New Covid strain spreading across the UK that's less likely to cause symptoms
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How serious is the Omicron variant? What we know as cases rise.
As the world scrambles to make sense of the new coronavirus mutation and come up with plans to defend against it, Tom Whipple and Rhys Blakely analyse the story so far
We have three facts. There are three things that we know to be true. First, there is a new variant with troubling mutations. Second, that variant is now in many countries, including the UK. Third, it is already spreading fast in South Africa.
That information was enough. Even as the scientists in South Africa released their data to the world they predicted the world would punish them for it, that their economy and travel industry would suffer precisely because they had been skilled enough to sound the alarm. And their prediction was right.
Geopolitical predictions, though, are easy compared with epidemiological ones.
Beyond those three stark facts, there is so little data that everything is informed conjecture — back of the envelope calculations with uncertainties so large that the same figures can be used to give succour or presage doom.
But that has not stopped the world from trying. Already, we are getting a preliminary idea of what we are facing and — just as importantly — what to look for as more data comes in.
How fast is the Omicron variant spreading?
Gauteng province in South Africa had its pandemic under control. Like the rest of the country, cases were steadily decreasing. Until, suddenly, starting in the end of last month they weren’t. This was the first signal that something was wrong. From that signal — from the rise that we now know was caused by the new variant — we can estimate Omicron’s relative advantage
Louis Rossouw, a member of the Actuarial Society of South Africa’s Continuous Statistical Investigation Committee, calculated the reproduction rate in September — the one associated with Delta — to be 0.8. This meant that if ten people were infected they could pass it to eight: the pandemic shrunk. He calculated the R of Omicron to be above 2. Ten people were instead infecting 20.
There are caveats to this data. When numbers are small they can be skewed by what are known as “founder effects”. A single superspreader event can greatly inflate the apparent R. This time last year, the R in Britain was 0.8, but in one small part of Kent it was about 1.2. That difference, the difference caused by the Alpha variant, was enough to cause our devastating winter wave
Why is it spreading?
There are two attributes, not mutually exclusive, that would give Omicron the ability to outcompete Delta. It can beat Delta by spreading faster — by, for example, causing infected people to release more viral particles — or by spreading in people Delta cannot reach.
Which one it is doing matters. This time last year, with a population mostly lacking antibodies against coronavirus, a more transmissible variant was the real concern. Now, with an international wall of immunity built up, the big worry is whether it can knock out some of those bricks. Answering which it is requires complex epidemiological work, matching cases to vaccine and infection status. But Trevor Bedford, a virologist at the Fred Hutchinson institute, has computed the parameters.
Assuming the R numbers in Gauteng are correct, and that 85 per cent of the population already have antibodies, then the spread we see could be achieved with a variant that, for example, has the same transmissibility as Delta but escapes 50 per cent of immunity, or has 50 per cent higher transmissibility but escapes 30 per cent of immunity.
A study released yesterday may help fill in part of the picture. It suggests that Omicron is about 2.4 times as likely to cause a reinfection in somebody who has already tested positive in the past three months. “This finding is consistent with the hypothesis that unlike previous waves that were because the variants were intrinsically more infectious, Omicron appears to have substantial immune escape — at least from immunity caused by a natural infection,” Professor Paul Hunter, of the University of East Anglia, said.
“The big uncertainty is whether this increases the risk of severe disease, hospital admissions and deaths,” Hunter added. “With previous variants, protection against severe disease was better maintained than protection against infection. It remains to be seen how much protection against severe disease is maintained for Omicron.”
How serious is it?
So far, all we have is anecdote. Initial cases appear mild. But then the same is true with Covid in general: the vast majority recover, especially as preliminary spread is in the young. Despite a virology folk wisdom that viruses tend to mutate to spread more and kill less, Alpha and Delta were probably slightly more virulent. The assumption has to be that Omicron is equally deadly until proven otherwise. Even so, it may appear less deadly simply because so many people are protected. Yesterday South African scientists said that reinfections appeared to be less severe, just as we would hope.
How well will boosters work against Omicron?
Nobody can know for sure but the latest data is encouraging. A trial published today in The Lancet shows that a Moderna booster increased levels of antibodies by about 30-fold in people who had initially been given two doses of AstraZeneca. Pfizer achieved about a 25-fold increase. Importantly, another important part of the immune system — T-cells — were also lifted, with levels rising around three-fold with both boosters. The immune defences of people who had initially had two doses of Pfizer rallied to comparable levels.
