As many suspected from the outset, travel bans against South Africa and neighboring countries could turn out to be little more than a case of punishing the whistleblower. As CBS reports, Dutch health authorities are now reporting that the omicron variant was found in the Netherlands as far back as November 19, well before scientists in South Africa and Botswana first sounded the alarm about the highly-divergent new form of COVID-19. Similar tests in Belgium and Germany have also indicated the presence of the variant in those nations previous to the announcement out of South Africa.
This news is not likely to generate an immediate lift of the travel ban. That’s because the significant number of omicron cases in the area around Johannesburg represents the largest known outbreak of this new variant, and limiting travel to and from that region may hold some value. But the news out of Europe is another demonstration that South Africa is paying the price both for having one of the best systems for conducting genetic analysis, and for being transparent about the results of its analysis. The reaction to that transparency is troubling in terms of what happens the next time someone detects a particularly interesting variant — or a wholly new infectious agent.
In some ways, the not-unexpected news that omicron has been around longer than we thought could be good; because it could indicate that when it comes to outcompeting delta to become the dominate variant, omicron is not moving as quickly as some feared. On the other hand, the fact that is has now turned up in at least 20 nations (as of Tuesday morning), is a strong indicator that this variant can be easily transmitted through casual contact.
When it comes to the three big questions: How contagious is it? How evasive is it? How virulent is it? The answer to all three is the same. We still don’t know. But we are getting a few clues.
As of Tuesday morning, there’s some bad news and some potential good news on omicron.
The bad news, as reported by The Wall Street Journal, is absolutely expected. Early tests of monoclonal antibody treatments, like the one manufactured by Regeneron Pharmaceuticals, appear to be significantly less effective against the omicron variant. The same thing applies to a similar treatment from Eli Lilly.
Scientists expected this as soon as the high level of mutations in the omicron variant, and particularly the changes in the critical spike protein, became clear. Antibody treatments like those from Regeneron and Eli Lilly are, in a sense, frozen in time, targeting the version of the virus first sequenced by Chinese scientists in January 2020. The Emergency Use Authorization from Eli Lilly’s antibody cocktail, bamlanivimab, was suspended in the fall after it proved to be relatively ineffective in fighting delta.
Unlike these treatments, vaccines produce a much broader series of immune responses. That’s part of why vaccines have a much better efficiency rate of preventing hospitalization and deaths than antibody treatments. States like Texas and Florida, where governor’s Greg Abbott and Ron DeSantis have been heavily leaning on antibody treatments while fighting against vaccine mandates, are going to see their already bad policies made worse, and everyone who develops COVID-19 may soon see the antibody option removed from the table—at least until these companies update their antibodies.
However, there’s also a ray of sunshine amidst all the gloom. Bloomberg reports that at least one physician dealing with omicron patients in South Africa is seeing radically different symptoms.
So far, the cases of omicron have been described as less life-threatening than delta. “I don’t think it will blow over,” said Dr. Coetzee, “but I think it will be a mild disease hopefully. For now, we are confident we can handle it.”
This is still extremely early. Most patients who die from COVID-19 do so after a struggle of weeks, and right now South Africa is looking at what seems to be a small number of verified omicron patients who had been symptomatic only for a few days. That said, it’s a hopeful sign. It’s certainly better than signals that omicron could be worse.
As omicron begins its spread, there’s been a resurgence of the myth that, over time, viruses decline in virulence until they become “just colds.” On the surface, this seems to make a kind of sense. After all, viruses need a host to replicate, and if that host is dead, their ability to spread is limited. So keeping the host alive and relatively healthy seems like a competitive advantage for the virus.
In the real world, there are multiple reasons why keeping the host around long term is such a minor factor as to be completely unimportant. The only evolutionary pressure present on a virus is reproduction. In a sense, that’s the only pressure on any organism, but in complex organisms, other behaviors can disguise that basic fact. In viruses, replication is all they do, and they can’t even do that without the help of a host organism.
In the case of the SARS-Cov-2 virus, what makes it so successful when compared to close relatives SARS and MERS is that SARS-CoV-2 is contagious even before symptoms appear.
SARS hits peak levels of virus in the respiratory system a couple of days after cough, fever, and other symptoms appear. So does MERS. When it comes to stopping an epidemic, the early presence of symptoms allows health care workers, as well as the infected, to make decisions that limit exposure of others.
But SARS-CoV-2 has “front-loaded” the period of contagion. The peak levels of infection for COVID-19 come right around the point of first symptoms. That includes a day or two before symptoms appear. The delta variant improved on this by significantly increasing the level of virus present in the respiratory tract. So people infected with delta literally walk around leaving plumes of virus particles, often at a point when they feel just fine. That’s the recipe for the mess we’re in right now.
