What does "survival of the fittest" mean? in the corona epidemic

Charles Darwin popularized the concept of "survival of the fittest", the mechanism that underlies natural selection and drives the evolution of life. Organisms with genes that are better suited to the environment are the ones that survive and pass their genes on to the next generation. The phrase "survival of the fittest" is a distraction that has been used for many years by racist regimes, but nevertheless, are the strong also the appropriate ones in the case of the corona - not so much

By: Prakash Nakarkati Vice President for Research, University of South Carolina and Mitzi Nagarkati, Chair, Center for Cancer Drug Discovery, Department of Pathology, Microbiology and Immunology, University of South Carolina. Translation: Dafna Raviv

Charles Darwin popularized the concept of "survival of the fittest", the mechanism that underlies natural selection and drives the evolution of life. Organisms with genes that are better suited to the environment are the ones that survive and pass their genes on to the next generation. So, when a new infection the world has never seen before breaks out, the process of natural selection starts all over again.

So in the context of the corona virus - who is the "most suitable"?

This is a challenging question. But as immunology researchers at the University of South Carolina, one thing we can say clearly: without effective treatment options, survival against the corona infection is entirely dependent on the patient's immune response.
We already know that the immune response is a double-edged sword - on the one hand it helps the host body fight infections, while on the other hand it causes significant damage in the form of autoimmune diseases.

The two phases of the immune response

The immune response is similar to a car. To reach your destination safely, you need both an accelerator (stage 1) and a brake (stage 2) functioning properly. A failure of either could have significant consequences.

An effective immune response against an infectious agent (pathogen) relies on a delicate balance between the two stages of action. When the pathogen attacks, the body begins phase 1, which promotes inflammation - a state in which a variety of immune cells gather at the site of infection to destroy the pathogen.

Then comes phase 2, during which the immune cells (called T cells) suppress the inflammation and thus the infected tissues can be completely healed. A deficiency in the first stage can allow the uncontrolled growth of the contaminating agent, such as a virus or bacteria. A defect in the second stage can cause massive inflammation, tissue damage and even death.

The corona virus affects cells by attaching to a receptor called angiotensin-converting enzyme 2 (ACE2), which is present in many tissues throughout the body, including the respiratory and cardiovascular systems. This infection triggers phase 1 of the immune response, in which antibody-producing B cells secrete neutralizing antibodies capable of attaching to the virus and preventing it from binding to ACE2. This action prevents the virus from infecting additional cells.

If the immune system is compromised and working poorly in stage 1, the virus can replicate rapidly. People with weakened immune systems include the elderly, organ transplant recipients, patients with autoimmune diseases, cancer patients undergoing chemotherapy treatments and people born with immunodeficiency diseases. Many of those people cannot produce enough antibodies or T cells to fight back against the virus, a condition that allows the virus to multiply and cause severe infection.

Long-term damage as a result of the inflammation

Increasing the replication rate of SARS CoV-2 causes additional complications in the lungs and other organs. Normally, the lungs have a wide variety of microorganisms, both harmful and benign, that exist in harmony with each other. But as the virus spreads, it is likely that the infection and resulting inflammation will disrupt this delicate balance, allowing harmful bacteria present in the lungs to take over. This condition leads to the development of pneumonia, in which the air sacs of the lungs begin to fill with fluid or pus, making it difficult to breathe.

This condition encourages further inflammation in the lungs, leading to acute respiratory distress syndrome (SRDS), which has been observed in a third of COVID-19 patients. The immune system, unable to control the viral infection and other pathogens developing in the lungs, provokes an even stronger inflammatory response by releasing even more cytokines, a situation known as "cytokine storm".

At this point, it is likely that phase 2 of the immune response aimed at suppressing inflammation has failed and cannot control the cytokine storm. Such cytokine storms can trigger friendly fire - destructive corrosive chemicals designed to destroy infected cells released by the body's immune cells - which can lead to serious damage to the lungs and other organs.
Also, because of the presence of ACE2 throughout the body, T cells can destroy virus-infected cells in many organs of the body, causing more widespread destruction. Thus, patients who produce excessive amounts of cytokines and T cells can die from damage not only to the lungs but also to other organs such as the heart and kidneys.
The balancing action of the immune system
This scenario raises several questions regarding the prevention and treatment of COVID-19. Since most people recover from the corona virus infection, it is likely that a vaccine that activates neutralizing antibodies and T cells and blocks the virus from entering the cells and replicating - will be a success. The key to an effective vaccine is that it does not trigger excessive inflammation.

In addition, in patients in whom there is a deterioration to a more severe form such as respiratory distress syndrome and cytokine storm, which is often fatal, there is an urgent need for innovative anti-inflammatory drugs. These drugs can widely suppress the cytokine storm without causing excessive suppression of the immune response, thus allowing patients to clear the virus without damaging the lungs and other tissues.

There may be only a narrow window of opportunity in which immunosuppressive drugs can be used effectively. Such drugs should not be given early in the infection, when the patient needs the immune system to fight the infection, but also cannot be delayed for too long after the development of respiratory distress syndrome, when the massive inflammation is uncontrollable. This window for effective anti-inflammatory therapy can be determined by monitoring antibody levels and cytokine levels in patients.

With COVID-19, then, the "strong" are individuals who normally go through phase 1 and phase 2 of the immune response. This means a strong immune response in phase 1 to clear the initial infection of the virus. This is followed by an optimal phase 2 response, to prevent excessive inflammation in the form of a cytokine storm.

Vaccines and anti-inflammatory therapies need to carefully manage this delicate balance to be successful. With this virus, it is not easy to know who are the most suitable. It is not necessarily the youngest, strongest or most athletic people who are guaranteed to survive this virus. The strongest are those with the "correct" immune response that is able to clear the infection quickly and without excessive inflammation following it, which could be fatal.

to the article on The Conversation website

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