There has been a lot of speculation about the ‘new variant’ of the Covid-19 virus. But how is it different and why? Is it really responsible for the intensity of this second wave of infections? And is the government really giving us the best advice to avoid infection?
The new variant of the virus is different in that it has 14 mutations to its genetic material, in particular to the ‘spike’ proteins that help it latch onto and infect human cells. It was detected quickly because the Polymerase Chain Reaction (PCT) Covid tests check for the presence of three different spike proteins, one of which is different in the new variant. So the new variant shows up positive in PCT tests for two of the proteins, but not the third.
It’s not clear at the moment why the new variant is more infectious. It doesn’t seem to be any more virulent – there’s no evidence that symptoms are worse, or that death rates are higher, for the new variant. However, the fact that the new variant has quickly become more prevalent than the original strain seems to imply that it has a competitive advantage over the original strain. There could be all sorts of reasons for that. It could, for example, survive better in air, so is more easily transmissible through aerosols (more about those later). Or it could be that it causes more frequent asymptomatic infections than the original strain, meaning that its victims are more likely to come into close contact with people who are infected, but don’t know they are.
It’s important to note that these changes to the virus occur through purely random mistakes that crop up when copying the viral genetic code. Most of these mistakes will result in changes that are inconsequential, or are disadvantageous to the virus, so quickly die out. But once in a while, an error in copying viral genetic code will result in a change that benefits the virus, by making it more infectious, or displaying less severe symptoms in its host. This copying error process isn’t peculiar to viruses – it happens in all living things. It happens in humans, too. But for us, 20 years or so has to pass before each generation can pass its genetic code on to the next generation. For a virus, that generation time is just hours or minutes. This is evolution in action – it’s just much quicker for viruses than it is for humans.
However, this evolutionary process means that it’s unlikely that a new emerging strain will cause more severe symptoms or higher death rates, unless that’s coupled to much improved transmissibility. For the virus to succeed in making more copies of itself, it needs its host to mix as much as possible with new hosts. That’s not going to work if the symptoms it generates in the host are so severe that the host has to stay in bed and can’t mix with new hosts, or if it kills its host. The ‘perfect’ virus would be one that troubles its host very little, with symptoms limited to modifying host behaviour to help the virus infect new victims. The viruses that have got closest to this are arguably the ones that cause the common cold – not a single virus, but a collection of sophisticated viruses that cause similar symptoms, including some Coronaviruses. They never (or hardly ever) kill their host, and produce only symptoms of coughing and sneezing that help the virus get into a new host.
There are some exceptions to all that, perhaps. Smallpox was a scourge of communities across the globe for centuries. Smallpox had a death rate of 30%, with lower death rate strains never evolving. However, it was extraordinarily transmissible. The Variola virus that causes smallpox can survive in completely dry conditions for weeks, meaning it could be transmitted around the globe on cotton and wool bales. However, the severity and extreme transmissibility of this virus invoked an international vaccination programme that led to the extinction of the virus outside of laboratories – a remarkable achievement for international scientific endeavour, but not great for the virus. From a viral point of view, it failed to adapt through evolution, and paid the price. Why didn’t smallpox evolve to become less lethal? Its ability to survive as a dry, dormant particle means it doesn’t depend on host-to-host transmission, so isn’t particularly obstructed by killing its host. For centuries it had been so successful, that it evolved stable genetic material that was unable to mutate and adapt to changed conditions when it needed to.
But let’s return to our familiar Covid-19 virus. This new strain does seem to be more transmissible, the evidence being that it’s almost replaced the original strain, in the UK at least. But there has, until recently, been a flaw in the advice and rules given to control the virus, particularly for this new variant. At the start of this pandemic, the line was that Covid-19 was transmitted by surface contact, with the virus able to survive for 72 hours on indoor surfaces, and droplets expelled by coughing, shouting, singing, and generally by infected people projecting bits of wet muck out of their noses and mouths.
The two-metre rule emerged because it was believed that surfaces and droplets were the main source of transmission. Two metres was deemed to be the maximum distance expelled droplets would travel before falling to the ground. In the early weeks, no-one much was talking about aerosols. But that view changed. In September 2020, 200 leading scientists wrote to the WHO asking them to emphasise aerosol transmission rather than droplet transmission. And an article in The Lancet in October pointed out that of all the studies carried out around the world on Covid transmission from surfaces, none had succeeded in isolating viable viruses in sufficient quantities to cause an infection in ‘real world’ rather than laboratory settings.
So what’s the difference between droplets and an aerosol? It’s all about size. Droplets expelled by an infected individual are about 100 microns across (0.1mm). These do indeed fall to the ground. Think of it like a can of spray paint – squirt it into the air, it falls to the ground quite quickly. But if the virus is simply breathed out by an infected person as individual viral particles, those are much smaller. They’re around 100 nanometres – a tenth of a micron. That means they’re small enough to remain suspended in air, not fall to the ground.
To visualise how an aerosol behaves, think of cigarette smoke. Cigarette smoke is an aerosol. The particles are a bit larger than Covid-19, but not much – about five times the size, on average. Think back to the days before the smoking ban. If you were in an unventilated bar or restaurant, and a couple of people were smoking, you were well aware that you were breathing it in, all the time you remained in the room. But if you walk past someone on the seafront who’s smoking, you might get a whiff of it, but that’s all – it quickly disperses. The cigarette smoke analogy isn’t a bad test to use when assessing risk from Covid aerosols. Of course, an infected person will still expel virus in droplets when they cough, shout, sing, or whatever. But it’s not the only route to infection, and probably not the riskiest. It’s not difficult to see how pubs, restaurants, gyms and indeed schools are such fertile ground for the virus.
However, despite all this, the core safety messages from the government remained the same, until quite recently. Even now, the difference between infection by droplet and infection by aerosol hasn’t been made clear. True, the advice now includes ventilating rooms and not meeting anyone at all in an enclosed space. But the nature of the risk is not well understood by most people. Social distancing is still valuable, but not in a ‘1.5 metres bad, 2.5m good’ sort of way. It’s all about graduated risk. And if you’re spending a long time in an unventilated room with other people, it’s not going to help much at all.
So the new variant might be more infectious because it transmits better as an aerosol. To me, that seems the most likely explanation. But the fact that aerosols are now believed to be the commonest route to getting infected needs to be communicated more effectively. Yes, washing hands is still a good thing to do, and helps to reduce risk. Wearing face masks is a good way to prevent droplets being expelled, but doesn’t do all that much to stop aerosols. Not getting infected by aerosols is all about avoiding those aerosols. Just stay away from other people, particularly indoors. Treat everyone outside your household as if they’re infected. Think of them breathing out cigarette smoke – would there be a risk of you inhaling it? If yes, then you’re at risk of getting Covid.
We will be out of this soon. As spring comes, the combination of increased UV light and warmer temperatures will help to make aerosol virus particles unviable, as it did last spring. But this time, we have the vaccine too. We can keep that infection curve sloping downward, and avoid a third wave. Until then, it’s up to all of us to keep ourselves safe, and in doing so, keep everyone else safe too. And its up to government to provide the advice that best helps us all to do that.