The point is that these were people who already had excellent protection against Delta — from their first two shots — against severe disease and death.
That T-cells showed a good response is seen as particularly encouraging. Omicron is a concern, in part, because it has a large number of mutations in the spike protein that the virus uses to latch onto and break into cells. This may mean that antibodies, which bind to the spike to prevent new infections, work less well.
There are only a limited number of places on the spike that are recognised by antibodies, with six being particularly important for preventing infection. The fear is that Omicron’s mutations will alter them
But T-cells, which can destroy infected cells and are thought to guard against severe disease, can recognise more of the spike, making them less sensitive to mutations. One possibility spoken about by immunologists — and at this stage it really is only a theory — is that Omicron will cause infections by foiling the antibodies, but that the T-cells will step in and prevent people from becoming seriously ill.
As Professor Eleanor Riley, of the University of Edinburgh, who was not involved with the study, told The Times: “The T-cell results are definitely good news. The data suggest not much difference in T-cell response to Wuhan and Delta variants, suggesting that most variants remain susceptible to T-cells. Hopefully that is also the case for Omicron.”
What if the worst still happens?
The earliest breakthroughs gave us drugs that can help people who are seriously ill. Crucially these medicines do not attack the virus itself.
This means that they are unlikely to be affected by Omicron’s mutations.
Instead they calm the body’s response to the virus, by lessening the damaging surge of inflammation the bug leaves in its wake.
They include dexamethasone, a cheap, widely available steroid. Professor Sir Martin Landray, who co-led the trial which discovered that it works, said it was very unlikely to be affected. Neither would tocilizumab, which also suppresses the immune response.
Combined, the two drugs cut the risk of death by about a third for patients on oxygen and halve it for those on a ventilator. They remain at the centre of the NHS toolkit.
Will any drugs not work?
Medicines designed around the virus itself will be more vulnerable to Omicron’s mutations. These include treatments that contain lab-made mimics of the antibodies produced naturally by the immune system. These antibodies are designed to stick to the virus’s spike, preventing it from latching on to and infecting new cells.
But Omicron’s spike contains about 30 mutations, which may mean that antibodies developed to tackle earlier coronavirus strains might stick to it less well. Sajid Javid, the health secretary, has said that one of these antibody treatments, Ronapreve, may be less effective against Omicron
A similar drug made by GSK, called sotrovimab or Xevudy, was approved by the UK’s medical regulator today, after data showed it reduced the risk of needing treatment in hospital, and death by 79 per cent in high-risk adults with Covid symptoms. GSK said this morning that sotrovimab targeted parts of the virus spike not usually affected by mutations.
Penny Ward, a visiting professor in pharmaceutical medicine at King’s College London, said that sotrovimab had been designed to bind to a region on the spike protein of virus that causes Covid-19 that was also present in the coronavirus which caused the Sars epidemic of 2002. It is hoped that this will make it variant-proof.
A third class of drugs have been the hardest to get right, so-called “anti-virals” that sabotage the coronavirus’s ability to replicate during the early stages of infection. These don’t target the spike protein, and so there are grounds to think that they should work for Omicron, Landray said.
They include molnupiravir. Taken as a pill, it works by inserting itself in the virus’s genetic code, introducing errors. In essence, it forces the bug to mutate itself to death.
It was heralded as a wonder drug when the first press release was released detailing trial results and Britain has bought almost 500,000 doses.
However, newer findings have indicated that it is less effective than originally thought, cutting the hospital admissions rate by about a third.
The trick with these will be working out how to use them most effectively.
The country’s half a million doses would last the UK only a couple of weeks, if everybody with Covid was given molnupiravir. So the most vulnerable would have to be prioritised, Landray said
The country’s half a million doses would last the UK only a couple of weeks, if everybody with Covid was given molnupiravir. So the most vulnerable would have to be prioritised, Landray said
“At the beginning of the pandemic, if you got admitted to hospital with this virus there was nothing anyone could do other than put oxygen into your lungs and pump your lungs up and down. If things got bad, that was all there was,” Landray said. “We are a long way better off than we were back then.”
https://www.thetimes.co.uk/article/how-serious-bad-is-omicron-variant-zc9zt3cx0
As the world scrambles to make sense of the new coronavirus mutation and come up with plans to defend against it, Tom Whipple and Rhys Blakely analyse the story so far
We have three facts. There are three things that we know to be true. First, there is a new variant with troubling mutations. Second, that variant is now in many countries, including the UK. Third, it is already spreading fast in South Africa.
