Omicron was first really discovered last week.
Seriously, it was last Wednesday, Nov. 24, when South Africa detected the unusual coronavirus variant and immediately told the World Health Organization. And essentially the whole coronavirus world of scientists — a huge number of professionals involved, at this point — has been trying to figure it out around the clock since then.
To be honest, this means that there just hasn’t been a lot of time for the experiments with the information you’d really want to know most of all to happen.
But there are hints — things we can guess at with low or medium certainty, given the information we have so far. We, of course, don’t want to claim that we know things that we don’t, but we’re not completely in the dark either. In particular, I’d like to give a shoutout to epidemiologist Kristian G. Andersen, whose informative Twitter thread compiled those hints and helped shape this story.
So let’s dig in. My hope is that this article will give you the contours of what scientists are thinking right now about omicron, what information is to come, and what to look for in the news in the coming weeks. Here’s all you need to know about omicron — the variant with the unfortunate honor of being named after the scariest-sounding of all the Greek letters.
Why are scientists worried about omicron?
You know how airport security checks everyone, but selects a small number of people for random, more invasive inspection? Some coronavirus testers do the same, randomly sending a number of samples from their day-to-day testing to labs to find out about how the virus is changing.
When South African scientists did that last week on a sample gathered at the beginning of the month — and props to South Africa on inspecting as many samples as it does — they found the viruses they were seeing were very different than the ones they saw as recently as last month. In particular, the new viruses had about 40 differences in their genetic sequence compared to the original coronavirus in its spike protein (the part of the virus that gives it its distinctive spiky-crown shape). Those differences are called mutations, randomly inserted as the virus makes errors in the copying process.
Those differences were notable. Some of the changes were ones we’ve seen in the other variants you’ve heard of: alpha, beta and delta. Those changes, we know from significant experimentation, are ones that make the virus more contagious and make it a little easier to evade antibodies.
For some other changes among the 40, we have good hypotheses on what they do; unfortunately, we think they make the virus stronger, either by making it easier to transmit from person to person or by making it easier to evade antibodies.
And, finally, there are some changes among the 40 that we don’t have any idea what they do. They could be good or bad; we just don’t know yet.
We also don’t know yet how these mutations interact with one another. There is the possibility that these mutations, most of which likely help the virus out individually, actually counteract one another in practice. That’s something that happened with the beta variant, which led to it petering out.
Is it spreading more than other coronavirus variants?
The mutations-canceling-out theory is hurt by one piece of evidence: omicron took over in South Africa as the major form of the coronavirus there, and quickly, too. It took only about two weeks for omicron, in the blue, to gain the lion’s share of sequenced samples in the nation.
Not only that, cases are also rising in South Africa, too. A graph of cases there shows a sharp uptick in positive tests. It’s not yet huge, but it doesn’t portend a good trend.
Remember that South Africa is in the Southern Hemisphere, so this isn’t an expected winter rise in cases but a summer one. That’s not a good sign, and so South African doctors raised the red flag to the WHO really quickly.
How did it develop?
Just like biologists do with animals that evolve from one another over millennia, epidemiologists keep track of the evolution of viruses using trees, to try to figure out how different features of the viruses came about.
The story of omicron is actually super interesting. It clearly didn’t evolve from the most common variant, delta. Overall, the omicron sequence actually has more in common with the original Wuhan strain from the beginning of the pandemic.
That’s pretty unusual for one virus type to have such a long branch, where we don’t see evolutionary progress for so long, and then all of a sudden see big changes. So what happened here? Well, there are essentially three guesses:
1. That the virus evolved in human populations that we weren’t studying closely, like those in significant parts of sub-Saharan Africa.
2. That the virus evolved in the friendly confines of one individual with a very, very long case of COVID-19, battling it out with an immune system for months in a way that led to these mutations.
3. That an animal population caught the old version of COVID from a human, and as it spread among the animals, it mutated. Then, eventually, the evolved form was passed back to humanity.
Option No. 1 is generally regarded as unlikely due to just how quickly omicron spread in South Africa and that there is still some virus surveillance in sub-Saharan African nations. No. 2 might be the most commonly cited hypothesis right now. If true, and it may well be, it’s a remarkable story — and individually unlikely, though certainly plausible in the aggregate, when you consider how many people struggle with long infections. No. 3 might be the most worrying, because of the implications of this kind of mutation-gathering in animals that is going to be very difficult to track.
It doesn’t much matter where omicron came from, but knowing more about its origins will give us an idea where to look even earlier for other future variants. More research in this space is to come.
Why is it winning in South Africa?
So why would omicron be spreading so quickly in South Africa? Well, there are basically two nonexclusive possibilities:
1. It is more transmissible than delta.
2. It escapes previously held immunity better than delta.
The problem is that both of these would look pretty similar on case graphs. You’d need more detailed data to be able to figure out what kinds of people are getting the disease.
But because we are so early in this, we don’t really have that data. So we have to be content with not knowing for a couple of weeks — a period that we’re in the middle of now.
OK, but what if you had to guess? Yes, reader, we’re officially entering in to “slightly informed speculation” territory now. I wouldn’t say this is irresponsible speculation, but we do have to acknowledge the high likelihood of error.
Here’s one early hint, compiled by computational epidemiologist Christian Althaus. Essentially, Althaus studied how quickly omicron took over from delta in South Africa, and then asked: What if all of that speed was due to increased transmissibility? Well, while delta has an estimated transmission coefficient (or R0) of 5-6, Althaus calculated that omicron would need to have a coefficient of somewhere between 10 and 30.
