New omicron subvariant spreads in Europe

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The omicron subtype “BA.2” is spreading rapidly in Norway, Sweden and Great Britain and has already overtaken the previous omicron variant BA.1 as the dominant form in Denmark. Not much is known yet about the once again modified variety, as geneticist Ulrich Elling explained. However, the mutability of the SARS-CoV-2 pathogen shows that only the broadest possible immune response will pave the way to the longed-for endemic.

BA.2 has also already been detected in Austria through the systematic analysis of samples from sewage treatment plants, as the head of the “School Site Monitoring”, Heribert Insam, recently explained. In Denmark, which is well informed about the distribution of variants in the country, cases with BA.1 are declining again, but infections with Omicron BA.2 are increasing. A similar trend is emerging in England, said Elling, who works at the Institute of Molecular Biotechnology (IMBA) at the Austrian Academy of Sciences (ÖAW).

Lower immunity to subvariant conceivable
The spike protein of the two subtypes differs significantly – specifically in 18 mutations. By comparison, the delta variant has a total of only eight mutations in the spike protein compared to the original virus. It is conceivable that BA.2 is even better able to escape a built-up immune protection. This could mean that people whose immunity was still able to ward off an infection with BA.1 may be less immune to a BA.2 infection. That’s plausible because BA.2 has relatively many mutations in the receptor-binding domain – the part of the spike protein that the pathogen uses to dock with cells and that many antibodies target, Elling said.

Another possible explanation is that BA.2 could be even more infectious and replicate more quickly. That’s conceivable, he said, because it has entirely new but fewer mutations overall in the “completely different” N-terminal domain (NTD) compared with BA.1. The NTDs are the three tips of the S protein considered from above. These structures are responsible for the fusion of the virus and the human cell. The many changes there in BA.1 could be a disadvantage in replication for this descendant, which BA.2 may have less to contend with. This is probably also the key to the fact that the previous BA.1 variant of Omicron has a harder time penetrating deeper into the lungs and that the courses are milder.

In principle, many people are already protected against severe courses of all SARS-CoV-2 variants, including Omicron, either by vaccination or by having been through the disease. Ellling: “Omicron is milder on average because it largely infects protected people.” That’s not likely to be much different with BA.2, the scientist expects. But it is unclear whether the subtype itself “is not another step in the wrong direction for the unvaccinated. We don’t know so far.”

So even within the Omicron variant, predatory competition has apparently begun. BA.2 is expected to take the lead, he said. Therefore, one should take a close look at what constitutes its advantage, Elling emphasized. The first data on this could be available in the coming week.

If the new sub-variant now catches on in Denmark or the UK, the Omicron wave could become a kind of “double whammy.” However, those who have caught the first variant are unlikely to be infected with BA.2, the researcher estimates.

Where the development of the coronavirus as a whole will go is “still unpredictable”. The respective new variants kept coming from other directions. For SARS-CoV-2 to ultimately become endemic – that is, a seasonally recurring pathogen that does not, however, cause a major epidemic – it requires, above all, an immune system whose T cells recognize the pathogen in as many different manifestations as possible. T-cells are a group of white blood cells whose job is to recognize new threats and drive the acquired immune response. They can react more flexibly to a virus than the antibodies, which are usually more specific.

It’s not yet possible to declare the pandemic over, even for people who have been through an omicron infection, Elling said: “We simply don’t know yet which variants are yet to come.” With each confrontation through vaccination or infection, however, the immune system builds a broader response, and the likelihood of milder and milder courses increases. That’s why the geneticist hopes for complex vaccines that include many varieties of the virus, similar to influenza vaccines. The fact that T-cell immunity presumably works quite well across all variants gives hope, he said.