‘Overwhelming’: Israeli virus sleuth researchers work flat-out on Omicron puzzle

Quantity and location of mutations are ‘big surprise,’ says Prof. Adi Stern, as her team works to build a picture of variant’s origins

Nathan Jeffay is The Times of Israel's health and science correspondent

Illustrative image: A photographer takes a photo of a projector image showing immunofluorescence staining of Omicro- infected Vero E6 cells in Hong Kong, December 1, 2021. (AP Photo/Kin Cheung)
Illustrative image: A photographer takes a photo of a projector image showing immunofluorescence staining of Omicro- infected Vero E6 cells in Hong Kong, December 1, 2021. (AP Photo/Kin Cheung)

A team of genetic sleuths in Tel Aviv is working flat-out to answer some of the big questions about the Omicron variant of the coronavirus, including its origins and its ability to dodge vaccines.

“We are trying to see when it first came into being, how it first came into being, and how long it has been spreading without being detected,” Prof. Adi Stern, head of Tel Aviv University’s lab dedicated to virus evolution, told The Times of Israel.

Stern has been working using models of the virus strain since details of its composition first became available last week, and said that exploring a coronavirus variant that is so different from its predecessors is “overwhelming.”

“What we’re learning is that this variant is confusing and puzzling. There is a huge number of mutations in Omicron, some of which we’ve seen before in different variants, but some of which are new,” she said.

“We’ve seen nothing at all so far, in terms of variants, with this many mutations in general, or specifically in the spike protein, which is a very important region and the target for most vaccines. A particular surprise related to the RBD, the receptor binding domain, of the spike protein,” Stern said.

Scientists expected minimal mutation in this region, as it is responsible for ensuring the virus’ entry into human cells. Until now SARS-CoV-2 has been highly successful in entering human cells, and the received wisdom was that the virus would largely retain the existing structure of the RBD — but there are more than a dozen RBD mutations in Omicron.

Prof. Adi Stern of Tel Aviv University’s School of Molecular Cell Biology and Biotechnology (courtesy of Tel Aviv University)

“We expected this part to stay relatively similar but have been very surprised,” said Stern.

Stern’s lab is looking at the patterns of mutations found in all the sequences of Omicron patients it can obtain, and at their phylogenetic tree, which is a diagram that depicts the lines of evolutionary descent.

It is examining different hypotheses to explain how Omicron came into being, including the possibility it arose in an immunocompromised patient who couldn’t shake the virus and became host to multiple mutations.

Illustrative — In South Africa, where Omicron was first discovered, a woman is tested for COVID-19. (AP Photo/ Shiraaz Mohamed)

“It could have been an immunocompromised patient with cancer or other illnesses, a recombination of two variants, a set of hyper-mutations that occur more quickly than normal, or a range of other possibilities,” said Stern, adding that findings will help manage future variant outbreaks.

She cautioned against jumping to the conclusion that Omicron will become dominant, that it will dodge vaccines, or that it will cause more serious illness than other variants.

“There were variants that became very widespread in South Africa but were largely limited to that country,” she said. “At the start of the year there was the British variant, which widely infected Israel, and what was called at the time the South African variant, which hardly spread. We don’t really know what leads to one variant taking over in one country or across much of the world and others not doing so.”

“At this point, everything is possible. It’s possible that this variant is more infectious but actually less virulent. In fact, some early reports from South Africa suggest this is the case, but it’s too early to say.

“In terms of vaccines, we’re waiting for what we call neutralization assays, namely to see how the virus reacts in labs to serum from vaccinated people. And despite the many mutations, I’m optimistic because the vaccine is normally good for the virus even after changes, and attacks the virus in more than one place, meaning that if there are mutations in one place it can still target elsewhere.”

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