Will Covid-19 Become a Common Cold?

The omicron variant is claimed to be clinically milder than delta. Is this the first step down the endemic path?
16 December 2021


The Omicron variant of Covid-19


Rolling down my sleeve post my Covid-19 booster, I pull up a pew alongside my fellow vaccinees in the after-jab “chill out” room where you loiter afterwards while they make sure there are not going to be any complications...

As the clock ticks and I await my escape back to work on the wards, the pause gives me a moment to reflect on whether this present pattern - variant; surge; looming lockdown; new booster; do pass furlough (if you’re lucky); do collect £200 - will be the pattern of our lives for the months and years ahead. But, somehow, I don’t think it will be. And I have history, and evolutionary biology, on my side.

The reason we’re all dashing headlong for boosters at vaccine centres - which are, incidentally, easy to spot - you just look for the long queue of disaffected people standing outside in the rain, socially distanced and with only Facebook for friends - is because of Omicron. This is the WHO - World Health Organisation’s – new diplomatically-dubbed Covid-19 variant, the naming of which involved skipping a few letters from the Greek alphabet to avoid offending anyone called Xi. Clearly they’re not on Dominic Raab’s Christmas card list, or at least they didn’t get the memo about the new anti-wokery Bill.

Omicron was first picked up about a month ago in southern Africa. Patient zero was a young man who walked into South African GP Angelique Coetzee’s surgery with a set of symptoms remote from the usual Covid-19 “Holy Trinity” - of anosmia (loss of smell and taste), fever and a cough - that we’ve been schooled to look out for as heralding possible Covid-19. This man chiefly had a “scratchy” throat and felt very fatigued. Despite Covid cases being very low in South Africa at the time, and in spite of his unusual symptoms, he was tested anyway. And when a further 7 people walked in with identical symptoms that day, and the PCR test results began to come back from the lab – signalling coronavirus infection – the decision to test was proven to be the right one.

But what was even more informative was the genetic make-up of the virus behind these cases: when the South African scientists lined up the genetic codes of the existing Delta variant that had been causing the majority of the country’s few hundred daily cases alongside the sequence from the latest infections, it was a chalk and cheese comparison. The virus behind the new infections was shot full of changes or mutations – 50 or so in all – with a big concentration of them centred on the part of the genetic code that the virus uses to code for the spike component of its outer coat.

That’s when alarm bells began to ring. The spike is the linchpin part of the virus that it uses to grab hold of and bust its way into our cells. Its key role means it’s also the structure targeted by the present generation of Covid-19 vaccines, making a mutant virus bearing a dramatically altered spike structure a huge potential risk for a world that has so far vaccinated over 50% of its population.

More alarming was the rapidity with which the cases of this new variant began to flood in. South Africa’s few hundred daily Covid cases turned into more than 10,000 a day, nearly all of them this new variant, provoking the WHO to declare it a variant of concern and Christen it “Omicron”. Some scientists said it should have been called “Oh my God”, based on its fearsome looking genetic profile.

But then came the paradox: despite many cases, including among vaccinated, unvaccinated and previously Covid-infected individuals indicating that Omicron does appear - as predicted - to be swerving quite nicely around the barriers of pre-existing immunity, there hasn’t been the same intensity of consequences. The proportion of people on oxygen, or requiring more intensive hospital care, is much lower than with Delta. People are recovering more quickly too, and the number of affected older people seems to be a lot lower. So far, medics in South Africa estimate that the case fatality rate of their Omicron outbreak is about 0.5% compared with 3% for Delta.

Admittedly, it’s still very early days. Patients don’t catch Covid and immediately head off to hospital, or worse to the mortuary, and it’s too soon to gauge the risk of longer term sequelae, like long Covid, but these data do look very encouraging. Perhaps encouraging enough to make one seriously entertain the idea that perhaps this is a glimpse of where the Covid-19 pandemic is ultimately heading: towards a more mild illness that is a tolerable inconvenience for all, rather than a death sentence for some.

