Why is survival of the fittest so important to a population of organisms?

Natural selection is Darwin’s most famous theory; it states that evolutionary change comes through the production of variation in each generation and differential survival of individuals with different combinations of these variable characters. Individuals with characteristics which increase their probability of survival will have more opportunities to reproduce and their offspring will also benefit from the heritable, advantageous character. So over time these variants will spread through the population.

Describe the process of evolution by means of natural selection

Natural selection is the process by which species adapt to their environment. Natural selection leads to evolutionary change when individuals with certain characteristics have a greater survival or reproductive rate than other individuals in a population and pass on these inheritable genetic characteristics to their offspring (Survival of the Fittest). Simply put, natural selection is a consistent difference in survival and reproduction between different genotypes, or even different genes, in what we could call reproductive success.What happens is:

• A mutation occurs
  
• If the mutation is beneficial, the animal will survive longer and reproduce more
  
• Some of its offspring will inherit the mutation
  
• These offspring will also have better chance of survival, meaning they live longer and reproduce more
  
• Over a long period of time this process is repeated and gradually the mutation becomes a common gene in a species and those with the mutation become the only ones, as those without cannot compete with those expressing the mutated gene
  

Describe variation and state that competition leads to differential survival of, and reproduction by, those
organisms best fitted to the environment

Some of the characteristics possessed by an individual in a population can be said to be inherited.  These characteristics are passed on as a result of sexual reproduction. Sexual reproduction also introduces an element of randomness, so that variation is brought about in a population. These two almost contradictory factors - dependable inheritance of characteristics from parents, and variation within the population - are essential to an understanding of the process of evolution.

Assess the importance of natural selection as a possible mechanism for evolution

Natural selection is one of the driving mechanisms of evolution. The compelling logical process of natural selection is clear in producing adaptive changes within a species, such that it evolves to be more competitive in its environment. 


Natural Selection is often used synonymously with Evolution; however, they have very different meanings. Here are some very important points about natural selection and evolution:

1. Natural selection is a mechanism (differential reproductive success due to traits)
   
2. Evolution is a process (change in allele frequencies over time)
   
3. Natural selection is one mechanism that can lead to evolution
   
4. Evolution can also be caused by all of the other forces mentioned here (drift, migration, mutation, nonrandom mating)
   
5. Natural selection may not lead to evolution if the trait under selection is not heritable.  
   

Determine that evolution is the process of biological change within a population over time

Evolution is a change in the gene pool of a population over time. A gene is a hereditary unit that can be passed on unaltered for many generations. The gene pool is the set of all genes in a species or population.

Recognize that the theory of evolution is a scientific explanation based on a large accumulation of evidence

A scientific theory is "a well-substantiated explanation of some aspect of the natural world, based on informational facts that have been repeatedly confirmed through observation and experiment. Theories are formed from hypotheses that have been subjected repeatedly to tests of evidence which attempt to disprove or falsify them. In the case of evolution through natural selection.

Define natural selection as the greater chance of passing on of genes by the best adapted organisms

Describe the development of strains of antibiotic resistant bacteria as an example of evolution by natural selection

Key Terms:

Antibiotic Resistance

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Charles Darwin popularized the concept of survival of the fittest as a mechanism underlying the natural selection that drives the evolution of life. Organisms with genes better suited to the environment are selected for survival and pass them to the next generation.

Thus, when a new infection that the world has never seen before erupts, the process of natural selection starts all over again.

In the context of the coronavirus pandemic, who is the “fittest”?

This is a challenging question. But as immunology researchers at the University of South Carolina, we can say one thing is clear: With no effective treatment options, survival against the coronavirus infection depends completely on the patient’s immune response.

We have been working on how the immune response is a double-edged sword – on one hand helping the host to fight infections, while on the other hand causing significant damage in the form of autoimmune diseases.

The two phases of the immune response

The immune response is like a car. To reach a destination safely, you need both an accelerator (phase 1) and a brake (phase 2) that are functioning well. Failure in either can have significant consequences.

An effective immune response against an infectious agent rests in the delicate balance of two phases of action. When an infectious agent 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.