That information was enough. Even as the scientists in South Africa released their data to the world they predicted the world would punish them for it, that their economy and travel industry would suffer precisely because they had been skilled enough to sound the alarm. And their prediction was right.
Geopolitical predictions, though, are easy compared with epidemiological ones.
Beyond those three stark facts, there is so little data that everything is informed conjecture — back of the envelope calculations with uncertainties so large that the same figures can be used to give succour or presage doom.
But that has not stopped the world from trying. Already, we are getting a preliminary idea of what we are facing and — just as importantly — what to look for as more data comes in.
How fast is the Omicron variant spreading?
Gauteng province in South Africa had its pandemic under control. Like the rest of the country, cases were steadily decreasing. Until, suddenly, starting in the end of last month they weren’t. This was the first signal that something was wrong. From that signal — from the rise that we now know was caused by the new variant — we can estimate Omicron’s relative advantage
Louis Rossouw, a member of the Actuarial Society of South Africa’s Continuous Statistical Investigation Committee, calculated the reproduction rate in September — the one associated with Delta — to be 0.8. This meant that if ten people were infected they could pass it to eight: the pandemic shrunk. He calculated the R of Omicron to be above 2. Ten people were instead infecting 20.
There are caveats to this data. When numbers are small they can be skewed by what are known as “founder effects”. A single superspreader event can greatly inflate the apparent R. This time last year, the R in Britain was 0.8, but in one small part of Kent it was about 1.2. That difference, the difference caused by the Alpha variant, was enough to cause our devastating winter wave
Why is it spreading?
There are two attributes, not mutually exclusive, that would give Omicron the ability to outcompete Delta. It can beat Delta by spreading faster — by, for example, causing infected people to release more viral particles — or by spreading in people Delta cannot reach.
Which one it is doing matters. This time last year, with a population mostly lacking antibodies against coronavirus, a more transmissible variant was the real concern. Now, with an international wall of immunity built up, the big worry is whether it can knock out some of those bricks. Answering which it is requires complex epidemiological work, matching cases to vaccine and infection status. But Trevor Bedford, a virologist at the Fred Hutchinson institute, has computed the parameters.
Assuming the R numbers in Gauteng are correct, and that 85 per cent of the population already have antibodies, then the spread we see could be achieved with a variant that, for example, has the same transmissibility as Delta but escapes 50 per cent of immunity, or has 50 per cent higher transmissibility but escapes 30 per cent of immunity.
A study released yesterday may help fill in part of the picture. It suggests that Omicron is about 2.4 times as likely to cause a reinfection in somebody who has already tested positive in the past three months. “This finding is consistent with the hypothesis that unlike previous waves that were because the variants were intrinsically more infectious, Omicron appears to have substantial immune escape — at least from immunity caused by a natural infection,” Professor Paul Hunter, of the University of East Anglia, said.
“The big uncertainty is whether this increases the risk of severe disease, hospital admissions and deaths,” Hunter added. “With previous variants, protection against severe disease was better maintained than protection against infection. It remains to be seen how much protection against severe disease is maintained for Omicron.”
How serious is it?
So far, all we have is anecdote. Initial cases appear mild. But then the same is true with Covid in general: the vast majority recover, especially as preliminary spread is in the young. Despite a virology folk wisdom that viruses tend to mutate to spread more and kill less, Alpha and Delta were probably slightly more virulent. The assumption has to be that Omicron is equally deadly until proven otherwise. Even so, it may appear less deadly simply because so many people are protected. Yesterday South African scientists said that reinfections appeared to be less severe, just as we would hope.
How well will boosters work against Omicron?
Nobody can know for sure but the latest data is encouraging. A trial published today in The Lancet shows that a Moderna booster increased levels of antibodies by about 30-fold in people who had initially been given two doses of AstraZeneca. Pfizer achieved about a 25-fold increase. Importantly, another important part of the immune system — T-cells — were also lifted, with levels rising around three-fold with both boosters. The immune defences of people who had initially had two doses of Pfizer rallied to comparable levels.
The point is that these were people who already had excellent protection against Delta — from their first two shots — against severe disease and death.
That T-cells showed a good response is seen as particularly encouraging. Omicron is a concern, in part, because it has a large number of mutations in the spike protein that the virus uses to latch onto and break into cells. This may mean that antibodies, which bind to the spike to prevent new infections, work less well.
