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Home Trends How the new strains of COVID-19 increase their infectious role

How the new strains of COVID-19 increase their infectious role


The variants of the new coronavirus put health systems in check again – REUTERS / Gonzalo Fuentes / File Photo

It has been shown that Vaccination programs around the world reduce transmission rates of COVID-19 and hospital admissions. But news of rapidly emerging and spreading COVID variants remains a concern.

In late 2020, a new variant of the SARS-CoV-2 coronavirus emerged in Britain. Named B.1.1.7, it is endowed with greater infectivity. According the COVID-19 UK Genomics Consortium, in December 2020 more than 50% of new infections in Great Britain were of this variant, that today is dominant in the islands. Presents a increased transmissibility Come in 38 and 130% compared to the original variant. The news of his appearance caused a wave of news and aroused fear in the public. But what is a viral variant and how does it become a problem?

SARS-CoV-2 seen in an electron microscope (NIAID via The New York Times) -
SARS-CoV-2 seen in an electron microscope (NIAID via The New York Times) –

A virus is essentially genetic information. A manual for generating copies of yourself. They can evolve through changes in their genetic information called mutations. Information needs support: cells use nucleic acid. Life is sustained by two types: DNA and RNA, which are similar, although with essential chemical differences. Human cells contain the information in DNA, but the coronavirus stores it in an RNA molecule with approximately 30,000 “letters.” When it infects, the cell becomes a factory of copies of its components, based on the information contained in the genomic RNA. When the components have been manufactured, they are assembled to form new viral particles, which leave the infected cell.

Genetic information is written in a language made up of three-letter words, or codons, combined from a four-letter alphabet. The copy of this language is imperfect and gives rise to mutations, which are changes in the letters of the sequence (among other possible errors). These changes can lead to evolutionary advantages, but they can also be lethal. Mutations are essential for evolution. The delicate balance between the size of the genome and the number of mutations that occur in its copies makes the diversity of life possible.

A virus makes copies so fast that it is possible to assist its evolution, driven by its mutations. These give rise to new variants, in which definite mutations are identified with respect to the original virus, but with which the vaccines continue to work. When so many mutations accumulate that the virus changes and escapes the immune system, a new strain emerges. This is the case of the flu, whose virus generates new strains periodically, forcing vaccines to be modified every season. Every time the virus replicates, the new copies always contain mutations. Sometimes, mutations can arise that reduce the infective capacity of the virus, or others that could give it an advantage by improving its adaptation to the host.

Each point represents a SARS-COV-2 genome, with branches connecting the viruses to their ancestors.  The center represents the virus introduced to humans.  Viruses that are farther from the center have more mutations.  The three new variants are highlighted in yellow.  (NextStrain / CC BY 4.0)
Each point represents a SARS-COV-2 genome, with branches connecting the viruses to their ancestors. The center represents the virus introduced to humans. Viruses that are farther from the center have more mutations. The three new variants are highlighted in yellow. (NextStrain / CC BY 4.0)

Mutation to survive

A recent analysis carried out by Cesar Menor-Salvan of the Department of Systems Biology of the University of Alcalá, wields a step-by-step development of the new strains, opening concrete information on their infectious power.

LA viral infection depends on a chemical subtlety: the ability of proteins to bind to other molecules, using (mainly) hydrogen bonds. To initiate the infection, the spicules of the virus are anchored to the receptor protein through these links, fitting together like a puzzle. The more hydrogen bonds that are formed, the more affinity the virus has for the cell and the less inoculated virus will cause infection.

Thanks to coronavirus data are public, anyone can investigate if the N501Y mutation gives an advantage to B.1.1.7. This mutation seems essential, since it occurs at the attachment point of the virus to the cell. With the help of a computer tool, in the University of Alcalá showed that the mutation causes the appearance of new links between the virus and the cell. This increases the affinity and infectivity.

