- It's been confirmed that SARS-CoV-2 has mutated in a way that’s enabled it to spread more quickly
- However, the spike mutation may also make the virus more susceptible to a vaccine
- As the study was not carried out on humans, additional studies are needed to track the consequences of these mutations
The new coronavirus has a complex biology, and, according to ScienceMag, accumulates about two changes per month in its genome (the genetic material).
Now, a new study by scientists from the University of North Carolina at Chapel Hill and the University of Wisconsin-Madison has revealed that, while SARS-CoV-2 has mutated in a way that's enabled it to be more infectious than other coronaviruses, the spike mutation may also make it more susceptible to a vaccine.
The findings, published in Science, note that the new strain, called D614G, emerged in Europe and has become the most common in the world.
Strain more sensitive to neutralisation
"The D614G virus outcompetes and outgrows the ancestral strain by about 10-fold and replicates extremely efficiently in primary nasal epithelial cells, which are a potentially important site for person-to-person transmission," study author Ralph Baric, professor of epidemiology at the UNC-Chapel Hill Gillings School of Global Public Health and professor of microbiology and immunology at the UNC School of Medicine, said in a UNC news release.
However, despite the D614G strain replicating faster and becoming the most common worldwide, the research team found that it is slightly more sensitive to neutralisation by antibody drugs.
Baric has studied coronaviruses for more than three decades. He was also integral in the development of remdesivir, the first FDA-approved treatment for Covid-19.
Why does the strain dominate?
Researchers believe the D614G strain dominates because it increases the spike protein’s ability to open cells for the virus to enter.
"The original spike protein had a 'D' at this position, and it was replaced by a 'G'," said Yoshihiro Kawaoka, a virologist at the University of Wisconsin-Madison." Several papers had already described that this mutation makes the protein more functional and more efficient at getting into cells."
The newly discovered mutation causes a flap on the tip of one spike to pop open, the researchers explained, thereby allowing the virus to infect cells more efficiently. It also creates a pathway to the virus's vulnerable core, they said.
On the bright side, with one flap open, it's also easier for antibodies, such as the ones currently being tested in vaccines, to infiltrate and disable the virus.
For this study, the researchers ran hamster experiments and performed replication and airborne transmission studies with both the original virus and the mutated version created by the team.
"We saw that the mutant virus transmits better airborne than the [original] virus, which may explain why this virus dominated in humans," said Kawaoka.
Pathology also examined
In addition to the above, the researchers also looked at the pathology of the two coronavirus strains.
After infection, the hamsters displayed more or less the same viral load and symptoms, suggesting that while the mutant virus is much better at infecting hosts, it doesn't cause significantly worse illness.
However, the researchers caution that these results may not reflect in human studies.
"SARS-CoV-2 is an entirely new human pathogen and its evolution in human populations is hard to predict," Baric said.
"New variants are continually emerging, like the recently discovered mink SARS-CoV-2 cluster 5 variant in Denmark that also encodes D614G.
"To maximally protect public health, we must continue to track and understand the consequences of these new mutations on disease severity, transmission, host range and vulnerability to vaccine-induced immunity," he commented.
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