Tomàs Pumarola: "The virus changes because we are making things difficult for it"

SabadellThe emergence of two new and apparently more contagious strains of covid-19 virus has led many countries this week to restrict the entry of people from the UK and South Africa. Dr. Tomàs Pumarola, head of microbiology at the Vall d'Hebrón Hospital in Barcelona, analyses the usefulness of these measures and explains why the coronavirus is changing.

Why are these new strains appearing?

This tells us that the virus is evolving, nothing more, and it is a common process in viruses that are RNA, such as flu, hepatitis, AIDS... They're constantly evolving.

It has been said that the UK variant is 70% more contagious than the original virus, and 70% more contagiousthe South African one, even more

I mean, what are we basing this on? We can't just jump to conclusions from the headlines: we have to be careful, we have to wait. I would like to read it in a statement from a clear scientific institute and published in a journal that has gone through scientific reviewers. We have this in part with the English strain, and we do know that it is transmitted more, even though it is not more pathogenic. But with the African one we have to wait until we have more information.

So, could it be that the virus is more contagious but not more dangerous?

One thing is that it is more transmissible and another is that it is more virulent, one thing has nothing to do with the other: the coronaviruses of the cold are still transmitted much more than those of covid-19 and they cause us a common cold; we have five or six every year. They are two different things that can go together but there is no reason for that to be the case.

Could there be other strains that have not been detected?

There is a type of study, which is microbiological surveillance, which consists of constantly following the microorganisms that we know can cause us problems, to see how they evolve day by day. We do this with influenza, meningococcus, pneumococcus, measles, pertussis... with many. Governments need to understand that this surveillance is important and they need to subsidize it. This means that there is a lot of heterogeneity worldwide in the degree of surveillance that is carried out. In the UK they set up a consortium for genetic surveillance of this virus and so they detect it, but there are other areas of the world where this surveillance is reduced or non-existent. However, it is also true that we are in an interconnected world and, therefore, a variant that appears on the other side of the world, once it reaches Europe, where we have quite powerful surveillance systems, is immediately detected. In April/May another strain appeared that was being transmitted much more, and it is the one that now predominates throughout the world. It is practically the only one that is circulating. Now others are appearing, we will see if these will dominate or not.

So, could it be that these mutations have been circulating for some time?

There is no reason for this to be the case: the good thing about surveillance is that you can detect mutations the moment they appear. What we need to know is what these mutations will actually mean in the future.

Does it make sense to limit the arrival of people from the United Kingdom and South Africa, or is it possible that these variants are already here and we have not noticed them?

I think it makes sense. They are variants which are being passed on a lot and we have to try to prevent them from spreading as much as we can. If these mutations do not really affect the biological capacity of the virus, it is like putting doors in an open field, but if these mutations reduce the effectiveness a little, we could contain them or at least delay them. In these moments of uncertainty, when we don't know what the real meaning of these mutations is in terms of the predominance of the virus in the future, of virulence, of how it will affect the vaccine, we have to try to stop them as much as possible.

What changes in the virus so that it is more or less easily transmitted?

On the surface of the virus there are some glycoproteins that we call the spicule. The spicule is what binds to the cell receptor and allows the virus to enter the cell. In other words, it is a key, which enters a lock on a door, opens it and the virus enters. Imagine that you have a key that the locksmith hasn't done well enough and you have to force it very hard to turn it: this is what happens when viruses start infecting people. What do you do? You take the key to the locksmith, file it down and there comes a moment when this key turns very gently and opens the door very well. This is what these mutations on the spicule do: they allow it to adhere to the cell and enter more effectively.

And why do these mutations occur?

The virus has to change, it has to adjust the key, because we are making things difficult for it: the antibodies that we generate when we are infected block the key, prevent it from entering the lock. So, the virus tries to change the key minimally so that the antibody cannot neutralize it. This is what we are forcing it to do with the immune response of all the people who have already been infected, and from now on we will do it in a much more important way through vaccination.

Will the vaccines work against these variants as well?

Right now no one can say what will happen. There are several questions. One is that the vaccine induces a strong cellular-type immunity, which is not blocked by these mutations. The second is that the spicule is very large, but the part that binds to the cell receptor is small, and not all mutations affect this part: therefore, it is possible that antibodies will continue to be effective in neutralizing the spicule. Could we find that the vaccine's efficacy drops from 95% to 70%? Maybe, but this is not a problem: we are assuming vaccines such as the one for the flu, with a 50% effectiveness. We are sure that there will be a vaccination effect, although it may be a little lower. And thirdly, microbiological surveillance is not only used to see how the virus changes, but also to make decisions, for example on how the vaccine should be modified. Precisely with the platform that we are using in these vaccines, messenger RNA, it is quite easy to modify the vaccine very quickly. This will be a dynamic process that we will have to carry on with, regardless of whether we have this strain now or not, because we will have others later on. This is what we do every year with the flu: we have to be vaccinated every year. The virus changes and therefore we have to reformulate its vaccines.

Can a mutation appear for which the vaccines that we have now are not useful?

No, it's not a possibility.

And if a vaccine has to be adapted to affect one of these variants, will it have to go through a validation process again?

No, because the vaccine is identical, it's the same but with minor modifications. It does not have to go through a whole process of clinical trials and validations again, because it has already been done.