Maximizing the period of contagion into the first few days of infection makes it possible for COVID-19 to spread not just before people are aware they are sick—and before the body can mount a successful counteroffensive. That front-loading of contagion also means that what happens next has almost no value to the virus. COVID-19 spreads fast and early. Patients could go on to completely recover. They could experience spontaneous combustion. Either result would have only a tiny effect on the overall level of spread.
That might not be completely true, since if there really were millions of people going up in flame, it would be nice to think that levels of caution would increase considerably. But given what we’ve seen over the last two years.…
In any case, there is such a small evolutionary pressure on the “get milder” side of the scale that it might as well not exist. An effect that can be seen in decades of dealing with HIV, centuries of battling polio, and thousands of years of smallpox. Despite appearing sometime around 10,000 BCE, smallpox still killed 300 million in the 20th century alone. How contagious is smallpox? Its rate of transmission is almost identical to that of the delta variant. How much did it decline in potency over a period of 12,000 years? Not at all.
Even so, there are a bevy of articles like this one from NPR circulating around, pushing the idea that we can simply wait COVID-19 out until it doesn’t matter. Articles that contain paragraphs like this:
This is a fundamental misreading of the experiment at the top of the article, one in which people had repeated exposure to a mild virus and developed a moderate degree of immunity. It’s based on treating SARS-CoV-2 as it it is already nothing more than a mild virus. Such that this is seriously put forward as a good idea:
The American Academy of Pediatrics reports that there have been 6,767,762 cases of COVID-19 among children. Of those, 25,747 have been hospitalized. 636 have died. For a statistician, those numbers don’t sound bad. For 25,747 families who have seen their child taken to the hospital, they’re terrifying. For 636 families they’re beyond reconciliation. As a policy, they’re incredibly unsupportable. For one thing, this completely ignores that millions of adults would die in such a national COVID party. In October, the CDC reported that at least 140,000 children in the U.S. had already lost a parent or guardian to COVID-19. Multiplying that number many times is a cruel price to pay for failing to develop better policies.
We can hope that omicron turns out to be a milder form of COVID-19. But if it is, that’s not because it’s being driven to that point by any evolutionary pressure. It’s because COVID-19 is incredibly widespread and RNA viruses tend to mutate easily. The result is that we’re getting hit by a variant that’s extremely different from what’s come before. Unless we adopt a policy that minimizes the number of infections, it won’t be the last one.
And the odds of a variant that is far more deadly, are just as good as the odds of one that is less.
Tuesday, Nov 30, 2021 · 7:56:18 PM +00:00 · Mark Sumner
This news is not likely to generate an immediate lift of the travel ban. That’s because the significant number of omicron cases in the area around Johannesburg represents the largest known outbreak of this new variant, and limiting travel to and from that region may hold some value. But the news out of Europe is another demonstration that South Africa is paying the price both for having one of the best systems for conducting genetic analysis, and for being transparent about the results of its analysis. The reaction to that transparency is troubling in terms of what happens the next time someone detects a particularly interesting variant — or a wholly new infectious agent.
In some ways, the not-unexpected news that omicron has been around longer than we thought could be good; because it could indicate that when it comes to outcompeting delta to become the dominate variant, omicron is not moving as quickly as some feared. On the other hand, the fact that is has now turned up in at least 20 nations (as of Tuesday morning), is a strong indicator that this variant can be easily transmitted through casual contact.
When it comes to the three big questions: How contagious is it? How evasive is it? How virulent is it? The answer to all three is the same. We still don’t know. But we are getting a few clues.
As of Tuesday morning, there’s some bad news and some potential good news on omicron.
The bad news, as reported by The Wall Street Journal, is absolutely expected. Early tests of monoclonal antibody treatments, like the one manufactured by Regeneron Pharmaceuticals, appear to be significantly less effective against the omicron variant. The same thing applies to a similar treatment from Eli Lilly.
Scientists expected this as soon as the high level of mutations in the omicron variant, and particularly the changes in the critical spike protein, became clear. Antibody treatments like those from Regeneron and Eli Lilly are, in a sense, frozen in time, targeting the version of the virus first sequenced by Chinese scientists in January 2020. The Emergency Use Authorization from Eli Lilly’s antibody cocktail, bamlanivimab, was suspended in the fall after it proved to be relatively ineffective in fighting delta.
Unlike these treatments, vaccines produce a much broader series of immune responses. That’s part of why vaccines have a much better efficiency rate of preventing hospitalization and deaths than antibody treatments. States like Texas and Florida, where governor’s Greg Abbott and Ron DeSantis have been heavily leaning on antibody treatments while fighting against vaccine mandates, are going to see their already bad policies made worse, and everyone who develops COVID-19 may soon see the antibody option removed from the table—at least until these companies update their antibodies.
