Scientists in Canada have analyzed the Omicron in more detail thus far. This is what they saw

VANCOUVER – Canadian research has drawn the curtain to offer a glimpse of how the Omicron variant of COVID-19 is managing to infect human cells while evading the immunity and protection of the vaccine.

The extremely detailed look at Omicron has come thanks to the University of British Columbia, which announced Wednesday that it had completed the world’s first molecular-level analysis of the variant.

The analysis was performed with cryoelectron microscopy, which uses electron beams to visualize tissue shapes. Some of these microscopes are up to four meters tall, according to UBC.

The study shows that the variant’s spike protein has three to five times more mutations than previous COVID variants.

The Star spoke with Sriram Subramaniam, from the Department of Biochemistry and Molecular Biology at UBC School of Medicine, one of the researchers behind the project.

This is the first molecular level analysis of the Omicron variant. What was its purpose?

We have seen these images of viruses with these things sticking out of the surface called spike proteins. These spike proteins are what the virus uses to enter and infect cells. Over the course of the last year or so, we’ve been looking at the structures of all the spike proteins in these different variants.

To try to better understand exactly what are the principles by which the virus enters cells and what these changes mean, and in particular in the case of Omicron, the important question is: How does it manage to be so transmissible despite having such large number of mutations? (When a virus mutates, there is usually a chance that it will become weaker and less transmittable.)

The number of mutations in the spike protein is more than 37 … this is around three to five times more mutations than we have seen in other worrisome variants compared to where we started with this virus two years ago.

So when you have such a large number of mutations, what’s remarkable about this particular variant is that it still retains roughly the same level of recognition efficiency in our cells (as previous variants).

How does this variant avoid antibodies?

There are some common patterns in these spike proteins, but when you have such a large number of mutations … the immune system doesn’t recognize them as effectively, so what these mutations do for the virus is lower the barrier so effective, so it’s easier to get in because it’s not blocked by as many antibodies as it could be in other variants.

It just doesn’t meet as much resistance as the other variants simply because it made all these changes to its surface and the antibodies don’t recognize it. But normally, when you have so many changes, you might have thought that maybe those changes would also affect the ability with which it adheres to our cells.

It’s still as good as the Delta variant at sticking to itself while still making enough changes to keep the immune system from tackling it much less successfully in people who have antibodies.

What have we learned from this analysis that we did not know before?

A couple of important things. One of the central questions that we are all trying to understand is what exactly makes the Omicron variant that much more transmittable. We thought the Delta variant was very transmissible; this is even more so. Therefore, the molecular understanding of the origins of this transmissibility is important.

The second aspect of our work was to get an idea of ​​those who, for example, have been twice vaccinated compared to those who have recovered … How does that affect the ability to block the virus?

That kind of knowledge is important; they are being done all over the world now. I think the more information we have structurally and the more information about the strategies that the virus has developed to evade antibodies, all of that will help us design better therapies as we deal with this variant.

Was there anything that surprised you when you looked so closely at the variant?

The surprise was the fact that the interface looks different but still manages to be just as effective at binding to cells. We knew it was pretty much the same, as good as Delta, because of the experiments we had done, but it’s always helpful to focus on this kind of atomic resolution to see exactly what the interactions are.

From what you’ve seen so far, are you more concerned with this variant than the previous ones?

I think there are always reasons for concern when we see variants like this, especially here. The rapid spread is of great concern and I think we have just literally seen in the last two weeks that it has been spreading so rapidly. I think it is definitely a source of concern and we just have to do our best to limit its spread.

This interview has been edited for clarity and length.

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