Out of 100 million people with coronavirus, more than a half have been infected in the past two months. The epidemic is still on the rise. In addition, the virus began to seriously mutate. Georgy Bazykin, a molecular virologist, talks about why precisely these dangerous mutations have happened and what awaits us next.
Georgy Bazykin is the Doctor of Biological Sciences, Princeton University PhD, professor at the Skolkovo Institute of Science and Technology, head of the Laboratory of Molecular Evolution at the Institute for Information Transmission Problems of the Russian Academy of Sciences, molecular virologist.
— Some of the restrictions imposed due to the coronavirus were lifted in Moscow. Sobyanin said that “the situation with the spread of infection continues to improve”. Is the season on the wane?
— It is the height of winter, and everyone spends most of their time indoors with other people, so infectious diseases should transmit more, and not less. It is different in the summer, when people go on vacation, spend more time outdoors, so respiratory infections do not spread so much.
Unfortunately, there are no reliable data on the number of cases in Russia right now. Official reports should be treated with caution because they are very different from other data sources. The main one is what we call excess mortality: this is how many more people die in a given month, such as December, compared to the average mortality for December in previous years. The discrepancy is great, so I find it difficult to interpret the dynamics of changes. To be honest, I do not see any signs of the situation changing for the better at the moment.
— When will you personally decide not to wear a mask in subway?
— When the epidemic is brought under control. A year ago, it was possible to hope that we could crush the virus with few losses. However, it seems that this will not happen until we have a collective immunity, when most of us would either get vaccinated or have had COVID-19. I hope for the former. And this will not take only a month or two to happen.
— How much is enough for collective immunity?
— No one knows the exact number. It depends on how the population is structured, how long the protection will remain, how new variants of the virus with new properties will spread. Anyway, we are far from collective immunity: thousands of people get sick in Moscow every day, so I would still wait before getting rid of masks.
Are the Brazilian and South African mutations already with us?
— What will happen to the morbidity dynamics when new variants of the virus, like the British one, come here?
— The virus mutates all the time, which causes new variants to appear, and some of them become more frequent. That is the point of biological evolution. Most mutations do not significantly change the properties of the virus, but variants with new characteristics occasionally spread. One such mutation, which allowed the virus to be more easily transmitted, spread in the spring, but it went almost unnoticed. Now we are seeing the same process again.
Three new variants have been described and they are provisionally called “British”, “South African”, and “Brazilian” according to the countries where they were first discovered, although they could have originated somewhere else. These variants have higher transmissivity: that is, the virus is more likely to be transmitted from one person to another; this is true for the British variant and most likely true for the other two. That is enough to cause great concern: a more contagious strain is not something that we need right now.
Moreover, according to preliminary data, the British variant is more severe and has a higher percentage of deaths, while South African and Brazilian ones cause the immunity developed in response to previous variants lose the partial recognition of the virus.
— And when should we expect them?
— The British variant was registered in Russia in early January, but it did not spread further, according to Anna Popova. The trouble is that Russia does not have a unified system for state supervision over virus variants. And there should be one in order to understand whether we have variants that are dangerous, what their frequency is, where they originated and how they are transmitted.
The coronavirus genome is read in about every tenth patient in the UK and in every thousandth in Russia. Besides, this is done by three different institutions in our country and they do not always share information even with each other, which is no good. Such work should be centralized, not dispersed.
Essentially, I wish that the moment when Brazilian and South African variants come to Russia could be postponed, but it is likely that they are already with us and we simply do not know about this.
When the British variant comes, you can expect it to spread quite quickly. If we really do not have these variants yet, then I think that more substantial measures for closing the borders would be justified.
— Are they not closed?
— They are basically open: you can fly to Russia from anywhere through Istanbul, for example. In New Zealand, new arrivals are quarantined in a hotel, they do not get to go home on taxi to self-isolate, infecting the taxi driver and everyone along the way, but they spend two weeks in a single hotel room. Thanks to this, New Zealand has no new cases, except for those that were intercepted at the border. People go to bars, stadiums, the economy is booming. There may be cases of transmission in communities, but when there are a few of them, they can be tracked. and further spread can be contained.
The complete elimination of coronavirus is not an impossible task to do. But at least in Russia, we have to try to prevent new variants from coming here so that they do not take even more lives.
New variants of the virus “elude” the immune system
— Will vaccination help against new variants?
— It will. Studies show that effectiveness of both the vaccines and previous immunity partially remains against all three new variants. Unfortunately, there is no such data for Sputnik vaccine yet, but we can expect that it is a similar situation there.
How is this studied? You apply those antibodies that have been developed in response to the previous infection to the new virus in a test tube and observe how well they bind. It turns out that you need to add, roughly speaking, 10 times more antibodies to South African and Brazilian variants so that they bind as well as with the “old” virus.
However, the vaccine is reportedly so effective that the protection deteriorates from “very good” to just “good”. This means that vaccination is still the best remedy we have.
The problem is that no country in the world will have time to get vaccinated in the next couple of months, except perhaps Bahrain, where 100 people live. Everywhere, including Russia, this will be a long process, so we need to bear until the moment when the significant proportion of the population will be vaccinated.
— However, some completely new version of the virus will come out and the vaccines will be powerless.
— In our experience with other viruses, partial protection is better than no protection.
For example, let’s take a look at the flu vaccine. If it turns out that to neutralize a new variant of the virus, you need to take 10 times more antibodies, this is a sign from the World Health Organization that the fragment of the virus that is included in the vaccine needs to be changed. Nevertheless, the old vaccine retains partial effectiveness. It is better to have partial immunity than none.
— To what extent are existing vaccines ready to be quickly “updated” for new variants?
— A lot of smart people are thinking about it now. It will not be really easy, but obviously easier and faster than creating a new vaccine from scratch.