Is that possible? Sure. Is it likely? Probably not. That R0 would just be higher than any other coronavirus (SARS or non-SARS) that we’ve seen.
Probably most likely is a combination of the two factors: that the virus spreads well and that mutations in the virus make it a bit harder for immune system antibodies to deal with, leading to more reinfections and vaccinated people being infected. That certainly would make sense, too, given the mutations in the spike protein. But again, we’ll need more data to know for sure.
Does it cause stronger disease?
We don’t have evidence that it does. There’s no anecdotal evidence of surprisingly severe omicron cases. In fact, the limited evidence would point in the other direction, but perhaps most likely is no difference at all.
A graph of case growth vs. hospitalization growth in South Africa, compiled by Financial Times writer John Burn-Murdoch, shows that cases have exploded more quickly than in previous coronavirus waves, but hospitalizations largely have followed the same pattern as with other variants.
But there are caveats: Much of the spread in the first couple of weeks has been in university students. And then there’s the fact that it’s only been a couple of weeks. Sometimes it takes people a couple of weeks to be hospitalized after contracting COVID. We’re possibly missing some of these just because it’s early.
Why would omicron be weaker? Well, one possible explanation is that, if it is indeed better at attaching to cells in your body than previous forms of the coronavirus, thanks to its mutations, that you might see its effects take hold in the upper respiratory tract (your nose, your throat) rather than in the lower respiratory tract (your lungs). That means a more transmissible disease, but also one that’s less severe — a scratchy throat is better than a scratchy lung.
But, again, we’re really, really early. And the simplest result — and maybe most likely, if you’re a believer in Occam’s razor — is that there’s no significant change in disease severity.
How well will your vaccination work?
OK, I saved this question for last. Forgive me, but I had to make you read through the rest of the article somehow! This is really what you want to know: Will your vaccination work against omicron?
Given that the early evidence limply points to partial immune evasion, there is a possibility that your vaccine will be less effective in preventing infection. Likely not totally ineffective, but less effective.
Remember, this was true of the delta variant, too. Take Pfizer’s vaccine, for example: we saw 90% to 95% effectiveness against infection against the original coronavirus, but various studies found that it was 64% to 87% effective in preventing infection against delta.
But the vaccines did continue to do an amazing job at preventing hospitalization. In various studies against various variants, we’ve seen vaccine efficacy numbers between 89% and 96%. Alpha, beta, gamma, delta, you name it, were all largely stopped from sending people to the hospital.
Is there a possibility that omicron, thanks to its larger number of mutations, bucks this trend? Sure. But it’s essentially implausible to think that the vaccines wouldn’t work at all; just that their efficacy could be mitigated.
It’s possible that high-risk people would need to get an omicron-targeting booster, but previous studies with delta-targeting boosters essentially found no significant difference between that and a third standard boost. Both were essentially equally helpful.
The increased efficacy of vaccines against hospitalization makes some sense, given what we know about how the immune system works. Essentially, there are different levels of response in the immune system — preventing infection is one task given to one type of cells and fighting infection is another task given to another type of cells. While we care about both, the latter is certainly most important.
For those who do face significant disease, we also have far more effective treatments now than ever before. While monoclonal antibody treatments like Regeneron might become less effective, there’s no real reason to think that other staples like dexamethasone or tocilizumab would stop working. Around the corner, new pill-form treatments like Paxlovid and molnupiravir should work just as well, too.
What should you watch for in the next couple of weeks?
Here’s a partial list of what to watch for.
• As you’ve seen, omicron has been detected all over the world, including in the United States on Wednesday. Many of those index cases, though, have travel ties to South Africa. Do we start to see widespread community spread elsewhere — including here?
• We’re running experiments on how effective our vaccines are against the new variant. At first, these will be experiments in petri dishes, essentially measuring how many virus cells antibodies created by the vaccines neutralize.
You’ll probably see some misleading headlines about this. Let’s say they find that vaccine antibodies are two times less effective in killing the variant virus. Does that mean your vaccine is half as effective? No. Because your body is adept at creating lots of antibodies to meet demand, it means your vaccine drops from something like 95% effective to 90% effective.
On the other hand, if you see that the vaccine antibodies are 100 to 1,000 times less effective against omicron, then that’s probably worse news.
• We’re also running surveys and compiling data on how many South Africans have been infected and hospitalized by vaccination status. Vaccination is less common there than it is here, so this will take longer to get a valid sample size.
• We’re also getting more data on the severity of omicron infections.
• Watch for the development of omicron-targeting boosters, in case they’re needed.
In short, the fear of omicron essentially acting as a reset button on the pandemic is certainly overblown. We’ve made too many advances in the past two years to get to there.
But there is a real risk of some more familiar worries: higher transmissibility and/or immune evasion leading to another spike in cases, in both new infections and some reinfections from the unvaccinated and some vaccine breakthrough for the vaccinated. Those boosted with a third dose would likely fare best in this scenario.
While people with both vaccination-created immunity and immunity from previous infection are significantly less likely to be hospitalized with future cases, it’s also true any spike in cases will result in more hospitalizations in general than if there weren’t a spike. What we don’t know at this point is how large that spike could be. It could be a bump in the road, or it could be another wave of sickness that stresses our health care system, leading to lesser care for some with and without COVID.
Andy Larsen is a data columnist for The Salt Lake Tribune. You can reach him at firstname.lastname@example.org.