The virus that causes COVID-19 is evolving, with new and more infectious variants taking hold.
Key points:
- Most mutations are harmless, but occasionally the virus acquires genetic changes that give it an advantage
- Mutations in the spike protein on the surface of the virus can make it easier for it to attach and enter human cells
- The more the virus spreads, the greater the chance a dangerous mutation will occur
Last week, Victoria entered a seven-day lockdown due to another COVID-19 outbreak.
That has now been extended for at least another seven days in Melbourne.
But what makes this outbreak different from others is the spread of a “highly infectious” variant that was first detected in India in October last year.
The variant is one of four that the World Health Organization (WHO) has identified as a global concern, with the others originally emerging in the UK, Brazil and South Africa.
Authorities in Vietnam have also identified a “dangerous” new hybrid variant that is a mix of the types first detected in the UK and India.
But how do these variants occur and what makes some more contagious than others?
Getty Images: Juan Gaertner/Science Photo Library
)
Variants with significant mutations in their spike proteins are listed as “variants of concern” by WHO, as they are associated with increased transmissibility and severity, and could have an impact on immunity.
“Those mutations can make the spike protein bind more tightly to the receptors of human cells, so you may get a better rate of success than you would if it didn’t bind as well,” Professor Mackay said.
“That might mean that more cells get infected in that person than happened with the previous variant.”
The B.1.617 variant that was first detected in India has two defining mutations in its spike protein: E484Q and L452R.
These mutations help the virus infect cells more easily and dodge the immune system’s antibody response.
The B.1.617.1 sub-lineage of the Indian variant — also known as Kappa — that is circulating in Victoria has an additional mutation in its spike protein called Q1071H.
The more infectious B.1.617.2 sub-lineage that is surging in the UK — also known as Delta — contains more mutations in its spike protein, but lacks the E484Q mutation found in Kappa.
Instead, it has T478K, another mutation that has been associated with high infection rates, particularly in Mexico and the United States.
How much more contagious are they?
While there is still not a lot of data on the Kappa sub-lineage, the spread of its more infectious counterpart in the UK can give us an idea of how it may spread, said Raina MacIntyre, who specialises in global biosecurity and infectious diseases at the University of New South Wales.
Read more about COVID-19 vaccines:
Delta is up to 50 per cent more transmissible than the B.1.1.7 variant — also called Alpha — first identified in the UK in December last year, Professor MacIntyre said.
On top of that, Alpha is already between 50 and 100 per cent more transmissible than the D614G variant that dominated in 2020.
“That means it may be much harder to control,” she said.
Professor MacIntyre also said that the Indian variant is now the most common type to escape hotel quarantine, accounting for over 20 per cent of all strains sequenced in Australia.
What about other mutations?
While spike mutations have gained the spotlight, other mutations may also give SARS-CoV-2 variants an advantage.
Other errors in the genetic sequence can help the virus make more copies of itself inside human cells.
“The virus just replicates more actively and more aggressively,” Professor Mackay said.
But he also said there was more to learn about the effects of these mutations and whether they helped the virus stay one step ahead.
“It’s still an open question as to how those other mutations interact and what role they play in creating variants that are more transmissible.”
How many more variants will we see?
While it’s difficult to predict how many new SARS-CoV-2 variants we can expect to see in future, one thing’s for sure: the virus, like all pathogens, will continue to evolve.
Getty Images: SOPA Images/Contributor
)Mutations occur randomly, but keeping an eye on how quickly they happen can give us an idea of whether these genetic changes will give rise to a variant, said Sebastian Duchene, a genomic epidemiologist at the University of Melbourne.
For instance, the UK’s Alpha variant accumulated around 20 mutations over three months — far more than the average rate of one or two mutations per month, Dr Duchene said.
“It had to move a lot faster for that period of time to accumulate mutations.”
In other words, the more people the virus infects, the greater chance it has of acquiring a mutation that gives it an advantage, according to Professor Mackay.
“With the sheer number of people that this virus has jumped from, there have been lots of opportunities for the virus to mutate into new and better versions,” he said.
“It’s the nature of pathogens that they continue to evolve and generate new mutants,” Professor Howden said.
“The more people are infected, the greater the probability of more variants emerging.”