Coronavirus mutation: is the fear justified and where does it come from?


A new strain of the coronavirus could be responsible for the faster spread of the virus in London and the south-east of England, it was announced. Unconfirmed reports suggest that the coronavirus variant is called N501Y. This particular strain has increased in frequency since August.

The idea of ​​a mutating virus, breaking down into new strains, is enough to scare most people. But are these fears justified and where do they come from?

Hollywood certainly has to take some responsibility for our misconceptions about mutation. After all, the concept has inspired filmmakers for decades, starting with Die, Monster, Die! in 1965 until big budget franchises, such as X-Men. Both tell stories of changes in DNA resulting in superhuman abilities.

Special effects filmmakers like to show off these DNA changes in the most dramatic way possible – often accompanied by vibrant colors and explosions – but actual genetic mutations are a much quieter affair. So you shouldn’t be too worried when you hear that the the coronavirus is mutating. It’s a normal part of evolution.

However, to understand mutations, one must first detour into the world of proteins. Reading the side of my “Taste of the East” microwave lunch (unfortunately eaten at home with tired kids rather than on the beach in the picture on the package), there is a unique value for “protein. “. But the word can be misleading. The thing on my driveway is both a car and simultaneously a different type of car from the rest. The same word means both the individual and the group to which he belongs. The same applies to the term protein.

About a fifth of your body is made up of protein. Proteins are the molecules in your body (or your breakfast) that are made up of chains of amino acids. Protein is an umbrella term that captures everything from protein molecules that act like enzymes in your stomach, to structural proteins that make up your skin and hair.

There are only 20 types of amino acids with which to build all proteins on Earth. Of 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 amounts, nature creates a dazzling array of very different proteins with specific jobs within an organism. Just like 20 types of Lego bricks can be used to make a lot of different models, the 20 types of amino acids are used to make your 6 million different types of proteins.

Changing 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 number or type of amino acids that make up a particular protein changes. This, in turn, has the potential to alter the properties of the protein. However, this is the Hollywood spoiler: most mutations do not result in 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 strengthen it.

Only mutations that confer an advantage (or make no difference) persist in DNA. To speak of a virus having “goals” and “intentions” with mutations is to speak from a human point of view. Likewise, there is debate as to whether the “ultimate virus” is the one that has survived undetected in you all your life, or that jumps quickly and easily between new hosts. Both would require extensive mutations, the results of which are too random to be planned.

Proteins are folded into extremely complex 3D shapes, based on interactions between amino acids in the same chain. Changing an amino acid that is essential for keeping the shape together, such as replacing a positively charged acid with a negatively charged acid, will change that shape.

Those billions of years of molecular sculpting that allow proteins to have the right shape to cooperate with are not compatible with sudden mutations and radically different shapes. No extra abilities, no superpowers – usually the protein doesn’t work the way it should. What if this protein is the key to the virus that infects you? Good news! This particular virus particle cannot harm you and this version of the mutated virus goes out.

So how does an organism, human or virus, continue if most mutations are bad for it? A common approach is to go back and correct the mutation.

During the administration of its system of transforming the DNA code into chains of amino acids to make a protein, evolution incorporated certain steps to verify the changes. If you’ve spent billions of years fine-tuning your plan, you want some protection for all that previous hard work. Therefore, humans and coronaviruses have corrective mechanisms for their DNA / RNA patterns.

This evolutionary proofreading is there to correct the “errors” that would change the proteins and inhibit the virus. Replay also reduces the speed of acquisition of beneficial mutations.

Not all amino acids are formally important, and changing them does not alter the protein. The most common mutations found in the coronavirus spike protein that crossed it and became established fall into the ‘no significant protein change’ group: replacing a large amino acid with another large amino acid. The biological equivalent of putting different tires on your car. Although these amino acids are different, the spike protein appears largely unchanged in its functioning. No better or worse for getting into cells.

Viruses act from generation to generation much faster than large organisms like us, and clusters of small changes can cluster together into meaningful differences more quickly. However, in the case of the newly identified variant in South East England, we do not yet have any evidence that this mutation makes the virus more harmful or transmissible.The conversation

Matt webster, Head of the Allied School of Health, Anglia Ruskin University

This article is republished from The conversation under a Creative Commons license. Read it original article.

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