There are only a limited number of places on the spike that are recognised by antibodies, with six being particularly important for preventing infection. The fear is that Omicron’s mutations will alter them
But T-cells, which can destroy infected cells and are thought to guard against severe disease, can recognise more of the spike, making them less sensitive to mutations. One possibility spoken about by immunologists — and at this stage it really is only a theory — is that Omicron will cause infections by foiling the antibodies, but that the T-cells will step in and prevent people from becoming seriously ill.
As Professor Eleanor Riley, of the University of Edinburgh, who was not involved with the study, told The Times: “The T-cell results are definitely good news. The data suggest not much difference in T-cell response to Wuhan and Delta variants, suggesting that most variants remain susceptible to T-cells. Hopefully that is also the case for Omicron.”
What if the worst still happens?
The earliest breakthroughs gave us drugs that can help people who are seriously ill. Crucially these medicines do not attack the virus itself.
This means that they are unlikely to be affected by Omicron’s mutations.
Instead they calm the body’s response to the virus, by lessening the damaging surge of inflammation the bug leaves in its wake.
They include dexamethasone, a cheap, widely available steroid. Professor Sir Martin Landray, who co-led the trial which discovered that it works, said it was very unlikely to be affected. Neither would tocilizumab, which also suppresses the immune response.
Combined, the two drugs cut the risk of death by about a third for patients on oxygen and halve it for those on a ventilator. They remain at the centre of the NHS toolkit.
Will any drugs not work?
Medicines designed around the virus itself will be more vulnerable to Omicron’s mutations. These include treatments that contain lab-made mimics of the antibodies produced naturally by the immune system. These antibodies are designed to stick to the virus’s spike, preventing it from latching on to and infecting new cells.
But Omicron’s spike contains about 30 mutations, which may mean that antibodies developed to tackle earlier coronavirus strains might stick to it less well. Sajid Javid, the health secretary, has said that one of these antibody treatments, Ronapreve, may be less effective against Omicron
A similar drug made by GSK, called sotrovimab or Xevudy, was approved by the UK’s medical regulator today, after data showed it reduced the risk of needing treatment in hospital, and death by 79 per cent in high-risk adults with Covid symptoms. GSK said this morning that sotrovimab targeted parts of the virus spike not usually affected by mutations.
Penny Ward, a visiting professor in pharmaceutical medicine at King’s College London, said that sotrovimab had been designed to bind to a region on the spike protein of virus that causes Covid-19 that was also present in the coronavirus which caused the Sars epidemic of 2002. It is hoped that this will make it variant-proof.
A third class of drugs have been the hardest to get right, so-called “anti-virals” that sabotage the coronavirus’s ability to replicate during the early stages of infection. These don’t target the spike protein, and so there are grounds to think that they should work for Omicron, Landray said.
They include molnupiravir. Taken as a pill, it works by inserting itself in the virus’s genetic code, introducing errors. In essence, it forces the bug to mutate itself to death.
It was heralded as a wonder drug when the first press release was released detailing trial results and Britain has bought almost 500,000 doses.
However, newer findings have indicated that it is less effective than originally thought, cutting the hospital admissions rate by about a third.
The trick with these will be working out how to use them most effectively.
The country’s half a million doses would last the UK only a couple of weeks, if everybody with Covid was given molnupiravir. So the most vulnerable would have to be prioritised, Landray said
The country’s half a million doses would last the UK only a couple of weeks, if everybody with Covid was given molnupiravir. So the most vulnerable would have to be prioritised, Landray said
“At the beginning of the pandemic, if you got admitted to hospital with this virus there was nothing anyone could do other than put oxygen into your lungs and pump your lungs up and down. If things got bad, that was all there was,” Landray said. “We are a long way better off than we were back then.”
https://www.thetimes.co.uk/article/how-serious-bad-is-omicron-variant-zc9zt3cx0
zouzounaki
Olympian
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we are doomed. 
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Nah, article just looks long. Make a cup of tea and sit down to read it.... You'll be a'ight.we are doomed.
mick brown
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zouzounaki
Olympian
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what’s he saying today? positive? doom? no time to watch it just now…
knome
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Fairly positive. Omicron is not the end of the world despite the terrifying name putting the fear of a feary deity in Facebookies and Twitterers and the Sun.
zouzounaki
Olympian
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good to hear. so the end of the world is not nigh yet?
mick brown
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Looking good so far. Far less hospitalisations.
andipandi
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