Last week, researchers in Africa reported a new suspected variant of the coronavirus. The World Health Organization (WHO) almost immediately listed it as a variant of concern and named it the letter of the Greek alphabet “omicron. Since then, this variant has been found in dozens of countries on every continent except Antarctica.
What is known about “omicron” is that it carries 50 mutations, most of which are in the spike-like protein of the virus. The spiky-shaped protein, which gives the viral particle a crown shape, is needed to penetrate human cells, and this is where most of the neutralizing antibodies bind. This is why “omicron” is a cause for concern.
However, it is not yet known whether the mutations have changed the properties of the coronavirus. There is reason to believe that SARS-CoV-2 could have become either more or less dangerous.
Four questions are more important:
- Whether “omicron” is more easily transmitted from person to person;
- Whether it is more likely to cause complications and death;
- Whether and to what extent it can overcome the immune system defenses built up after illness or vaccination;
- Whether it will supplant the “delta” that is prevalent everywhere.
At this point, we can only make more or less educated guesses about all of this. Most of the quantitative estimates (by how much, by how many times) are not derived from experimental or observational data, but are prompted by the intuition of the experts who share them.
Perhaps the results of laboratory experiments will come out next week, but they will have to be interpreted with caution: life is not a laboratory. Some questions can only be answered months later. For example, to calculate the lethality of “omicron,” we need to accumulate data on the dead.
What’s cleared up in a week
Epidemiological data from South Africa show that “omicron” probably has advantages over “delta,” and this variant is very contagious. Axios reports that 11,500 cases of COVID-19 were detected in the country the day before, and 22.4% of tests were positive. Just ten days ago there were 300 new cases in South Africa and only 2% tested positive.
The Financial Times writes that scientists at South Africa’s National Institute of Infectious Diseases retrospectively analyzed epidemiological data from March 2020 to November 27, 2021 and calculated that over the past four weeks, which is when the new variant began to spread, the risk of reinfection increased significantly. It is likely that sometimes omicron is able to overcome the protection developed after the disease.
There is also information from pharmaceutical companies – developers and manufacturers of monoclonal antibodies against COVID-19. Unlike antibodies produced by the body, monoclonal antibodies are identical. Of these, the most potent ones are carefully selected and then industrially produced in cultured cells. Often the drug uses not just one antibody, but two or more (“cocktail”).
Regeneron reported Tuesday that its “cocktail” is probably less effective against the new variant. The Financial Times quote suggests that the conclusion is based only on the presence of individual mutations in the virus, but the note goes on to say laboratory tests and computer modeling have been done. Be that as it may, Regeneron is not yet convinced that this is the case, but says they have other, potentially more potent antibodies.
According to the Financial Times, GlaxoSmithKline and Vir Biotechnology announced yesterday that their monoclonal antibody-based drug, in contrast, remains effective against omicron as well. These results were obtained in laboratory experiments, where neutralization was tested on pseudoviruses that had been supplemented with a spiking protein with some “omicron” mutations. But to speak with certainty, more research is needed.
Where did “omicron” come from?
Until recently, scientists thought that if a new suspicious variant of SARS-CoV-2 appeared, it would be a descendant of “delta”, because there is almost nothing left except “delta”. However, “omicron” is so different from the other variants that it is even difficult to establish its closest ancestor. Because of this, the assumption arose that “omicron” mutated for months in an organism with a suppressed immune system, for example in a person with a neglected HIV infection. Now scientists are considering two more hypotheses, and one of them is particularly troubling. STAT and Science report on them.
On the “family tree” of the coronavirus, the “branch” of the new variant is extremely long. “Omicron” could have separated as early as mid-2020 or even earlier, but has only been discovered now. This is highly unusual. SARS-CoV-2 accumulates changes in the genetic code gradually, so intermediate variants are visible. And “omicron” looks like it acquired all the mutations almost immediately.
Something similar happened a year ago with “alpha.” Then scientists suggested that the virus had evolved in a person with a suppressed immune system. Usually the body copes with the infection in a few days, but if it lacks strength, the virus can circulate for months. The immune system still pressures SARS-CoV-2, so it has to adapt – that’s how the resulting mutations take hold.
This hypothesis is indirectly confirmed by observations of patients with chronic COVID-19 (not to be confused with “prolonged” COVID-19, or the post-cure syndrome that develops after cure; however, it is possible that this syndrome, at least in some cases, is caused by the virus hiding in the tissues). SARS-CoV-2 does accumulate mutations of variants of concern in their bodies.
However, the hypothesis is inconsistent with observations of other chronic viral infections in people with suppressed immune systems. Typically, the variants that arise do indeed “learn” to slip away, but are worse transmitted from person to person. True, it is possible that the same mutations in the coronavirus help spread both within and between organisms.
According to another hypothesis, “omicron” originated in southern Africa in places where human testing is rare and viral genomes are even more rarely deciphered. Critics of this hypothesis point out that such a deafening place is hard to imagine. “Omicron” or its ancestor would still have penetrated somewhere else and been seen.
Finally, a third hypothesis states that humans infected animals, the “omicron” evolved into them, and then crossed over to humans. This conjecture is supported by a recent study, which found that as recently as a year ago, 80 percent of white-tailed deer tested in the U.S. state of Iowa were infected with SARS-CoV-2.
In Africa, the intermediate host may have been a rodent. At first, the coronavirus could not infect these animals, but over time it “learned.” Seven mutations are known to have something to do with adaptation to rodents – and all of them are present in “omicron”. This is not enough to recognize the hypothesis as correct, but we can do experiments with wild animals and see if they have chronic infection and how SARS-CoV-2 changes with it.
Whether or not “omicron” has emerged in an animal, the coronavirus definitely infects many different species, so other variants may emerge in them in the future.