Vaccines face new variants of the virus (Andrew Testa / The New York Times)
Vaccines face new variants of the virus (Andrew Testa / The New York Times)

“We have seen – explains the author of the research -, in a simplified way, how scientists can predict what effect the mutations will have on the behavior of the virus. In the case of variant B.1.1.7, at least one of its mutations makes it more contagious, prevailing over the one without the mutation. This type of selection is key in the evolution of life ”.

The mutation they showed does not seem to increase the severity of the infection –although there are preliminary data that point to this–, nor does it affect the action of the vaccines. Surveillance of new variants and identification of their mutations is essential for monitoring the pandemic and predicting the performance of vaccines. Without alarmism, mutations and the appearance of better adapted variants is a natural process in a virus that has just started its evolution with humans.

“Viruses mutate,” explains Amir Khan, an NHS doctor and senior lecturer at the University of Leeds School of Medicine and the University of Bradford in the UK. This is to be expected. And, as the coronavirus spreads and infects more people, it will be given more opportunity to do so, particularly in countries that have been slow to block, enforce social distancing or close borders. ” The new variant in Brazil has overwhelmed hospitals in that country. Within a few weeks of identifying the new variant, Manaus saw that cases began to increase exponentially, even in people who had previously been infected with the original virus.

Infections have increased worldwide in recent weeks - REUTERS / Pascal Rossignol
Infections have increased worldwide in recent weeks – REUTERS / Pascal Rossignol

The P1 variant has been caused by a number of mutationsBut three in particular worry scientists. The first is the E484K mutation, which has also been identified in the South African variant. It is called an “escape” mutation, as it changes parts of the peak protein of the virus that our immune system depends on to recognize and initiate our immune response. These changes may mean that you can evade an immune response triggered by the vaccine or a previous infection. More research is needed to fully understand this.

The spike protein is found on the outer surface of the virus. When the virus enters a human host, it has to enter cells to infect them. It does this by connecting its spike protein to receptors on the outer surface of human cells, called ACE2 receptors.

The E484k mutation has changed the spike protein of the original virus so that it binds more easily and forms a stronger connection with host cells, making it more infectious. The same mutation also means that the virus can evade the neutralizing antibodies that a previous coronavirus infection has created more effectively. This may explain some of the reinfections in Manaus.

So far there are 3 dangerous variants of the new choroanvirus - REUTERS / Pascal Rossignol / File Photo
So far there are 3 dangerous variants of the new choroanvirus – REUTERS / Pascal Rossignol / File Photo

The second is the mutation N501Y , which is also present in the UK variant. This mutation also affects the coronavirus spike protein, but specifically its “receptor-binding domain.” This is the part of the spike protein that comes into contact with human cells, attaches itself to them, and then allows the virus to enter. This mutation not only makes the virus bind more closely to human cells, it also makes it more likely to remain attached to them, thus increasing the probability of infection. This mutation has allowed the UK variant to become the dominant strain in the UK and is most likely what helped the Brazilian variant to become dominant in Manaus.

According information from the UK government, this mutation can make the virus up to 50 percent more infectious than the parent virus.

The third is the K417T mutation, which is not as well understood as the other two. It also occurs in the receptor-binding domain of the spike protein and can facilitate the virus to bind to human cells, increasing its infectivity. More research is needed on this mutation, but there is a school of thought that suggests that this, combined with the N501Y mutation, will significantly increase the virus’s binding ability to human cells, making the Brazil variant especially dangerous.

Vaccine manufacturers have agreed that if this variant becomes the dominant strain, their vaccines can be quickly adjusted to accommodate it. The time it takes to make these adjustments will vary from vaccine to vaccine. Those from Pfizer and Moderna, which use messenger RNA technology, can be done more quickly, in about six weeks, according to information provided by Pfizer-BioNTech. The Oxford-AstraZeneca vaccine, which uses DNA technology, will take longer and the manufacturer has said it expects to have an adjusted vaccine for the South African variant in the second half of this year.

KEEP READING:

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