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Ômicron: it is simplistic to blame non-vaccinated people for the emergence of the variant

The month of November ends with the advent of a new variant of the new coronavirus declared of concern by the WHO, omicron, which is spreading across southern Africa. It is genetically differentiated from the other worrying strains—delta, alpha, beta, and gamma; accumulating many mutations. First identified earlier this month in Botswana, monitored more rigorously by South Africa, where it already dominates the Johannesburg region, cases have already been found in Hong Kong, Scotland, Germany, Australia, Italy, Canada and Israel.

The mutations are about 16 in the S protein, which is very important in the virus’ ability to infect. This is the virus protein that is produced in human cells with the messenger RNA contained in Pfizer and Moderna vaccines, and presented to the immune system, which creates defenses targeting the protein. As these vaccines are based on a version of the S protein of previous variants, it may be that these acquired defenses are not sufficient against the S protein of the omicron variant, which would no longer be a recognizable target because of these mutations. However, it is important to highlight that, at this time, it cannot be said that the omicron escaped the defenses acquired by vaccines or previous infection. Some of these mutations were present in other variants like delta, which ultimately failed to break through vaccine defenses and natural immunity.

Speaking to Nature, frontline researchers like virologist Penny Moore of the University of the Witwatersrand in Johannesburg make it clear that they still don’t know whether the omicron is actually more transmissible or that it actually escapes immune defenses. At the moment what we have are computer models. To find out if the variant escapes defenses and causes a more or less severe disease, at least two weeks of work will be necessary.

In the opinion of specialist in viral evolution Trevor Bedford, from the Research Center of the Cancer Fred Hutchinson, as the omicron does not share some of the mutations outside the S protein that aided in the delta’s high transmissibility, it may be that the former is less transmissible than the latter, similar in this respect to the gamma variant. However, he emphasizes that he is speculating. Evolutionary biologist Jesse Bloom of the same center told Science magazine that he thinks it unlikely that the immunized will completely lose their ability to resist the micron, but that their specific combination of mutations suggests that they will escape antibody neutralization more than the other large variants. .

Variants: where they come from, whose fault is it

The progressive interpretation that already appears in large media outlets is that “vaccination inequality ” and insufficient vaccination are direct causes for the emergence of the omicron variant. In Botswana, where it appears to have originated, the proportion of the population that has taken at least one dose of vaccines is 37%. The political opinion of even many scientific leaders is that the emergence of variants such as delta in India and omicron in Africa is karma because rich countries did not donate the that they could in doses to poorer regions of the world.

It is not clear whether this progressive interpretation survives scientific scrutiny. CNN states that “scientists know that the virus is much more likely to mutate in places where vaccination is low and transmission is high.” The statement is technically incorrect: mutations are errors in copying genetic material, and these errors can be induced by environmental factors — the antiviral drug Molnupirvir, for example, induces these copy errors in viruses. Ultraviolet light also has this ability. These copying errors happen even without any environmental factor accelerating them, because the enzymatic molecules that copy RNA or DNA make mistakes at low rates. However, non-vaccination is not a mutagenic environmental factor.

What happens is that, in unvaccinated populations and without natural immunity, a virus reproduces more, makes more copies of itself. The chance of a die falling six points face up is always the same each time it is thrown: one in six or ,7% . The chance of seeing at least one face with six points grows with the number of turns. Similarly, the chance of new mutations at each copy of the virus, in the absence of mutagenic substances, is always the same. Some copying errors make the copying process difficult, and so they soon disappear. Others help the process, and get ready for another round of copying, which will have errors that can either help or hinder the copying process, and so on. This is the process of natural selection, and this is what happens with variants full of new mutations like the omicron.

A matter of evolution

Natural selection is imposed by whatever environmental difficulties a particular copy of the virus faces: whether it is more or less efficient at the key and lock mechanism that allows it to enter cells, whether it is more or less capable of spreading through the air within droplets of mucus, if it is sensitive to the season of the year, and even if it is more or less able to escape some defense presented by the organism.

These difficulties are called “selective pressures”, and it is not possible for a virus, the simplest replicating biological entity that exists, to become perfect in all: one reason is that responding to one pressure can make responding to another worse. Vaccine-acquired immunity is a constant selective pressure on disease-causing viruses and bacteria, and they vary in their ability to respond to that pressure. The smallpox virus showed low capacity and was eradicated, but the flu virus (influenza) is more successful, hence the annual update of vaccines to fight it. The new coronavirus is between these two extremes.

While it is true that unimmunized individuals are breeding grounds for viruses and provide opportunity for natural selection by the sheer large population of viruses they make possible, the progressive interpretation errs by default , not to mention the possibility that the vaccines themselves may be selective pressure on the coronavirus. Especially when these vaccines reduce but do not prevent transmission, that is, they allow the virus to make some tentative copies. In the PNAS magazine, in September, biologist Emanuel Goldman says something similar to the explanation above, but, strangely, he blames the non-vaccinated for variants that might escape the defense of vaccines, even knowing that the vaccinated need to be present in the population for this to happen. .

A counterpoint to Goldman was published in the journal PLoS Biology in 2004. Andrew F. Read of Pennsylvania State University, along with colleagues, showed that vaccines with a partial reduction in the transmission of a virus allow for a selection environment that favors more lethal variants. Read’s study analyzed the case of a virus that affects chickens.

As Samuel Alizon of the MIVEGEC Laboratory in Montpellier and colleagues discuss in a review of the journal Ecology Letters, in 2004, different studies indicate that viruses have their peak of transmission not in the highest mortality, but also not in the lowest, but in an intermediate value . When there is more than one variant of the same virus, they compete with each other for a place in the cell, which they depend on to copy themselves, and this competition seems to favor the lower-lethal variant — at least that’s what a study with simulation by researchers suggests. of the Swiss Institute of Bioinformatics.

The lethality of a virus also depends on its ability to survive for a long time outside the human body. Bruno Walther and Paul Ewald of Amherst College confirmed in 37 that human respiratory pathogens show a positive relationship between the ability to survive long in the environment and lethality. There is a “sit and wait” strategy: the smallpox virus, for example, killed many of those infected, and it survived a long time in the environment.

The coronavirus has the opposite pattern: it depends more on closed environments. , does not “sit” outdoors, and has a much lower mortality rate than smallpox. Therefore, Ewald predicts, the coronavirus, which has durability in the environment similar to that of the flu virus, should follow the flu’s direction and lower its lethality to about 0.1%. This will be the likely end of the COVID19 pandemic: it will become endemic, that is, one of the diseases we live with, such as the flu and the colds.

In conclusion, it is pure simplism to blame non-vaccinated for the emergence of more virulent or more lethal variants, we do not know if the omicron is an example of this type of variant, and, if so, the The general pattern of human respiratory pathogens is indicative that the new coronavirus must evolve towards causing a less worrisome disease.

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