent the same virus from increasing in number again. It’s these IgG antibodies that also, in many cases, prevent reinfection when the virus is introduced again at some point in the future.

We can look for both IgM and IgG antibodies with serological (blood) tests to help us determine who has been infected with the COVID-19 virus. It is important to realize how to apply the results of these tests, to understand not only what they tell us but also what they DON’T tell us.

As previously stated, we become contagious prior to the onset of symptoms AND prior to antibody production which means a negative antibody test does NOT rule out infection. In other words, antibody tests are of limited value in diagnosing active infection. The best test to look for active infection is a test that looks for the virus itself (called a PCR test).

In one study, it was found that viral genetic material (RNA) declined slowly after the detection of antibodies in the blood which could mean that even though antibodies are present, an individual may still be shedding infectious virus. In this case, the PCR test is the best way to know if someone is still contagious.

There’s also the question of whether or not the presence of COVID-19 IgG antibodies means we are protected against reinfection. We cannot say for certain that just because you have the antibody now means you are not at risk for being infected again at some point in the future. We really have no idea how long immunity might last or how robust it may be, and there are conflicting opinions on the subject. We simply need more time and more tests to gather the data.

In general, antibody test results should NOT be used as the sole basis for confirming that an individual has or has had the disease. Results must be applied individually, taking into account the clinical course of symptoms and timeline of illness. In this way, results can be of great value to a patient and their community.

When used appropriately, these tests and others can help us to better understand the bigger picture; like what percentage of the population has been infected, how many people infected die, and how we can prevent further spread. The more data points we have, the closer we will get to answering the many questions that remain — ultimately helping us understand how we can move forward without compromising the health and safety of our communities.

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