Alpha, beta, delta, gamma, lambda: a succession of fast-spreading variants are raising Covid-19's risk – and experts say we can expect to see many more. Science reporter Jamie Morton looks at the three big questions surrounding them.
Why are we seeing variants?
From the moment Sars-CoV-2 broke out of China and spread across the globe, the threat of new variants emerging wasn't just a possibility, but a certainty.
Nearly 20 months later, scientists have recorded many new strains of the new coronavirus, all of which share a common ancestor in the parent strain, or so-called "wild type".
Not all of them are worrying, but four in particular - B.1.1.7 (Alpha), B.1.351 (Beta), B.1.617.2 (Delta) and P.1 (Gamma) – very much are.
Officially designated as "variants of concern" by the World Health Organisation, they've been shown to spread quickly - and often cause worse infections and death.
While alpha was between 43 and 90 per cent more transmissible than earlier variants, delta - the driver of India's devastating second wave and Sydney's current mass-outbreak - could even be between 30 and 100 per cent more transmissible than alpha.
Meanwhile, scientists are closely watching another variant, labelled C.37 or lambda, and so far deemed a "variant of interest", that's been tearing through South America.
By the time the main variants emerged at the end of last year, the parent strain had already done an effective job of travelling around the world and infecting millions.
So why did they arise?
"Viruses, like all life, evolve," Otago University virologist Dr Jemma Geoghegan explained.
When a virus replicated by copying its own genome it sometimes made mistakes.
We know these mistakes better as mutations.
If they occurred in other biological entities, like ourselves, mutations were usually quickly spotted and fixed.
RNA viruses typically didn't have that ability, but one of them – coronaviruses like Sars-CoV-2 – did to some extent, and thus evolved more slowly, at a rate about half that of influenza.
Viruses went through periods of evolution when they spilled over into new hosts, and learned how to better infect them.
That wasn't to say mutations didn't happen by chance.
But if a certain mutation provided some advantage, like more easily invading cells, then it became more likely that it increased in frequency.
And the longer a virus was able to spread from host to host, Geoghegan said, the greater was its opportunity to drive new variants.
"Once a variant starts to spread more quickly, it's a simple mathematical process that drives it to become a dominant variant," added Dr David Welch, a computational biologist at the University of Auckland.
For instance, the delta variant spread approximately twice as quickly as the parent strain, so would go on to infect more people before its ancestor had the chance to reach them.
In the variants of concern we've seen so far, Welch said there were a number of specific, structure-changing mutations that all come together to make those variants transmit more quickly.
These mostly tended to occur around the virus' "spike protein", which it used to bind to the ACE2 receptor that gave it entry to human cells.
In the case of high-risk variants like delta, which took mere months to spread across more than 80 countries, the changes meant they didn't just infect more people, but could do more harm.
One study into delta suggested a separate mutation could help its ability to fuse with human cells once it latched on – which then allowed it to infect more cells and ultimately overwhelm immune defences.
The Delta variant spreads more easily than other SARS-CoV-2 variants. Help stop the spread of Delta and other variants by getting vaccinated against #COVID19 as soon as you can.https://t.co/xbvNiaVJKV— CDC (@CDCgov) July 8, 2021
How far down the variant road are we?
"As long as the virus spreads, it will continue to evolve," Geoghegan said.
Because its evolutionary history could be tracked over time, scientists have been able to observe around two mutations each month, which gave some indication of the path ahead.
But still, Welch said, it was difficult to predict its future evolution.
"Any theories about the direction that transmissibility or severity may take only really apply in the very long term, so we can't predict what may happen over the next year or even decade, if at all," he said.
"The virus has now passed through many millions of people and a reasonable guess is that it has enough opportunity to find the variants which are fittest.
"But, we can't rule out there are other combinations of mutations that could make it even more effective at spreading, or cause more serious disease."
The emergence of the delta variant, which appeared to have achieved higher transmissibility through a very different collection of mutations than the alpha variant, was especially worrying, he said.
In another concerning development, the rare case of a 90-year-old Belgian woman who died in March with the alpha and beta variants showed it was possible to be infected with two strains at the same time.
Welch said that, once a large proportion of the population had some immunity to the virus, we could expect to see evolution driven more by "immune escape" – or the ability to infect those who've been vaccinated or have natural immunity.
"If such variants arise, they would have a large advantage over other variants in a largely vaccinated population."
