Alpha, beta, gamma, mu, now omicron – it seems you can barely move these days without bumping into a new variant of COVID-19, and those are just the ones deemed worrisome enough to name. There are a mind-boggling number of distinct variants already out there that simply aren’t distinct and widespread enough to take notice of.

But is this a feature of COVID, or of any virus? Are we hearing about variants more now because there really are more – or just because we’re in the middle of a pandemic?

In short: is this normal?

All Viruses Mutate

What is a virus? It’s a pretty fundamental question, but the answer isn't as simple as you might think – even people who have studied them their whole lives can’t agree on things as basic as whether viruses count as alive or not.

At their core, viruses can be thought of as tiny self-replicating machines. They are made up of a piece of genetic material – DNA or RNA – protected by something called a capsid. Sometimes these base ingredients are accompanied by other structural elements – for instance, the “envelope” which protects the genetic material inside, or the infamous spike protein that gives COVID-19 its incredible infectious ability.

Viruses have one goal: reproduce. With reproduction comes mutation – it’s a process you might know better as “survival of the fittest.”

“Most mutations are random errors, and most of them actually don’t benefit the virus,” explained Dr Hana Akselrod, assistant professor of medicine at George Washington University School of Medicine and Health Sciences, to SciLine.

“Some may break it and make it non-functional. But once in a while, a mutation will arise that is of benefit to the virus […] This process has been going on throughout the course of the pandemic.”

Those benefits could be higher transmissibility, or increased ability to evade immune responses – two of the mutations that made Omicron so worrying when it was first studied. Alternatively, a mutation may provide a way to more effectively bind to the host cells, or create more copies of itself, Akselrod said, resulting in higher viral loads in those the virus infects.

Which other viruses mutate?

Have you ever wondered why you need a new flu shot each year? With many vaccines, you can get one before you hit elementary school and never think about it again, but influenza is different. The reason: it can, and does, mutate.

“The influenza virus, like every virus, contains a set of genes that are wrapped in a coat of protein,” wrote Anthony L. Komaroff, MD, Editor in Chief of the Harvard Health Letter.

“Vaccines typically stimulate the production of antibodies that attach to outer structures on the protein coat, disabling the virus; indeed, that’s how the influenza vaccine works. Unfortunately, these outer structures are constantly changing, so a new vaccine is needed each year to target those structures on the flu viruses that are currently circulating.”

In fact, the flu mutates even faster than COVID-19. However, while influenza viruses mutate quickly, they often don’t mutate dramatically; they “drift,” Dr Pedro Piedra, professor in molecular biology and microbiology at Baylor College of Medicine, told Forbes.

With a broad spectrum vaccine – the most common flu vaccine in the US protects against four different strains at once – such minor changes in the virus are unlikely to completely negate our immune defenses. The problem, Piedra pointed out, is when some major and completely new mutation occurs.

“That can cause a pandemic, because we haven’t seen it,” he said. “Something similar to what happened in 2009 and 2010, with the novel H1N1 [swine flu].”

Do mutations always make viruses more dangerous?

It might seem silly to say it explicitly like this, but viruses don’t care about your health. Whether you live, die, or even notice their presence at all isn’t important to them – they only care about living long enough to replicate.

“Different mutations can be selected or emerge independently […] so long as they carry a benefit to the virus,” said Akselrod. “So the virus gets an advantage from them and kind of gets a reason to keep them as it spreads.”

Sometimes, those mutations do result in a more deadly virus. Apart from the many deadly flu pandemics peppered throughout history, we’ve also seen this happen as recently as this year, with the discovery of a new strain of HIV. It also happened with the virus that causes Ebola: in 2014, the normally rare disease killed more than 11,000 people across West Africa when a glycoprotein – a molecule that does the work of finding a way into host cells – mutated to make the virus more transmissible in humans.

“That mutation happened several months into the outbreak, and would never have happened if we had stopped the virus early,” Pardis Sabeti, who co-led one of the teams who discovered the mutation, told The Atlantic. “It’s a reminder of the importance of working fast, and not letting these viruses have a lot of opportunities to reproduce in humans and adapt to them.”

However, becoming more deadly isn’t always the smart move.

“If the virus kills someone, if it kills the host, it dies with the host. So it totally defeats the purpose,” Jared Auclair, associate teaching professor of chemistry and chemical biology at Northeastern, explained. “The easiest thing for the virus to do is to stay in the same person for as long as possible … It’s less work, so to speak, as opposed to hopping to another host.”

Some scientists think that might be what caused the mysterious disappearance of the so-called “sweating sickness” in Tudor England. When it first appeared, this disease could leave healthy people dead in a day – leaving barely any time for the virus responsible to find another host. Perhaps, speculated virologist Derek Gatherer, the disease never disappeared at all – it simply evolved to reproduce better.

“Its reign of terror barely lasted a century,” he wrote in an article for The Conversation. “If indeed it was an ancient variant of [hantavirus] […] the virus may have mutated to a less virulent form, perhaps in the process acquiring the capacity to be passed between humans as a more benign feverish illness, rather than being just a sporadic environmental hazard.”

Is COVID-19 unusual?

This leads to the million-dollar question: is SARS-CoV-2 mutating unusually fast? As you may have guessed by now, the answer is: “not really.”

“[The mutation] rate in SARS-CoV-2 is not particularly remarkable,” Katie Kistler, a postdoctoral researcher who studies viral evolution at the Fred Hutchinson Cancer Research Center in Seattle, told Live Science.

In fact, the perception of COVID-19 as being exceptional in this respect probably comes down to a handful of factors. First, there’s the fact that the virus is zoonotic in origin – jumpinh from an animal into humans. That means it would have to go through a period of rapid evolution, Kistler explained: “the virus needs to adapt to infect humans rather than bats […] There are a lot of beneficial mutations available to the virus during that [transition] phase,” she told Live Science.

On top of the fact that the virus is in this high-mutation phase of its evolution, there’s another important factor at play: COVID-19 is highly transmissible. That doesn’t make each viral particle more likely to mutate individually, but overall, the chances of a mutation occurring somewhere are vastly increased.

“Each mutation is kind of like pulling a slot machine – the chance of hitting the jackpot on any individual pull is small, but you pull millions of handles simultaneously the chances are dramatically increased,” explained Dr Thomas Friedrich, Professor of Pathobiological Sciences at University of Wisconsin School of Veterinary Medicine, to SciLine.

"Viruses that ‘hit the jackpot’ by accumulating a set of mutations that makes them more transmissible will then increase in the population due to natural selection. As more people become immune through prior infection or vaccination, while transmission rates remain high, we may expect this sort of adaptation to continue.”

The drive to develop vaccines and therapies may also be a reason behind the apparently high number of COVID-19 variants, Live Science notes. With each new weapon against the virus, a new motivation for mutation is created.

Of course, there is one final reason that we’re more aware of COVID-19 variants than other diseases: we’re paying attention. While scientists across multiple disciplines pivot to monitoring the unfolding pandemic, it’s easy to forget that we aren’t always so clued into the inner workings of diseases.

“You can’t ignore the fact that these viruses evolve and become better adapted to human infection,” cautioned molecular virologist Dr Jonathan Ball to The Atlantic.

“We’ve kind of ignored the MERS coronavirus, which is still rumbling along in the Arabian peninsula. It’s endemic in some camel populations, and there are constant spillover events into humans. For the moment, that doesn’t go very far, but you can’t always rely on that lottery to come down in your favor.”