Yet, the best thing would be to crush the epidemic. If there is no virus, there is nothing that could mutate. New variants are emerging because the number of new reported cases in the world continues to grow every day.
We have crossed the 100 million mark, and about half of those people got infected in the past two months.
Of course, when the virus is raging and moving around the globe, it has a lot of room for maneuver, and it constantly finds those rare and interesting combinations of mutations that allow it to infect us better with time.
I am sure that new variants will come from those countries where the epidemic is on the rise, such as the United States, Great Britain, Russia, and not from places where there are almost no new cases now: Singapore, China, Taiwan, and New Zealand.
Vaccinated people spread the virus less
— What do you mean by “crush”? Doing so that the vaccination rate outstrips the spread rate or isolating everyone again?
— The main thing is not to withdraw from simple measures available to each of us. We should continue wearing masks, exercise social distancing, go less to crowded spaces unless necessary. It is difficult to establish uniform rules for everyone, but at least you need to understand that is too early to relax.
Well, there is a new powerful measure: vaccination. It is difficult to increase its rate: it is impossible to produce billions of doses instantly. But in Moscow, for example, there is no great excitement now, and everyone can now make this decision for themselves whether to get vaccinated or not. In turn, I have been vaccinated as an education worker, and I advise everyone, who has the opportunity, to do the same.
— As far as I understand, you personally and your family live out of the city and try not to leave the house often.
— Part of my family works or studies offline; I work from home, but I also have to show up at the university sometimes, so now we have moved back to the city. I certainly feel more relaxed after the vaccination. Yet, the effectiveness of vaccination is below 100%, and we should still remain cautious.
— Do the vaccinated people not spread the virus as intensively as the unvaccinated people?
— So far, no one knows for sure whether vaccinated people transmit the virus and if yes, how intensively. We can measure how the vaccine reduces the chance of dying, how it reduces the chance of getting seriously ill, and how it reduces the chance of fever, but it is very difficult to measure how you transmit the virus to others. We can measure this in experimental animals and the studies show that vaccinated animals spread the virus less. However, with people, we need to know exactly who infected whom, and this is much more difficult.
General considerations are that vaccination reduces the amount of virus in the body, and when there is less virus, then you transmit it less intensively.
I am almost sure that vaccination reduces the likelihood of infecting another person, although, like I said, there is no solid data on this yet.
— We have heard that if a person is not vaccinated and gets infected, they are especially dangerous in the first 5-7 days after the onset of the disease. Is this still the case or have things been revised?
— The risk of you passing the virus on to someone else is greatest for 5 days before the onset of symptoms and 5 days after that. The risk becomes very small 10 days after the onset of symptoms.
— Pfizer, Moderna, Sputnik: which vaccine is better from your point of view and why?
— Different vaccines use different technologies. Pfizer and Moderna are RNA vaccines; Sputnik as well as, for example, Oxford-AstraZeneca and Johnson & Johnson are vector vaccines. Both vector and RNA vaccines cause our own bodies to produce virus proteins. RNA technology is quite new, and vector technology is older. Other vaccines include ready fragments of virus proteins; such are, for example, many flu vaccines, and EpiVacCorona vaccine for coronavirus.
Personally, I get vaccinated with the vaccine that is available in the country where I am. Pfizer and Moderna will not get to us anytime soon.
How the British variant could develop
— You have published an article (preprint) where you describe the evolution of the virus in the body of a woman who has had COVID-19 for more than four months. How can a person be infected for so long? What does it mean?
— This is our joint work with Institute of Influenza; my laboratory was responsible for analyzing the data. The patient we examined had a suppressed immune system. Viruses that are able to mutate quickly can evolve directly in the host body: this is what happens with chronic infections. This is well studied with the immunodeficiency virus, which quickly accumulates mutations inside the infected person, and they cause the virus to “elude” the immune system.
Coronavirus and influenza are acute diseases, they end within a week or two, and the virus does not have the time to evolve much. Yet, acute diseases in people with a suppressed immune system sometimes turn into chronic ones, they can have the flu or coronavirus for many months.
Several works on the study of such patients have been published now, and ours is one of them. They indicate that the virus really accumulates mutations unusually quickly in such a situation. Apparently, this is how it adapts to an organism with a poorly functioning immune system.
— If the immune system is already working poorly, why would the virus adapt to it?
— That is a good question. The thing is that the immune system of all patients, who were examined before us, was turned off, but their blood had antibodies: either after a transfusion of plasma from recovered people or as a result of introduction of monoclonal antibodies. Therefore, it was believed that the mutations of the virus are, first of all, its attempt to adapt to these antibodies.
However, our patient was not treated with any antibodies, and what is more, her virus also had a number of mutations in the spike protein. If there is no need to adapt to new hostile conditions, then why is there such intense evolution, indeed? We do not have an answer yet.
— Is it true that some of these mutations are the same as those that occurred in the rapidly spreading British variant?
— Indeed, some of the mutations that occurred in the virus in the bodies of patients with immunosuppression, including in our study, overlap with those that we observe in the famous variants with new properties: the Brazilian, British, and South African ones. Because of this, there is a hypothesis that these mutations also occurred in bodies of patients with a suppressed immune system.
This is just a hypothesis: no one has observed specific patients, but it is plausible since these mutations were accumulated surprisingly quickly. If you build an evolutionary tree of this virus, then the branches that lead to the British, South African, and Brazilian variants are unusually long: this means that there have been many mutations. We see the same thing in patients with a suppressed immune system.
However, all this does not add up to a single picture yet. Why is there this particular adaptation? Why does this happen in bodies of people with an altered immune system? How do these mutations help the virus spread to the rest of the community? All this must be studied.
Translated by Julia Frolova