New strains of coronavirus are causing more and more concern – vaccines are less effective against them, they infect humans better and more and more. There are so many of them that the new variants of SARS-CoV-2 will be called the names of the constellations – the Greek letters may end, said Maria Van Kerkhove, head of the technical group of the emergency diseases division of the World Health Organization. “Lenta.ru” understands why there are so many options for SARS-CoV-2 and what can be expected from COVID-19 in the future.
Alpha to Orion
“Probably, the Greek alphabet will not be enough for us, but we are already considering the next series of names. In fact, we're thinking about the constellation option, ”the epidemiologist told The Daily Telegraph in a comment. Earlier, according to her, officials had already dismissed the option with the names of the Greek gods – out of fear that not everyone would be able to pronounce them correctly. The working group on the evolution of viruses is currently working with WHO lawyers to “make sure we don’t upset anyone with these names,” said Van Kerkhove.
Maria van Kerkhove. Photo: Fabrice Coffrini / Pool / Reuters
They began to designate new strains of coronavirus in Greek letters at the end of May – for the convenience of pronunciation in unscientific conversation and in order not to discriminate against the countries where these strains were first detected. However, there are 24 letters in the Greek alphabet – and WHO has already “staked out” ten options. The organization has been tracking the evolution of the virus since the beginning of the pandemic, but the emergence of new, much more dangerous variants at the end of 2020 prompted WHO to accelerate the classification of two types of variants – of concern and interest.
The first category includes the well-known alpha, discovered in the UK in December; South African beta; gamma detected in January in Brazil and delta detected in India in October. There are also four interesting options now: “this”, “iota”, “kappa” and “lambda”
There were more of them, but after a certain time, some options were recognized as not posing a serious danger and were excluded from this list. Specifically, these are epsilon, zeta and theta.
Usefulness of translation
An eternity has passed since the beginning of the pandemic for the coronavirus – in viruses, generation is most often understood as the cycle of cell infection: attachment to its surface, penetration, gene expression and the release of new viral particles from the cell. The more generations there are, the more the laws of evolution begin to influence, although there is still debate as to whether the virus is a living creature.
By entering the cell, the virus forces it to make copies of itself. The polymerase enzyme “reads” the letters of the bases of viruses – for RNA viruses, to which the coronavirus belongs, it is uracil (U) – and according to this pattern begins “assembling” its copies. However, copies are not always perfect, sooner or later errors occur – for example, instead of A, T. is put. We know them as mutations.
Most RNA viruses, such as HIV or influenza, have no protection against such errors. Therefore, for example, a successful vaccine against HIV has not yet been developed – the virus changes so often that by the time a person develops antibodies, they are no longer suitable to fight against him. However, the coronavirus has such protection. The Nsp14 enzyme corrects transcription errors – but not all. Therefore, SARS-CoV-2 continues to mutate – albeit not as frightening as that of HIV or the flu, at a rate: it is estimated that the coronavirus genome accumulates two single-letter mutations per month. This is half that of the flu and a quarter of that of HIV.
It is not easy to understand what variants from these mutations will arise. The genome of the virus contains about 30 thousand nucleotides – several orders of magnitude smaller than the human (about three billion), but still there are enough places for mutations. It is difficult to study separately what changes in the structure and behavior of the virus will cause this or that mutation, but they rarely occur in isolation.
A group of viruses that differ from the original version in a certain set of mutations is a strain. The difference may be only a fraction of a percent of the entire genome, but each new RNA sequence can initiate a new branch of the virus.
Used on most of the errors in the transcription of the virus is almost not interfere, and do not contribute to its survival mutation often simply disappear. However, some prove to be useful and remain in the arsenal, allowing the coronavirus to “get better.”
Escape routes
There are several main directions for how the coronavirus can improve. SARS-CoV-2 can improve its transmissibility – the ability to infect as many people as possible. It is estimated by the average number of people infected from one person to his isolation. Thus, the transmissibility of the “alpha” strain is 50 percent higher than that of the Wuhan version, and that of the “beta” strain is 20 percent higher.
Virulence, the severity of the symptoms of the disease, may also increase. However, scientists note that most of the mutations that occur indicate a decrease in coronavirus. In addition, the coronavirus can better evade the immune response – antibodies and other defense mechanisms, such as T cells, for example. So did one of the closest relatives of SARS-CoV-2 – human coronavirus 229E, which has learned to get away from human antibodies in 20 years of evolution.
Based on how well a strain has progressed along one path or another, WHO categorizes them into concerns and interests. The latter include those variants with increased transmissibility and virulence, which lead to intensive transmission of infection among the population or the emergence of many clusters of COVID-19 in many countries. The options of concern have all these properties, but, among other things, weaken the epidemiological defense system – reduce the effectiveness of available diagnostics, vaccines and therapies.
There is evolutionary pressure for SARS-CoV-2, the main factor of which is vaccines and human immunity. That is why most often mutations occur in the genes encoding the peplomer protein – the main tool with which the coronavirus enters the cell. This increases the transmissibility of the virus and its resistance to antibodies. The large number of mutations in the peplomer protein may explain the extremely high transmissibility of the “delta” strain. A mutation in the protein that increased its degradability may explain the increased efficiency of the strain in the lungs. These mutations have allowed the “delta” strain to become the most common of all coronavirus variants at the moment.
Seeking herd immunity
The evolution of the coronavirus will slow down, scientists say, but not soon – so, in the case of the swine flu epidemic in 2009, the virus rapidly evolved over a couple of years, and only then the rate of its mutations began to decrease.
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Andrew Pollard. Photo: Steve Parsons / Pool Photo / AP
In addition, it is still unknown how long a person's immunity from the virus will last. It is short-lived against human coronaviruses: re-infection with them can occur after 80 days to a year. It has been shown that humoral – antibody-mediated – immunity against SARS-CoV-2 also weakens over the course of a year.
But even gaining seasonality cannot guarantee that the coronavirus will not continue to take lives. So, from seasonal influenza A – which caused the previous major pandemic of the Spanish flu of the H1N1 virus and its “descendants” – up to 650 thousand people die every year. SARS-CoV-2 may take a similar path, although, most likely, due to the lower mutation rate, there will be no need to update vaccines against it annually.