Many scientists have already suggested that Sars-CoV-2's future will be a permanently-circulating seasonal virus, like the flu.
But right now, Welch said there was still such a vast pool of susceptible people that the virus was comfortably able to circulate in summer.
As the level of immunity increased, he added, the underlying rate of transmission would need to be higher to spread within the population – and that might only happen in winter, thus making it a cold-season virus.
"A virus that spreads as easily as this could only be eradicated by co-ordinated worldwide action and, we have seen, most countries lack the appetite or ability to eliminate it," he said.
"As borders reopen and travel resumes in countries like Aotearoa that have eliminated it, we expect it to be reintroduced regularly and begin to circulate widely."
How are vaccines faring against variants?
The good news is that the vaccines we have today, like the Pfizer shot that most Kiwis will receive, are still highly effective at preventing disease, even against variants.
But Welch pointed out they were still somewhat less effective at preventing transmission.
"So even if we had very high vaccine uptake throughout the population, including in children, we'd still expect to see some circulation of the virus."
In Australia, the Victorian Premier has hinted at a "very different set of rules" at the start of next year - providing enough Australians have received both doses of vaccine.
Daniel Andrews said opening up communities and the country to the rest of the world was still risky even after one shot, and promoted variants and mutations.
It was just that fear that had led many epidemiologists to condemn the UK's decision to relax restrictions.
What do we know about the #COVID19 Delta variant so far? How can we assess our risk? What strategies should we play to protect ourselves whether we are in a low vaccination or high vaccination setting?#ScienceIn5 with Dr @mvankerkhove ⬇️ pic.twitter.com/QNJa5cmzu7— World Health Organization (WHO) (@WHO) July 5, 2021
Here, modelling by Te Pūnaha Matatini researchers has indicated that 83 per cent of Kiwis would need to be vaccinated against less transmissible virus strains, like the original wild type, for measures like lockdowns and 14-day quarantine to be no longer needed.
Yet 97 per cent of the population would need both Pfizer shots to abandon such measures if the country was hit by a wave of a strain as transmissible as the delta variant.
"If a person infected with a more transmissible variant leaked through New Zealand's border controls, and this sparked a community outbreak, it could be very hard to eliminate," Te Pūnaha Matatini modeller Dr Rachelle Binny said.
At the least, hard social distancing measures like level 4, rapid contact tracing and other measures would likely have to be thrown against an outbreak involving multiple variants.
"Even if the virus can be eliminated, it takes much longer on average, and we would expect high numbers of infections and fatalities before the outbreak is contained," Binny said.
"Every time someone gets infected with the virus, there is a chance of a new variant emerging by mutation so our best defence is to keep case numbers low."
Another new modelling study co-authored by Binny showed that vaccinating as much of the population as possible – and as quickly as possible – remained the best hope to stopping new variants.
It also suggested it could be better to prioritise giving updated variant-resistant shots to those who hadn't yet been vaccinated, over high-risk people who'd already received two doses of vaccine.
In one simulated scenario, which assumed no vaccine was available, the modelling showed that either the disease proved to be self-limiting and variants died out after the population reached herd immunity, or it evolved too fast to be stopped, hitting the point where it began circulating like influenza viruses.
In the latter case, the researchers observed how in the second of two waves, peaking around day 450 of their modelled outbreak, a large number of new variants sprouted, quickly rendering natural elimination through herd immunity impossible.
A second scenario they explored assumed that regularly-updated vaccines were available, and that they had 100 per cent effectiveness and take-up among the population.
Further, they assumed that each of the new vaccines were aimed at the variant that was most prevalent on the day the vaccines began to be rolled out, and which hadn't been targeted before.
While this modelling found that faster vaccine updates – happening as rapidly as every 50 days – were more effective in achieving elimination, this only had a marginal effect if the vaccination rate was slow.
"When enough people in a population are vaccinated, new variants are less likely to arise and outbreaks of existing variants can be more easily controlled with contact tracing and lower alert levels," Binny said.
"If new variants emerge that are resistant to current vaccines, then our model suggests that the faster vaccines can be updated to target these new variants, the better our chances of elimination."
Yet, even when New Zealand completed its vaccine roll-out, she said there'd still be a risk of new vaccine-resistant variants emerging in outbreaks abroad.
"This could undo a lot of our hard work, so it's also important that New Zealand works with other countries to achieve high vaccination coverage globally."