Science

Why do SARS-CoV-2 variants spread so quickly?

The very first variant identified at the end of 2020 in the United Kingdom, named B.1.1.7, is now present in at least sixty countries and territories according to the World Health Organization. Considered much more contagious, even “more deadly” according to Boris Johnson’s latest statement – a fact which remains to be confirmed by scientists, however, it is presented by the media as a potential second pandemic. How does this variant manage to spread so easily?

Sarah Otto, an evolutionary biologist at the University of British Columbia, studies how genetic mutations and natural selection combine over time to shape populations. SARS-CoV-2, more than 380,000 genomes of which have been sequenced in the space of a year by scientists around the world, offers a unique opportunity to study the evolution of an organism in near real time .

The specialist recalls that although most mutations do not promote the survival of a virus, it may happen that a specific mutation, or a set of mutations, gives it a certain advantage. This is a priori what happened for this British variant, which appears to be more transmissible thanks to the mutations it carries. The reason for its extremely rapid spread remained to be determined.

A particularly strong selection signal

A virus carrying a mutation can multiply in three ways: because its host is a “super-spreader”, because it is brought into a region that is not yet infected, or because it is introduced into a new segment. Population. The latter two possibilities are called “founding events”: a rapid increase in the frequency of a given variant can be observed if it is introduced into a new group and triggers a local epidemic.

The B.1.1.7 variant appears to be an exception, however: over the past two months, its frequency has increased more rapidly than “non-B.1.1.7” practically every week and in every region of UK territory. The following animation illustrates the ultra rapid spread of this new viral form:

This rapid predominance cannot be explained by the first type of founding event: indeed, the disease was already widespread throughout the territory. Likewise, the variant was not introduced into a new segment of the population (following a meeting of a large number of people, for example), because the preventive measures in place at the time already prohibited large gatherings. Experts deduce that the selection signal (for a higher transmission) is very strong in this variant.

To date, epidemiologists have concluded that B.1.1.7 is more transmissible (but there is no indication that it is more lethal). A team of researchers has estimated that this variant increases the number of new cases caused by an infected individual (what is called the basic reproduction number or R) 40 to 80%; another preliminary study concluded that the variant is 56% more transmissible on average.

The exponential increase in the number of cases of infection will occur several weeks after the appearance of the variant in the population. © Science Table – COVID-19 advisory for Ontario

A 40 to 80% increase in R is still remarkable. But Sarah Otto explains that even when the selection is so strong, the evolution of the virus is not instantaneous. She and her team have performed a mathematical modeling of this evolution, which shows that several weeks are necessary for the variant to reach a meteoric rise, because only a small fraction of the population initially carries the variant. A conclusion corroborated by a Canadian study. These few weeks of “respite” will nevertheless be essential to prepare for the massive influx of patients into the care units, due to the exponential growth of cases.

A race against viral evolution

When scientists looked at the genome of the B.1.1.7 variant, they were amazed at how much the initial virus had mutated in a short period of time: no less than 30 to 35 changes in a year! This viral form does not mutate faster, but appears to have undergone an episode of rapid change in the recent past. For example, the virus could have been carried by an immunocompromised person. In fact, people with a very weak immune system constantly fight the virus: they suffer from prolonged infections, because they undergo recurrent cycles of viral replication, and only offer a partial immune response … to which the virus is constantly evolving!

covid-19 virus genomes
Each dot represents a SARS-CoV-2 genome; branches connect related viruses to their ancestors. The center of the circle represents the virus introduced into humans. Viruses furthest from the center carry the most mutations. The three new officially identified variants appear in yellow. © NextStrain, CC-BY

Two other viral lines, identified in South Africa (B.1.351) and in Brazil (P.1) are currently the subject of in-depth studies. These variants also show a recent excess of mutations and spread rapidly among local populations; scientists are gathering the necessary data to confirm that this is again a selection for better transmission and not the result of chance.

It should be noted that the 23 mutations of B.1.1.7 and the 21 mutations of P.1 did not appear at random in the genome of the virus: they are grouped together at the level of the gene encoding the spike protein – protein which allows the viruses to attach to and enter human cells. One of these changes, named N501Y, appeared independently in all three variants, as well as in immunocompromised patients; other modifications are common to two of the three variants. The parallel evolution of the same mutations, both in different countries and in different immunocompromised patients, suggests that they convey a selective advantage for evading the host’s immune system.

The variants are therefore more resistant to the immune system. But how to explain the higher rate of transmission from one individual to another? Sarah Otto explains that it is unfortunately difficult to answer this question, because too many mutations have occurred at once and are now lumped into these variants. Therefore, only one of these mutations (as well as a combination of several mutations) can be the source of higher contagiousness. For example, one study showed that the N501Y mutation “alone” had only a small inheritance advantage, which increased rapidly when combined with other mutations (as seen in the B.1.1 variant). .7).

Today, the 40-80% higher transmission of B.1.1.7 – and potentially of the other B.1.351 and P1 variants – is the main factor to consider. According to the specialist, who evokes a “race against viral evolution”, this British variant will overwhelm many countries in the coming months and it is essential to vaccinate populations as quickly as possible, while limiting interactions and movement, to stem this flow of new viral forms.

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