The shape of COVID-19

Last month, I told you about an AI program that can predict protein shapes. Just like the letters that make up a word, the amino acid chain makes up a protein, and the 3D shape it forms determine what a protein does in the body. If one of the amino acids changes, the shape changes and the protein is altered, just like a word changes when a letter is replaced. With its new shape, the protein may act differently in the body. Some changes make a protein function better or worse, while others have little or no effect. These changes happen as random mutations, like how sometimes I mistype a word and the result convey a different meaning (though I hope autocorrect, or my editor, catches the error).

SARS-CoV-2, which we commonly call the coronavirus, has a protein on its surface with a shape permitting it to attach to cells in our body. Once attached, the virus can enter the cell, reproduce itself, and spread throughout our body, the end result being a respiratory infection, among other ill effects, which we call COVID-19. If the shape of this surface protein on the virus changes because a different amino acid occurs in one or more places, it may attach better and thus increase its ability to make us sick. As our infected cells make more viruses, this newer, more potent version of the virus spreads more, and overall, the virus becomes more dangerous.

This is what has happened with the so-called variants of the COVID-19 virus; the virus has become stickier, making it spread more easily. Viruses often change like this, and often such changes have no effect or make the virus less effective. But changes that do make the virus more effective are more likely to be replicated and become more common. Thus, the concern about the new versions of the virus, like the British, South African and Brazilian variants – more effective viruses will spread more, and therefore kill more people.

Still effective

There is a second and related issue with virus variants. What our vaccines do is take a small part of the virus – perhaps one of its proteins – and tell our immune system that the protein with this shape must be attacked and destroyed because it is dangerous. Our immune system learns slowly, or at least slower than viruses often work. Slow learning is why vaccine protection is not immediate and sometimes takes a second dose. But, once learned, our immune response can be rapid. Once our immune system knows which protein to attack, it can kill the virus that uses it. But if the virus mutates so that the shape of its protein changes, the immune system might not know it needs to attack, or it may be less effective. The potential for shape changes has led to concerns about the new variants of the COVID-19 virus. The evidence, to the best of our current knowledge, is that our vaccines are still effective against these variants, but further changes might mean we’ll need to rework the vaccine.

The more cases of COVID-19 in the population, the more opportunities there are for the virus to change. An initial random change like this is even thought to be responsible for the original emergence of the virus. A virus that lived in animals was transmitted to humans who had close contact with the animals. Some mutation occurred that then made the virus easily transmittable between humans. We occasionally see these types of infections among people in close contact with animals (often birds), but not every such infection is easily transmitted between humans. These animal viruses can lead to health professionals organizing large-scale killing of the birds, because an additional mutation may make the virus deadly to us. In the case of SARS-CoV-2, the ability to move from one person to another made it deadly to us, and now the new variants are even more dangerous.

In some viruses, mutations occur more frequently. The flu virus is the best example; it changes often, there are multiple families of the flu virus, and some strains are more deadly than others. As these changes are random, we have no way of predicting what they will be or how much they will change the flu and its effects. The Spanish flu was a variant that emerged at the end of World War I and killed 50 million people. It has been extensively studied in the fear that it may occur again. These relatively rapid changes in the flu virus are why there is a different vaccine each year, and why we need to get a yearly flu shot.

Waiting for the vaccine

The new RNA technology (it’s complicated) that developed the various COVID-19 vaccines is now being applied to other virus-based diseases to see if we can create better vaccines. The current technology used to make flu vaccine is slow, and production must be started months before flu season, with a guess as to which flu strain will be most active. If the guess is a good one, the flu vaccine works well. The hope is that the new RNA technology, as it is improved, will mean we can create effective vaccines more quickly. The production and distribution problems with the two approved COVID-19 vaccines suggest improvements with this technology would be welcome.

But until the vaccine has been widely distributed in this pandemic, we would all be wise to do as much as we can to prevent the spread of the virus. We know this can be done by wearing masks and keeping socially distant. If we take these two simple steps, we can help prevent the virus from mutating into something even more deadly.