Have you wondered how we develop immunity? Here’s an easy and straightforward explanation.
People infected with coronavirus can have markedly different symptoms. Scientists and doctors continue to be perplexed by how the same virus can cause a wide range of symptoms in different people. Some may exhibit no signs, some may show mild to moderate signs of infection, while some have shown severe manifestations such as inflamed and fluid-filled lungs or blood clots, which can potentially cause death.
As there are no vaccines or effective medicines to date, the current care standards rely on supportive treatments and a couple of repurposed drugs. And, it has become increasingly clear that our immune system largely determines our recovery from Covid-19.
So what exactly happens inside our body when a virus enters it?
The body’s incredible defense
Our immune system is composed of millions of white blood cells called leukocytes. Our bodies are teeming with these cells. A few of them travel from one site to another through the bloodstream. Many occur outside our circulatory system within tissues where they fight infections. As they move around, leukocytes act as security personnel, constantly screening the blood for threats, suspicious signs, and anything they don’t recognize.
Threats to our body can be varied, so leukocytes are equally adaptable to tackle invading microorganisms in different ways. Accordingly, there are many different kinds of leukocytes. And these are broadly divided into two main groups: phagocytes and lymphocytes.
Phagocytes in Greek means “eat cells.” As the name suggests, they destroy cells merely by consuming them. Phagocytes generate the same response to any microorganism and therefore are tools for innate immunity. In contrast, lymphocytes destroy cells by adapting their destruction strategy to the specific organism. So they are tools for adaptive immunity.
The phagocytes and lymphocytes coordinate a two-pronged attack against an invading microorganism — in this case, a virus.
A virus has a relatively simple structure — it contains DNA or RNA enclosed inside a protective coat. A virus cannot survive on its own. When it comes in contact with a living cell, it enters the cell (host), unpacks its contents, takes over the host cell’s control, and starts multiplying.
Our body’s immune system usually wards off many infections throughout our lifetime. But, it is harder to protect the body from a virus as our immune system cannot “see” a virus wreaking havoc inside a host cell. Once a virus replicates and makes abundant copies, the host cell either suddenly ruptures or gradually coughs up its offsprings. These then use the same strategy to attack the surrounding cells and continue a cycle of enter, hijack, replicate, and release. What remains is the discarded debris of host cells.
Fortunately, during this process of multiplication, a virus also makes some molecules that are unique to it. Some of these molecules appear on the surface of virus-infected cells and are like fingerprints, which differ from those on the host cell. So they are like markers and allow the immune system to recognize “self” from “other.” These markers are known as antigens and act as cues to trigger an immune response.
The virus-infected cells also release a substance called interferon as a defense response. Interferons signal nearby cells to heighten their anti-viral defenses, thereby preventing viruses from replicating within them. Therefore, they “interfere” with viral multiplication and restrict infection until our white blood cells take charge.
White blood cells to the rescue
When phagocytes circulate in the blood, they detect these unfamiliar markers on cells. And it takes only minutes for our body’s immune response to kick in. Like soldiers preparing to fight a war, it triggers a series of coordinated actions to fight off the virus.
The phagocytes first destroy the infected cells by consuming them, and record information about specific antigens present on virus-infected cells. They then secrete a substance called cytokines that transmit information about the virus-infected cells to lymphocytes, which then orchestrate an adaptive defense. Cytokines also cause inflammation. Once lymphocytes receive information about antigens on these virus-infected cells, a group of lymphocyte cells, known as T cells, search for infected body cells and kill them. Meanwhile, other lymphocytes called B cells and helper T cells, produce specialized proteins known as antibodies.
Each antigen has a unique antibody — like a lock and key. When an antibody attaches to a specific antigen on a virus-infected cell, it triggers a series of reactions that ultimately destroy the cell. So antibodies are the body’s resistance.
B cells produce billions of antibodies that circulate throughout the body and destroy virus-infected cells until the worst is neutralized. While all this is going on — we experience familiar symptoms like fever, inflammation, runny nose, or cough, which aid the immune response.
These familiar symptoms serve three purposes:
One is to alert the body that it is fighting an attack. For example, a warmer body makes it harder for temperature-sensitive bacteria and viruses to reproduce and spread.
The second is to try and get rid of the virus. For example, mucus washes off germs in our nasal cavity. As mucus goes into overdrive, the mucus lining in our nose swells, and the nasal cavity fills up with excess fluid, which can drip out. Once our body clears the invader, our immune system decreases its panic signals. The mucus lining then returns to its average level.
The third purpose is to direct white blood cells to specific regions to fight off the virus. For example, when body cells are damaged, they make fluid leak into its surroundings that cause swelling and inflammation. An inflammation attracts phagocytes, which then destroy both the invaders and the damaged cells. Inflammation of our pharynx causes a sore throat.
The immune response can depend on where in the body a virus has lodged itself. If a virus enters our body through the nose into our lungs, it can cause respiratory tract symptoms such as cough. If the virus stays in our gastrointestinal tract, we experience symptoms such as diarrhea. If a virus enters through our eyes, we experience symptoms such as conjunctivitis or redness in the eyes.
Our innate immunity causes these symptoms. Its goal is to localize a virus attack to a particular region until the adaptive immunity takes over and destroys it.
Usually, an immune response will eradicate a threat within a few days. It won’t always stop us from getting ill, as that’s not the purpose of our immune system. Its actual job is to prevent a threat from escalating to a dangerous level. And help us develop long term immunity by remembering specific markers or antigens and tackling the risk should it revisit. That’s how we build resistance to diseases like chickenpox.
So the question arises — if the body can tackle a virus, why is the coronavirus so deadly?
The virus itself does not cause most coronavirus-related deaths. But deaths occur due to the immune system going on an overdrive to protect our body.
In the case of coronavirus and many other flu viruses, this can have three different answers.
When an attack is mild enough, most of the time, our immune system is adept at destroying a disease-causing virus. In some conditions, the immune system can frantically churn out more inflammatory molecules to recruit more immune cells and regain control over the body. Such situations can lead to severe and more deadly symptoms, such as pneumonia and acute respiratory distress.
Secondly, viruses are adaptive and can develop new ways to evade the immune system. Structurally, many viruses are relatively small and have a simple composition. However, a simple structure is what makes it deadly. Every time our body fights and develops immunity, the adaptive viruses can mutate. Some mutations can cause viruses to establish new ways to sneak past the body’s immune system to cause mayhem. For example, the new D614G mutation in coronavirus makes it easier for the virus to fuse with host cells. Therefore, it may make it more contagious.
The third answer has been repeated so often and so loudly that it seems indisputable. People whose immunity is compromised or underactive are more susceptible to diseases. This category of people includes the elderly population and those with pre-existing conditions such as autoimmune disease.
What can we do to help ourselves?
These are challenging times for all of us. The uncertainly and rapidly evolving information on Covid-19 is eliciting a common reaction in almost everyone — fear and anxiety. But, we do not have to feel helpless. As the writer, Kurt Vonnegut Jr., said, “[Your body] is the greatest instrument you’ll ever own.” We can support our bodies to fight off viruses internally. The key is to maintain healthy lifestyle habits, with regular sleep and exercise, a diet high in fruits and vegetables, and thoroughly cooked meats.
As the well-known adage goes, “Prevention is better than cure.” At least until we have a reliable vaccine, our best defense is to avoid the virus altogether by maintaining social distance, wearing a mask, and thoroughly washing hands.
Let’s educate ourselves and help each other. Let’s do our bit at battling Covid-19.
This was first published on Medium.com on Jul 2, 2020.
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