Back in the late 1800s, the pathologist Theobald Smith (no relation, although that’s an easy mistake to make when there are so few of us around) hypothesised that illnesses naturally become more mild with time because it’s in the interest of both the host (us) and the disease to become better bedfellows. A more benign disease is better tolerated and less likely to provoke us to erect barriers to stop it spreading than something lethal that rapidly runs out of victims to infect.

Smith based his theories on cows rather than humans, and his ideas were certainly an over-simplification of the reality where, just like stocks and shares, the virulence of infections can rise as well as fall, but we’ve seen sufficient other examples of viruses attenuating their aggressiveness over time to make us take this idea seriously for Covid-19.

A handful of rabbits introduced to Australia alongside the first colonists swelled subsequently to a population measured in the hundreds of millions. To control their numbers, myxoma virus, a rabbit relative of smallpox, was introduced to the country in 1950 where it devastated the population, killing off over 99% of the animals. But, subsequently, the virus lost its virulence and the lethality fell as the rabbits adapted to tolerate the pathogen, and vice versa.

This happens because viruses are parasites. They are effectively an infectious – though very tiny - bag of genes. Without us they have no home, so for an entity that exists solely to reproduce itself, excessive virulence can sometimes be a serious shot in the foot.

So could this happen with Covid-19? Indeed, is this happening with Covid-19? Is the virus, in the face of the measures with which we confront it, including existing human herd immunity conferred by vaccines and prior infection, now adapting in a more benign direction, or is Omicron just a distraction that will eventually peter out? The answer is that it might be, and this is where history can help, because we have strong evidence that it’s happened before, including with a coronavirus that still circulates today.

In 1890 a pandemic swept the globe and the death toll was more than a million. It was put down to flu, but, in more recent years, scientists have pieced together various lines of evidence suggesting that it was instead caused by a bovine coronavirus. This virus, which we now imaginatively call OC43, jumped the species barrier into humans, probably in much the same way that Covid-19 owes its origins to a bat virus. Just as in Wuhan in late 2019, where urbanisation, high population density, live food markets and a highly mobile and densely-connected populace fed an explosive outbreak, the same factors provoked bovine coronavirus to spread among overcrowded city-dwellers.

The 344 page report on the outbreak, penned in 1891 by “Dr Parsons”, documents strikingly similar symptoms to Covid among those afflicted, and even talks about a post-viral syndrome eerily similar to “long Covid”. The extreme vulnerability of older people and those with pre-existing health conditions, as well as relative sparing of younger people are also highlighted.

So what happened in the aftermath? Scientists suspect that, having spread rapidly among a population devoid of any immunity, the 1890 coronavirus left in its wake a herd of immune survivors who then, throughout the rest of their lives, periodically caught the virus again as their immunity waned and was then “topped up” by the encounter, but the disease was never as bad as each individuals first mild childhood encounter owing to underlying immune memory. We suspect that the virus retreated into the background, acquiring some genetic changes along the way to facilitate its persistence in humans, to become one of four common cold-causing coronaviruses that we all periodically catch from the time we’re born to the time we die. And because we have a lifetime’s experience of catching it, just like Covid spares kids, it never makes us very ill.

This gives us an insight into a possible direction that Covid might be taking, with Omicron. This variant is highly transmissible – possibly twice as much so as its Delta cousin –  and, consequently, it’s rapidly displacing the more aggressive Delta to become the dominant circulating strain. You can never say never in medicine, and it’s not a given that other, more aggressive variants won’t surface from elsewhere in the months ahead, but wouldn’t it be a nice Christmas present if Omicron does turn out to be like OC43, and more mild in nature despite being here to stay...


Could we engineer a more contagious, less virulent strain of SARS-CoV-2 with a very short incubation period for release into the population in an attempt to displace the more virulent forms of it? Try to shortcut the process. Isn’t it true also that having one virus for some reason makes it less likely that you’ll get infected by another? So even in the short term a ‘weaker’ SARS-CoV-2 with a short incubation period could have immediate benefits in displacing Omicron.

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