However, there’s also a ray of sunshine amidst all the gloom. Bloomberg reports that at least one physician dealing with omicron patients in South Africa is seeing radically different symptoms.
So far, the cases of omicron have been described as less life-threatening than delta. “I don’t think it will blow over,” said Dr. Coetzee, “but I think it will be a mild disease hopefully. For now, we are confident we can handle it.”
This is still extremely early. Most patients who die from COVID-19 do so after a struggle of weeks, and right now South Africa is looking at what seems to be a small number of verified omicron patients who had been symptomatic only for a few days. That said, it’s a hopeful sign. It’s certainly better than signals that omicron could be worse.
As omicron begins its spread, there’s been a resurgence of the myth that, over time, viruses decline in virulence until they become “just colds.” On the surface, this seems to make a kind of sense. After all, viruses need a host to replicate, and if that host is dead, their ability to spread is limited. So keeping the host alive and relatively healthy seems like a competitive advantage for the virus.
In the real world, there are multiple reasons why keeping the host around long term is such a minor factor as to be completely unimportant. The only evolutionary pressure present on a virus is reproduction. In a sense, that’s the only pressure on any organism, but in complex organisms, other behaviors can disguise that basic fact. In viruses, replication is all they do, and they can’t even do that without the help of a host organism.
In the case of the SARS-Cov-2 virus, what makes it so successful when compared to close relatives SARS and MERS is that SARS-CoV-2 is contagious even before symptoms appear.
SARS hits peak levels of virus in the respiratory system a couple of days after cough, fever, and other symptoms appear. So does MERS. When it comes to stopping an epidemic, the early presence of symptoms allows health care workers, as well as the infected, to make decisions that limit exposure of others.
But SARS-CoV-2 has “front-loaded” the period of contagion. The peak levels of infection for COVID-19 come right around the point of first symptoms. That includes a day or two before symptoms appear. The delta variant improved on this by significantly increasing the level of virus present in the respiratory tract. So people infected with delta literally walk around leaving plumes of virus particles, often at a point when they feel just fine. That’s the recipe for the mess we’re in right now.
Maximizing the period of contagion into the first few days of infection makes it possible for COVID-19 to spread not just before people are aware they are sick—and before the body can mount a successful counteroffensive. That front-loading of contagion also means that what happens next has almost no value to the virus. COVID-19 spreads fast and early. Patients could go on to completely recover. They could experience spontaneous combustion. Either result would have only a tiny effect on the overall level of spread.
That might not be completely true, since if there really were millions of people going up in flame, it would be nice to think that levels of caution would increase considerably. But given what we’ve seen over the last two years.…
In any case, there is such a small evolutionary pressure on the “get milder” side of the scale that it might as well not exist. An effect that can be seen in decades of dealing with HIV, centuries of battling polio, and thousands of years of smallpox. Despite appearing sometime around 10,000 BCE, smallpox still killed 300 million in the 20th century alone. How contagious is smallpox? Its rate of transmission is almost identical to that of the delta variant. How much did it decline in potency over a period of 12,000 years? Not at all.
Even so, there are a bevy of articles like this one from NPR circulating around, pushing the idea that we can simply wait COVID-19 out until it doesn’t matter. Articles that contain paragraphs like this:
This is a fundamental misreading of the experiment at the top of the article, one in which people had repeated exposure to a mild virus and developed a moderate degree of immunity. It’s based on treating SARS-CoV-2 as it it is already nothing more than a mild virus. Such that this is seriously put forward as a good idea:
The American Academy of Pediatrics reports that there have been 6,767,762 cases of COVID-19 among children. Of those, 25,747 have been hospitalized. 636 have died. For a statistician, those numbers don’t sound bad. For 25,747 families who have seen their child taken to the hospital, they’re terrifying. For 636 families they’re beyond reconciliation. As a policy, they’re incredibly unsupportable. For one thing, this completely ignores that millions of adults would die in such a national COVID party. In October, the CDC reported that at least 140,000 children in the U.S. had already lost a parent or guardian to COVID-19. Multiplying that number many times is a cruel price to pay for failing to develop better policies.
We can hope that omicron turns out to be a milder form of COVID-19. But if it is, that’s not because it’s being driven to that point by any evolutionary pressure. It’s because COVID-19 is incredibly widespread and RNA viruses tend to mutate easily. The result is that we’re getting hit by a variant that’s extremely different from what’s come before. Unless we adopt a policy that minimizes the number of infections, it won’t be the last one.
And the odds of a variant that is far more deadly, are just as good as the odds of one that is less.
Tuesday, Nov 30, 2021 · 7:56:18 PM +00:00 · Mark Sumner