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A new strain of the coronavirus may be responsible for the faster spread of the virus in London and south-east England, it has been announced. Unconfirmed reports suggest that the coronavirus variant is called N501Y. This particular strain has been increasing in frequency since August.
The idea of a mutant virus, turning into new strains, is enough to scare most people. But are these fears justified and where do they come from?
Hollywood certainly must take some responsibility for our misconceptions about mutation. After all, the concept has inspired filmmakers for decades, starting with Die, Monster, Die! in 1965 to big-budget franchises, like X-Men. They both tell stories of DNA changes that result in superhuman abilities.
Movie special effects creators like to show these DNA changes in the most dramatic way possible, often accompanied by bright colors and explosions, but real-life genetic mutations are a much quieter affair. Therefore, you should not be overly concerned when you hear that the coronavirus is mutating. It is a normal part of evolution.
Wikimedia Commons
However, to understand mutations, we must first deviate into the world of proteins. Reading the side of my “Taste of the East” microwave lunch (sadly eaten at home with confinement-fatigued kids rather than on the beach in the package picture), there is a unique value for “protein.” But the word can be misleading. What is in my driveway is both a car and, at the same time, a different type of car from the others. The same word means both the individual and the group to which it belongs. The same applies to the term protein.
RELATED: A more infectious coronavirus mutation may be ‘a good thing’, says disease expert
About a fifth of your body is made up of protein. Proteins are the molecules in your body (or lunch) that are made up of chains of amino acids. Protein is a generic term that captures everything from protein molecules that act as enzymes in the stomach to structural proteins that make up skin and hair.
There are only 20 types of amino acids with which to build all the proteins on Earth. Within these 20, many are very similar and can be grouped into families based on their properties. There are positively charged, negatively charged, large, small, and some with more subtle differences.
By combining these 20 amino acids in different orders and different amounts, nature creates a dazzling array of very different proteins with specific functions within an organism. Just as 20 types of Lego bricks can be used to create a myriad of different models, the 20 types of amino acids are used to produce approximately 6 million different types of proteins.
Mutant coronavirus
DNA, or in the case of the coronavirus, RNA, is the set of genetic instructions that tell an organism what building blocks are needed and in what order to create the proteins it needs to survive.
Mutations affect these instructions, which means that the amount or type of amino acids that make up a particular protein is changed. This, in turn, has the potential to change the properties of the protein. Here’s the Hollywood spoiler, though: Most mutations don’t lead to any beneficial changes in protein properties. In fact, mutations that change the properties of a protein are more likely to weaken the virus than to make it stronger.
Only mutations that confer an advantage (or make no difference) persist in DNA. To speak of the virus having “targets” and “intentions” with mutations is to speak from a human perspective. Similarly, there is a debate as to whether the “ultimate virus” would be one that survives inside you undetected for your entire life, or one that quickly and easily jumps between new hosts. Both would require extensive mutations, the results of which are too random to plan.
Proteins fold into extremely complex 3D shapes, depending on interactions between amino acids in the same chain. Changing an amino acid that is key to holding the shape together, like swapping a positively charged one for a negatively charged one, will change that shape.
Those billions of years of molecular sculpting that allow proteins to have the correct shape to cooperate are not compatible with sudden mutations and radically different shapes. No additional abilities, no super powers; usually the protein no longer adjusts as it should. What if that protein is key for the virus to infect you? Good news! That particular virus particle cannot harm you and that mutated version of the virus becomes extinct.
So how can any organism, human or virus, continue, if most mutations are detrimental to it? A common approach is to go back and correct the mutation.
By managing its system of converting DNA code into chains of amino acids to produce a protein, evolution has incorporated a few steps to verify changes. If you’ve spent billions of years refining your plan, then you want some protection for all that old hard work. Therefore, both humans and coronaviruses have correction mechanisms for their DNA / RNA templates.
This evolutionary review is there to correct the “mistakes” that would change the proteins and inhibit the virus. Revision also reduces the rate at which advantageous mutations are acquired.
Not all amino acids are important for shape, and changing them does not alter the protein. The most commonly found mutations in the coronavirus spike protein that have survived and become established are in the group of “no significant change in protein” – swapping a large amino acid for another large amino acid. The biological equivalent of putting different tires on your car. While these amino acids are different, the spike protein appears virtually unchanged in its function. Neither better nor worse to enter cells.
Viruses work through generations much faster than large organisms like us, and groups of small changes can more quickly cluster into significant differences. However, in the case of the recently identified variant in south-east England, we still have no evidence that this mutation makes the virus more harmful or transmittable.
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Matt Webster, director of the School of Allied Health, Anglia Ruskin University. This article is republished from The Conversation under a Creative Commons license. Read the original article.
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