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In February of this year, back when the Delta variant was known only to a few experts under the name of B.1.671.2, I wrote an article about virus reproduction and how new variants form. A couple of months later, Delta was classified as a “variant of interest” by the World Health Organisation. A month after that, in May, Delta was classified as a variant of concern, and the news didn’t get better from there. Soon after, the Delta variant was detected in Australia, and in August it arrived in New Zealand. We all know how that story went.
Now, we are hearing about another frightening new variant – Omicron. So far, we don’t know much about it, but it is spreading, and it seems to be spreading fast. Faced with this news, I’ve decided to update my previous explanation of virus variants with new information about Omicron. I’ve included some of my original text from February, so if you are one of my most loyal readers, you may find some of this familiar. However, it has been updated and it bears repeating for those that are new.
Even if we didn’t realise it prior to the Covid-19 pandemic, most of us were already aware of the concept of viral variants. If you are like me, and get regular vaccinations against influenza, better known as the flu, then you are getting vaccinated against new variants, although with influenza they are usually called strains. There are so many new strains of the flu, that experts meet twice a year to discuss them. They analyse data collected by the World Health Organisation and use that data to predict which strains of the virus are likely to be the most common in the coming winters. From their predictions, they recommend which should be used to make the flu vaccine for the next season.
With the flu, we face an arms race against a virus that is constantly changing. Last year’s vaccine may not work to stop this year’s outbreak. But the experts’ meeting is not just about making the most effective vaccine. Some years, strains emerge that are particularly infectious, or particularly deadly. Flu experts are always looking out for the next pandemic.
To understand why this needs to happen with the flu and not, for example, measles, we need to understand more about the virus, or, more correctly, the virus group, since “the flu” is not a single disease caused by a single type of virus. There’s a whole world of influenza viruses out there, infecting people, cats, chickens, pigs, ducks, bats and even seals and whales.
There are four main types of influenza virus, usually known simply as influenza A, B, C and D. Of these, three are known to infect people, although only two, A and B, cause significant human disease. Although both A and B contribute to “seasonal flu”, it is influenza A which is the most diverse, which infects the greatest number of different animals, and which causes periodic pandemics.
Influenza viruses look similar to coronaviruses – they are both round viruses with protruding spikes made from protein. Inside, they both also carry their genetic code as RNA – a similar molecule to the DNA which carries the genetic code in human cells. When DNA and RNA are being copied, to make new cells or new viruses, there are sometimes errors in the copying process. These errors are known as mutations. However RNA is much more prone to error than DNA. Viruses with RNA, such as influenza, therefore have a higher mutation rate than DNA viruses, such as the virus which causes chickenpox.
RNA from a coronavirus (image credit: Crocothery/ Getty Images)
But even among the RNA viruses, mutation rates vary. Influenza viruses have a particularly high rate of error when they are reproducing, which explains, at least in part, why they are constantly evolving. Mutations are the raw material for evolution. Many mutations are harmful, and viruses with these mutations don’t survive. But some mutations are beneficial to the virus, and so viruses with these mutations are more successful. Over time, viruses with the beneficial mutations come to dominate, and the new variant replaces the previous one.
Coronaviruses, on the other hand, belong to a small group of RNA viruses that have a slightly different way of reproducing from influenza. The RNA copying process for coronaviruses includes a “proofreading” step, where mutations in the RNA are detected and fixed. As a result, coronaviruses have a much lower mutation rate than influenza. Based on the mutation rate, we wouldn’t expect to see Covid-19 change at the same rate as influenza, but there’s more to the story.
Evolution is a numbers game. With each new generation, whether it’s a virus, a weed growing in your garden or a human, some individuals will have mutations which are more beneficial to survival and reproduction. Those individuals will reproduce more effectively, meaning that there are more of them in the next generation. In the next generation, there will be even more, and so on, until the individuals are different enough to be called a new strain or variant. The faster the generation time, the faster this process happens. For a virus, the time can be measured in hours or, at most, a few days. In a single year, a virus can have as many generations as humans have had since we started sowing crops and domesticating animals.
There’s another factor in the numbers game as well. Over the last two years, fewer than 200 people have caught the Ebola virus. That hasn’t given it many opportunities to become better adapted to humans. Over the same period, more than 250 million people caught Covid-19. Even with a much lower mutation rate than influenza, the virus causing Covid-19 has had no shortage of opportunities to become better adapted. And that’s exactly what it has done – and will continue to do, until we get Covid-19 under control everywhere.
The latest variant, Omicron, is still very new. The earliest known case dates back only to the 9th of November. South African scientists first reported it to the World Health Organisation on the 24th of November. Two days later, an expert group met and decided it should be declared a “Variant of Concern”. Their conclusion wasn’t based on how the variant was behaving – it’s too soon to have much idea about that. Instead, it was mostly based on the number and type of mutations that Omicron carries.
Omicron has far more mutations than other Covid-19 variants. Mu – a variant which caused a lot of concern when it was labelled a “Variant of Interest” in August – has 6 mutations in the RNA that codes for its spike protein, while the Delta variant has 9. Omicron has 32. Some of Omicrons mutations aren’t new, for example, it has the one that makes Delta more transmissible than earlier variants. Other mutations are suspected to be a threat based on laboratory data (that is, a threat to us, not to the virus). Some mutations are completely new.
Although we know a lot about its mutations, we don’t know much about what Omicron actually does. There are suspicions that it may be more transmissible and that it may be able to overcome the immunity people have as a result of past infection or being vaccinated. It appears to be spreading rapidly in South Africa – but it’s not entirely clear whether the rapidly increasing case numbers are because people are now looking for it more. There are also indications of a much greater reinfection rate with Omicron when compared to other variants – meaning that a lot of people in South Africa who had Covid-19 before are now catching it again. However, because Omicron is so new, the paper reporting the reinfections is a pre-print – a draft version of an article that hasn’t gone through a scientific review process.
In fact, everything we know about Omicron so far is from preliminary information. Mostly we have pre-prints, blog posts and statements that scientists have made to the media. It is unsettling when the information is so uncertain, but there’s nothing much to do about it but wait for more definite answers. These answers will take time, but not too long. Based on the information I have seen so far, even in a week or two we will have much more certainty about rate of spread, the ability of the virus to evade existing immunity (whether due to past infection or vaccination), and whether Omicron can displace Delta.
More time be needed before we know how sick Omicron is making people. That is partly because there is often a lag between when people are infected and when they become seriously ill. But there is another reason as well. Each individual and each country is slightly different when it comes to Covid-19. At the individual level, we know that the severity of the disease depends on a range of complex factors such as age, underlying medical conditions and existing immunity. At the country level, how each variant behaves is related to vaccination rates, other public health measures, what happened in previous waves of the disease and population demographics. South Africa is very different from New Zealand. What happens in South Africa may not be repeated here.
We do know for certain that Omicron is already widespread. It has been found in more than 20 countries, including the United States, where it has been reported in 11 states. In many cases, it’s clear that it was already present before almost anyone had heard of it. The first cases in Australia were detected just one day after Omicron was declared a Variant of Concern. The first case detected in the United States was in someone who’d arrived from South Africa on the 22nd of November.
The situation with Omicron leaves us uncertain what is going to happen next. What does it mean for vaccination programmes, public health measures and international travel? Unfortunately it’s just too soon to know. In the meantime, the advice remains the same, wherever you are. Even if vaccines don’t work as well against Omicron, they are still likely to give some protection. While we wait and see what Omicron means for the world, it is still worth getting vaccinated.
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Nice explanation. Thank you.
Nice explanation Mel