WHAT will Covid become officially born in 2019, and which since that moment has been under the magnifying glass of scientists all over the world? In particular, what will become of the Omicron variant? Will it disappear, change and become stronger, or will it lose its power and become endemic? Or will the virus still stand out so much that it becomes SARS-CoV-3? These questions were posed by evolutionary biologist Jesse Bloom, who works at the Fred Hutchinson Cancer Research Center in Seattle, as early as the beginning of the pandemic in 2020. He looked into the future of SARS-CoV-2 and, like many virus specialists in that moment, he predicted that the new pathogen would not be eradicated. It would instead become endemic: the fifth coronavirus to permanently settle in humans, alongside four “seasonal” coronaviruses that cause relatively mild colds and have been circulating among us for decades or more.
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by Cinzia Lucchelli
The seasonal virus 229E
Starting from seasonal viruses to find out more, in order to draw a possible evolutionary path, and therefore draw a design of the future of the pandemic, 229E has been studied above all, capable of infecting people several times in the course of life. What was not clear, however, was whether the new infections depended on the weakening of immune responses in human hosts, or if the virus bypassed immunity thanks to mutations. To find out, Bloom took decades-old blood samples, taken from people probably infected with 229E, and tested them for antibodies against various versions of the virus, even dating back to the 1980s. The results opened a first door. Those blood samples had a high level of antibodies, capable of blocking an infection, but against a version of 229E dated 1984. Instead, they were much weaker against viruses that later appeared on the scene: they were much less able to neutralize a version. virus dating back to the 1990s, and even less effective against the 229E variants of the years 2000 to 2019. The same was true for the blood samples of the 1990s: patients were immune to viruses from the recent past, but not to future ones . This led to speculation that the virus was evolving to circumvent immunity.
The pinwheel of variants
So a first conclusion is that one variant drives out the other over time, with the risk that it strengthens by managing to “pierce” the antibody barrier of those who are infected. “Omicron is not the first variant to become dominant – explains Fausto Baldanti, director of the Molecular Virology Laboratory of San Matteo in Pavia -. They come in waves: the first was the D614G, then came the Alfa, which disappeared, then the South African Beta and immediately after the Delta, still dominant, which supports infections in Italy “. But all over the world Omicron is preparing to make the “turning point”, to cross the Delta. “The data must be contextualized – continues Baldanti -. Omicron emerged in South Africa with 20% vaccination coverage. South African authorities have argued that it is associated with mild symptoms. However, it is necessary to understand which places we are talking about. The average age in South Africa is much lower than ours, so the clinical context is also different: it is a classification carried out in a country different from ours, even in terms of age “. But even in England, Omicron is spreading like wildfire. “But England ran a very special vaccination campaign: they vaccinated everyone early with AstraZeneca, and with a single dose. Furthermore, the second followed after 6 months. Unlike what has been done all over Europe, which has administered it a long time before. This, therefore, does not tell us that this strategy has changed the immunological response “.
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How does the virus change?
Scientists following the evolution of SARS-CoV-2 are monitoring two broad categories of changes in the virus. One makes it more contagious or transmissible, for example by causing it to replicate more quickly, in order to facilitate its spread through coughing, sneezing and wheezing. The other allows it to overcome a host’s immune response. When a virus begins to spread in a person, there is little point in being able to circumvent a pre-existing immunity if it lacks it. So the first – and major – “advances” of a new virus tend to consist in increasing infectivity or transmissibility.
“I certainly expected this new coronavirus to adapt to humans in a significant way, that is, probably with greater transmissibility,” said Wendy Barclay, a virologist at Imperial College London.
The rate of mutation
Genome sequencing in the early stages of the pandemic showed that the virus diversified and underwent about two mutations of a single letter per month. Speed that is about half that of influenza and a quarter of that of HIV, thanks to an enzyme that corrects errors, present in coronaviruses but rare in other RNA viruses. However, few of these initial changes appeared to affect SARS-CoV-2 behavior or be favored by natural selection. An early mutation, called D614G, in the gene that encodes the virus’s Spike protein – the one that recognizes and invades host cells – seemed to offer a slight increase in transmissibility. However, this gain was by no means comparable to the leaps in transmissibility that researchers would later observe with the Delta and Alpha variants, as Sarah Otto, an evolutionary biologist at the University of British Columbia in Vancouver, Canada, pointed out.
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Evolution in equilibrium
Other well-established human viruses do not show the leaps in infectivity that SARS-CoV-2 has made in the past two years, and Bloom, as well as other scientists, expect this virus to have the same fate. In this regard, Trevor Bedford, evolutionary biologist at Fred Hutchinson, argues that he must find a balance between the ability to replicate abundantly in the airways of the hosts and the need to keep them healthy enough to be able to infect others: “The virus does not want to force you to bed, so sick that you can’t see many other people, “Bedford explains. For the virus, a solution could be to evolve so as not to multiply too much in the host’s airways, but by making the infection last longer in order to infect a greater number of new hosts. “Ultimately – say the researchers – there will be a trade-off between the amount of virus produced and the speed with which the immune system is stimulated.” Thus, going unnoticed, SARS-CoV-2 could ensure continued spread.
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Omicron has messed up the cards
Even today it is the Delta variant, along with its descendants, that monopolize infections in the world. And scientists expected that these Delta lines would eventually displace what remained of the other variants. But Omicron has messed up the cards. The rapid increase in cases of this variant in South Africa suggests that it has an advantage over the Delta: says Tom Wenseleers, an evolutionary biologist and biostatistician at the Catholic University of Leuven, in Belgium. The Omicron variant carries some mutations associated with the very high infectivity of the Delta. But if the increased infectivity were the only reason for its rapid growth, continues Wenseleers, it would mean an R0 over 30, and “it’s not at all plausible”. Wenseleers and other researchers suspect that Omicron’s advance is mainly due to its ability to infect people immune to Delta thanks to the vaccine or a previous infection.
The picture that scientists have on Omicron is not yet clear, but they know that, if it is spreading also thanks to its ability to circumvent immunity, this corresponds to the theoretical predictions on the probable evolution of SARS-CoV-2.
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Is it turning into SARS CoV-3?
So we come to the basic question: if Omicron has so many mutations, does it mean that it is characterizing itself as a new virus? Does that mean it’s about to become SARS CoV-3? Scientists’ response is one of skepticism. For example Baldanti, he has no doubts: “What do I say to those who support this thesis? I say you are wrong. Omicron mutations are many, but not so many that they constitute a new viral type. If we examined the variability of HIV or Hepatitis C, that of the Coronavirus would appear ridiculous “. And also Giovanni Maga, director of the Cnr of Pavia, moves along this path: “How is SARS CoV-1 identified from SARS CoV-2? By the percentage of genetic difference. Omicron has a genome of 30 thousand nucleotides (organic molecules that make up the monomers of the nucleic acids Dna and Rna). Changing 50 is not enough to argue that it is a different virus, given that its genetic structure is the same. We would have to see a difference in all genes to argue that it is a new viral strain: if the viruses have a 90% difference, then we could say that they are different strains. In this case, however, it is always the same virus: it has only accumulated more mutations concentrated on the Spike protein, in order to facilitate its entry into the cells “.
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