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July 7, 2022

Son of Omicron?

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Brought to you by The Echo and Cosmos Magazine

More like cousin of Omicron, it seems. But how worried do we need to be?

Over the weekend, word spread about “Son of Omicron”, a new Omicron sub-variant that was detected among a handful of COVID cases in Victoria and now New South Wales.

New variants and sub-variants, when they emerge, are a potent source of fear for a population that, just over a month ago, was confronted with the sudden spread of Omicron, and forced to throw out the existing pandemic rule-book. But public health officials say at this early stage there’s not a major cause for concern.

So, what’s the deal?

First thing’s first: is it actually the ‘son’ of omicron?

‘Son of omicron’ is actually a bit of a misnomer. This strain, known as BA.2, is not descended from the Omicron strain currently prolific across Australia’s eastern states (that strain is known as BA.1). In fact, BA.2 is more like a sibling or a cousin of Omicron.

It seems that it has a common ancestor,’ says Catherine Bennett, Chair in Epidemiology at Deakin University. Like with a lot of things, you end up with families of variants, not a single variant.’

In fact Omicron, which was first detected in South Africa, wasn’t descended from Delta or Alpha at all – it was found to have genetic ties stretching back to an unknown, undetected ancestral variant.

It looks like this new variant we’re talking about, BA.2, also derived from that same common ancestral Omicron, and it actually appears to tie more closely back to the original variants than it does to others circulating in more recent times,’ says Bennett.

So, it just shows us that we’ve still got this soup of variants out there.’

What do we actually know about BA.2?

BA.2 is not a ‘new variant’ per se, it’s just a slightly different version within a family of variants known as Omicron. While comprehensive data is lacking, scientists are cautiously optimistic that BA.2 won’t be drastically different in terms of severity or vaccination effectiveness.

This one’s different in the sense that this has clearly derived from Omicron, whereas Omicron did not derive from Delta,’ says Associate Professor Hassan Vally, an epidemiologist at Deakin. So, there’s reason to be potentially less worried about this one, because it may represent just a minor shift in the phenotype [the observable genetic traits] of the virus.’

It doesn’t look to be more virulent,’ agrees Bennett. We know that in Denmark, with this particular variant dominating, the country is still opening up and we’re not seeing the rise in hospitalisations that we have with previous variants.’

There’s also very early data suggesting vaccines provide similar protection against BA.2 as they do against BA.1.

BA.2 does appear to be more infectious, by about 120 per cent. But that’s in a variant that was already 500 per cent more infectious than Delta,’ says Bennett, so the difference isn’t a dramatic step-change like we saw in December and January as Omicron cases began to soar.

Another way BA.2 differs from Omicron is that it’s not characterised by ‘S-gene dropout’.

S-gene dropout was a key feature of Omicron that helped us distinguish it from Delta when using PCR testing platforms; Omicron lacked the S-gene that Delta had, and so this dropout became a key signifier of the new variant. BA.2 has therefore become known as the ‘stealth’ variant, because initially PCR tests weren’t picking it up as an Omicron infection at all.

Bennett says we’ve already had to drastically change the way we approach the pandemic thanks to Omicron, so further dramatic upheaval in response to BA.2 is unlikely.

Omicron was a game changer,’ she says. We had to give up on trying to control the virus with contact tracing and quarantining of contacts because it was so much more infectious and with a shorter incubation period. So, with BA.2, it’s a bit faster again, but it doesn’t impact public health settings because we’ve given up trying to contain it in the ways we did before, and now we’re relying on vaccine protection and slowing it down with broad public health measures.’

How worried do we need to be about new variants emerging?

Bennett points out that the mutations that ultimately cause new variants to emerge are happening all the time.

When you actually have an infection yourself, you have so much viral replication going on and that’s when mutations happen,’ she says.

We tend to think of variants as a fixed thing, and they’re not – we have this micro-evolution going on all the time. So, we draw a line and say “these are clades” or “these sublineages”, based on a degree of similarity or difference, but in reality it’s a continuum.’

In fact, this ‘micro-evolution’ was crucial early in the pandemic, because genomic sequencing allowed outbreak investigators to identify case clusters and trace them back to the source, even if those cases all stemmed from one single introductory case in the state.

But a high prevalence of infections provokes concerns about more and more variants emerging – some of which could have more severe impacts – because of this constant process of micro-evolution. Vally says that while we must not become complacent, it may be the case that as the world crests the Omicron wave the immunity that’s left behind could hold new variants at bay – at least for a while.