This is followed by phase 2, during which immune cells called regulatory T cells suppress inflammation so that the infected tissues can completely heal. A deficiency in the first phase can allow uncontrolled growth of the infectious agent, such as a virus or bacteria. A defect in the second phase can trigger massive inflammation, tissue damage and death.

The coronavirus infects cells by attaching to a receptor called the angiotensin-converting enzyme 2 (ACE2), which is present in many tissues throughout the body, including the respiratory tract and cardiovascular system. This infection triggers a phase 1 immune response, in which the antibody-producing B-cells pump out neutralizing antibodies that can bind to the virus and prevent it from attaching to ACE2. This inhibits the virus from infecting more cells.

During phase 1, the immune cells also produce cytokines, a group of proteins that recruit other immune cells as well as fight infection. Also joining the fight are killer T cells that destroy the virus-infected cells, preventing the virus from replicating.

If the immune system is compromised and works poorly during phase 1, the virus can replicate rapidly. People with compromised immune systems include the elderly, organ transplant recipients, patients with autoimmune diseases, cancer patients undergoing chemotherapy and individuals who are born with immunodeficiency diseases. Many of these individuals may not produce enough antibodies or killer T cells to counter the virus, which allows the virus to multiply unchecked and cause a severe infection.

Lung injury resulting from inflammation

Increased replication of SARS-CoV-2 triggers additional complications in the lungs and other organs.

Normally, there is a wide range of microorganisms, both harmful and benign, that live in harmony in the lungs. However, as the coronavirus spreads, it is likely that the infection and the inflammation that ensues will disrupt this balance, allowing harmful bacteria present in the lungs to dominate. This leads to development of pneumonia, in which the lungs’ air sacs, called alveoli, get filled with fluid or pus, making it difficult to breathe.

This triggers additional inflammation in the lungs, leading to Acute Respiratory Distress Syndrome (ARDS), which is seen in a third of COVID-19 patients. The immune system, unable to control viral infection and other emerging pathogens in the lungs, mounts an even stronger inflammatory response by releasing more cytokines, a condition known as “cytokine storm.”

At this stage, it is also likely that the phase 2 immune response aimed at suppressing inflammation fails and can’t control the cytokine storm. Such cytokine storms can trigger friendly fire – destructive, corrosive chemicals meant to destroy infected cells that are released by the body’s immune cells which can lead to severe damage to the lungs and other organs.

Also, because ACE2 is present throughout the body, the killer T cells from phase 1 can destroy virus-infected cells across multiple organs, causing more widespread destruction. Thus, patients that produce excessive cytokines and T cells can die from injury not only to the lungs but also to other organs such as the heart and kidneys.

The immune system’s balancing act

The above scenario raises several questions regarding prevention and treatment of COVID-19. Because the majority of people recover from coronavirus infection, it is likely that a vaccine that triggers neutralizing antibodies and T cells to block the virus from getting into the cells and replicate is likely to be successful. The key to an effective vaccine is that it doesn’t trigger excessive inflammation.

Additionally, in patients who transition to a more severe form such as ARDS and cytokine storm, which is often lethal, there is an urgent need for novel anti-inflammatory drugs. These drugs can broadly suppress the cytokine storm without causing excessive suppression of immune response, thereby enabling the patients to clear the coronavirus without damage to the lung and other tissues.

There may be only a narrow window of opportunity during which these immunosuppressive agents can be effectively used. Such agents should not be started at an early stage of infection when the patient needs the immune system to fight the infection, but it cannot be delayed too long after ARDS development, when the massive inflammation is uncontrollable. This window of anti-inflammatory treatment can be determined by monitoring the antibody and cytokine levels in patients.

With COVID-19, then, the “fittest” are individuals who mount a normal phase 1 and phase 2 immune response. This means a strong immune response in phase 1 to clear the primary coronavirus infection and inhibit its spread in the lungs. Then this should be followed by an optimum phase 2 response to prevent excessive inflammation in the form of “cytokine storm.”

Vaccines and anti-inflammatory treatments need to carefully manage this delicate balancing act to be successful.

With this coronavirus, it isn’t easy to know who are the fittest individuals. It isn’t necessarily the youngest, strongest or most athletic individuals who are guaranteed to survive this coronavirus. The fittest are those with the “right” immune response who can clear the infection rapidly without mounting excessive inflammation, which can be deadly.

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