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The coronavirus is mutating, just like most viruses, but the effect isn't as pronounced as some headlines suggest
You may have seen headlines popping up during the pandemic that SARS-CoV-2, the virus that causes COVID-19, has split into "strains" that are more contagious, more virulent or even easier to vaccinate against.
It's definitely something you've been asking us about:
I've heard that the coronavirus active during this second wave is a mutated version that's more contagious, which is somewhat responsible for the higher rates of infection. True or false or somewhere in between?
I read that in Australia, most infections, by proportion of age group plus actual case numbers, were in older age groups (60-70 and 70-80 year olds) prior to June, but now it's the 20-30 year age group. Why do you think this is? Has the virus changed/mutated to enable this, or is it just a factor of social/close contact?
Yes, the virus has mutated since it was first identified in Wuhan, China, in December last year. And yes, certain mutations are more common in different parts of the world.
But so far, these haven't made a material difference in how we should be fighting the virus, says Kanta Subbarao, a virologist at the Doherty Institute.
"[New strains] are certainly something that scientists are watching for. And, in the midst of a pandemic for which we need vaccines and we need to understand what's happening with the disease, it's an important question,"
Professor Subbarao says.
"But I don't think there's cause for panic.
"The mere fact we see a mutation doesn't mean it's advantageous or disadvantageous."
So why are some mutations completely benign and others potential cause for concern? Let's start with a quick back-to-basics on virus biology.
How viruses mutate
A mutation is a change in something's genetic material.
When a living thing replicates — whether it's a virus, or one of the cells in your body — it doesn't always make a perfect copy of the long, complicated strands of chemicals that make up its genetic material.
For living things made up of cells, like animals, plants, fungi and bacteria, that genetic material is in the form of DNA, and there's a built-in "proofreading" mechanism that picks up most of these errors.
On the other hand, many viruses' genetic material is in the form of RNA, a very similar long-stranded molecule but one that is a lot less stable and more prone to errors, or mutations.
"Most mutations lead to dead viruses," explains David Jacques, a virologist at the University of New South Wales.
But others are benign, and some might give the virus some kind of advantage — and get passed on to future copies of the virus.
Mutations can also be useful for researchers tracking the spread of the disease.
The small genetic changes, passed on as the virus travels from person to person, can draw links between different infections and show where someone most likely caught the virus.
This can be especially useful in cases where contact tracing draws a blank.
This virus is only mutating slowly
COVID-19 is often compared to influenza and has some common symptoms, but at a genetic level, the viruses themselves are quite different.
Influenza viruses are notorious for mutating rapidly, to the point where flu vaccines lose their effectiveness. That's why we're told to get a flu shot every year.
In contrast, coronaviruses don't mutate anywhere near as quickly.
Coronaviruses, the largest RNA viruses known, should be unstable and prone to lots of mutation. But unlike other RNA viruses, they have a proofreading enzyme that keeps them from mutating quickly.
"Coronaviruses mutate much slower than we might have expected for an RNA virus," Dr Jacques says.
"This gives hope that a vaccine will be successful."
Which mutations matter?
One recent study in the journal Cell described a mutation called D614G in a key protein in SARS-CoV-2, and found it was becoming more common as the pandemic progressed.
But there's no concrete evidence that this, or any other, mutation has changed the virulence of the virus, — that is, the severity of the disease it causes — says Edward Holmes, an evolutionary virologist at the University of Sydney.
The reason D614G has attracted more interest than many of the other mutations, which could fall anywhere among the 30,000-odd building blocks of the virus's genome, is that it's on the spike protein.
This protein makes up the bumps on the virus that allow it to enter our cells, and is the target of all the vaccines currently being developed.
"People are watching to see if there are any mutations that arise in the spike protein and become dominant," Professor Subbarao says.
"If you made your vaccine against the Wuhan strain, will it work against what becomes dominant?"
The D614G mutation is unlikely to impact the design of vaccines because it doesn't fall in a part of the spike protein that binds to protective antibodies, Professor Holmes says.
"However, there is some evidence the D614G mutation increases the infectivity of SARS-CoV-2 in a laboratory setting," he says.
"I also suspect that it gives some boost to the transmissibility of the virus in nature, although this is not completely proven yet and I doubt that any effect is substantial.
Professor Subbarao says the D614G mutation may be more common in some parts of the world, not because it gives the virus an advantage, but because of the "founder effect": the idea that it was simply present in the first cases that spread to those areas.
And while keeping an eye on mutations has important implications for vaccines and spread, it's unlikely the new coronavirus (or any other virus) will cause worse disease over time, says Dr Jacques.
"If I could make just one emphatic point, it would be that viruses almost never mutate to become more virulent," he says.
"They will try to mutate to avoid drugs and vaccines, but they almost certainly won't cause worse disease.
"There's no question that this coronavirus is bad, but its slow mutation rate gives us a really good shot at getting on top of it."
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