Experts think that the level of infection that we’ve seen with this Omicron wave around the world is going to mean such a shift in the level of immunity globally that it’s going to make a huge dent in the ability of the virus to mutate, because the less that’s transmitted, the less opportunity it has to mutate,’ he says.

On the other hand, he says identifying and sequencing new mutations in countries with extremely high caseloads and struggling testing facilities may still present a challenge.

So, there’s still challenges in terms of detecting these variants and responding to them quickly.’

Can we adapt better to new variants in future?

While new variants may be always around the corner, Bennett says that just as the virus is changing, so are we, both as individuals and as a collective.

Human conscious intervention is important here,’ she says. If the virus reaches a point where it’s causing too many problems, we stop it from spreading, or we slow it down. If you had a variant that was so mild we didn’t really notice it, we wouldn’t respond and that would give the virus an advantage.

So, moderation of transmission changes also in line with the virulence of the virus, which tends to select versions of the virus that are milder.’

Moreover, the science behind our pandemic response is becoming increasingly sophisticated, and Bennett believes eventually we’ll be able to apply a more selective approach to managing cases, variant by variant.

We’re getting better and faster at distinguishing between lineages, even using our frontline testing PCRs, which might allow us to target particular cases.

So, if another variant turned up that was more virulent and we didn’t want that circulating, we might increase our testing and pick out the clusters of cases with that variant and actively shut it down. And, in the process, you’re giving the other variant which you’re less worried about an advantage.’

The other big difference is that Australia, for the most part, is no longer an immunologically naïve population.

The risk with pandemics is that it’s incredibly transmissible and virulent because we can’t fight it off,’ says Bennett. But as the population is exposed to both the virus itself and the full course of vaccination, we’re becoming more resilient to COVID-19 as a disease, regardless of variant.

If you’ve had some exposure in the past, that can protect you from serious illness because you don’t need incredibly high levels of antibody to stop that disease progression. That’s why the vaccines work against every variant so far in preventing serious illness, but not as well in preventing infection for all.’

That means that being vaccinated, boostered and, potentially, exposed, makes you less vulnerable to severe disease, which makes the disease less virulent – even among the elderly and the vulnerable.

So, in fact, we’re changing,’ Bennett says. That’s not to say that we should throw caution to the wind: There is still a great benefit if we can bring transmission under control, and we do know that now, with Omicron, that will take a booster.’

Ultimately, the best way to get the pandemic under control is to stop hoarding resources and gun for vaccine equity. Just today, modelling published in Nature Human Behaviour found that if wealthy countries donated just under half of their Covid vaccine supply to low and middle-income countries, death rates in those nations would diminish and new variants would be less likely to emerge. It’s a win-win.

If we can get the world access to the booster over the next year or so, and if the booster reduces symptomatic infection by over 60 per cent, that’s probably reducing all infection by somewhere between a third and a half of what we’d otherwise see,’ says Bennett. Then you slow down your mutation clock, delaying the time to the next variant.’

This article was originally published on Cosmos Magazine and was written by Amalyah Hart. Amalyah Hart is a science journalist based in Melbourne.

Published by The Echo in conjunction with Cosmos Magazine.

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    • Double face masks….wow!

      The layers of concealing is revealing….whatever works for you I guess.

      One shoe (or mask) certainly doesn’t fit all.

  1. The first rule of being a parasite is “Don’t kill your host”
    All viruses evolve to cause you as little trouble as possible.
    If you think you are being hunted by a thinking, sentient virus, you have a mental illness called Hypochondria

    • “Don’t kill your host”…global Covid death toll only 5.7million and climbing all the time. In Australia, scores dying everyday, it is more deadly here now then ever before.

    • A bit contradictory Steve. Exactly right that the virus isn’t consciously plotting its moves – mutations are random. It therefore doesn’t consciously follow rules like “don’t kill your host”. Although this feature – along with others that promote survival – may win the day through natural selection it’s all still random and involves twists and turns.

      SARS-CoV 2 came into existence with a few features that made it capable of evading this selective force. One feature is the number of days of asymptomatic infectiousness where someone will have time to move around freely in robust health – infecting others before being laid low. These newly infected will have the same time to infect the next tier.

      SARS CoV 2 has not evolved to be less virulent but the opposite – Delta was thought to be more virulent than the original virus and genomic boffins tell us that Omicron did not evolve from Delta but from another iteration of the original virus. Other data suggests it is equally as lethal as the original. The same genomic experts tell us that while increased infectiousness seems the most likely outcome of natural selection, there is nothing to suggest that future variants will be any less or more virulent.

      All the randomness and chaos of nature – nothing to be complacent about.


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