The long COVID-19 and other chronic respiratory conditions after viral infections may stem from an overactive immune response in the lungs

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(THE CONVERSATION) Viruses that cause respiratory illnesses like influenza and COVID-19 can cause mild to severe symptoms in the first few weeks of infection. These symptoms usually go away in a few more weeks, sometimes with the help of treatment if they are severe. However, some people experience persistent symptoms that last for months or even years. Why and how respiratory diseases can develop into chronic diseases like the long COVID-19 is still unclear.

I am a PhD student and work at the Sun Lab at the University of Virginia. We study how the immune system sometimes goes awry after fighting off viral infections. We are also developing ways to target the immune system to prevent further complications without weakening its ability to protect itself against future infections. Our recently published review of research in this area found that it is becoming increasingly clear that it may not be an active viral infection causing a long duration of COVID-19 and ailments similar, but an overactive immune system.

The lungs in health and disease

Keeping your immune system dormant when there is no active infection is essential for your lungs to function optimally.

Your airways are in constant contact with your outside environment, taking in about 5 to 8 liters (1.3 to 2 gallons) of air – and the toxins and microorganisms it contains – every minute. Despite continuous exposure to potential pathogens and harmful substances, your body has evolved to keep the immune system dormant in the lungs. In fact, allergies and conditions such as asthma are byproducts of an overactive immune system. These excessive immune responses can cause the airways to constrict and make it difficult to breathe. Some severe cases may require treatment to suppress the immune system.

During an active infection, however, the immune system is absolutely essential. When viruses infect your airways, immune cells are recruited to your lungs to fight the infection. Although these cells are essential for clearing the virus from your body, their activity often leads to collateral damage to lung tissue. Once the virus is cleared, your body weakens your immune system to give your lungs a chance to recover.

Over the past decade, researchers have identified a variety of specialized stem cells in the lungs that can help regenerate damaged tissue. These stem cells can transform into almost all the different types of cells in the lungs depending on the signals they receive from their surrounding environment. Recent studies have highlighted the primary role the immune system plays in providing signals that facilitate lung recovery. But these signals can produce more than one effect. They can not only activate stem cells, but also perpetuate damaging inflammatory processes in the lungs. Therefore, your body tightly regulates when, where, and how loudly these signals are emitted in order to prevent further damage.

Although the reasons are not yet clear, some people are unable to turn off their immune systems after infection and continue to produce tissue-damaging molecules long after the virus has been cleared. This not only further damages the lungs, but also interferes with regeneration via resident lung stem cells. This phenomenon can lead to chronic illnesses, as seen in several respiratory viral infections, including COVID-19, Middle East respiratory syndrome (MERS), respiratory syncytial virus (RSV), and the common cold.

The role of the immune system in chronic diseases

In our review, my colleagues and I found that many different types of immune cells are implicated in the development of chronic disease after respiratory viral infections, including the long COVID-19.

So far, scientists have identified a particular type of immune cell, killer T cells, as potential contributors to chronic disease. Also called cytotoxic or CD8+ T cells, they specialize in destroying infected cells either by interacting directly with them or by producing harmful molecules called cytokines.

Killer T cells are essential in preventing the virus from spreading through the body during an active infection. But their persistence in the lungs after the infection resolves is linked to prolonged reduced respiratory function. Additionally, animal studies have shown that removing killer T cells from the lungs after infection can improve lung function and tissue repair.

Another type of immune cell called monocytes is also involved in fighting respiratory infections, serving among the first responders by producing virus and tissue damaging cytokines. Research has found that these cells also continue to accumulate in the lungs of long-term COVID-19 patients and promote a pro-inflammatory environment that can cause further damage.

Understanding the immunological mechanisms underlying the long COVID-19 is the first step to solving a rapidly worsening public health problem. Identifying subtle differences in how the same immune cells that protect you during an active infection can become harmful later could lead to earlier diagnosis of long COVID-19. Additionally, based on our findings, my team and I believe that treatments that target the immune system could be an effective approach to managing the long-lasting symptoms of COVID-19. We believe this strategy may prove useful not only for COVID-19, but also for other viral respiratory infections that also lead to chronic disease.

This article is republished from The Conversation under a Creative Commons license. Read the original article here: 186970.

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