November 12, 2020

The pandemic caused by the novel coronavirus SARS-CoV-2 has gripped the world for most of a year. The virus that now dominates the globe, however, is not the one that first emerged in Wuhan, China. Instead, most current cases are caused by a mutant variant of the virus called D614G.

This form of SARS-CoV-2 likely emerged in Europe in early 2020. It rapidly outperformed the original Wuhan variant, becoming the dominant strain around the world by late spring.

A study in Science shares some of the first concrete findings about how the now-prevalent mutated strain compares with the original. The study was led by researchers in the Baric Lab at the University of North Carolina at Chapel Hill’s Gillings School of Global Public Health.

Dr. Ralph Baric

Dr. Ralph Baric

“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,” says Ralph Baric, PhD, the William R. Kenan, Jr. Distinguished Professor of epidemiology at the Gillings School and a professor of microbiology and immunology at UNC’s School of Medicine.

Baric has studied coronaviruses for more than three decades and was integral in the development of remdesivir, the first FDA-approved treatment for COVID-19.

“[In this study,] you’re asking the two viruses to compete head-to-head,” Baric remarks in an episode of the BBC’s The Science Hour. (His interview runs from the 1:40 to 12:45 marks). “The contemporary variant completely dominates.”

Dr. Yoshihiro Kawaoka (Photo by Jeff Miller/University of Wisconsin-Madison)

Dr. Yoshihiro Kawaoka (Photo by Jeff Miller/University of Wisconsin-Madison)

For the recent study, Baric Lab researchers — including first author Yixuan J. Hou, PhD — worked in collaboration with Yoshihiro Kawaoka, PhD, and Dr. Peter Halfmann, PhD, both virologists on faculty at the University of Wisconsin-Madison.

“The original spike protein had a ‘D’ at this position, and it was replaced by a ‘G,’” Kawaoka says. “Several papers had already described that this mutation makes the protein more functional and more efficient at getting into cells.”

That earlier work, however, relied on a pseudotyped virus that included the receptor-binding protein but was not authentic. Using reverse genetics, Baric’s team replicated a matched pair of mutant SARS-CoV-2 viruses that encoded D or G at position 614 and compared basic property analysis using cell lines, primary human respiratory cells, and mouse and hamster cells.

Kawaoka and Halfmann contributed their unique coronavirus study model, which uses hamsters. Their team — including Dr. Shiho Chiba, who ran the hamster experiments — performed replication and airborne transmission studies with both the original virus and the mutated version created by Baric and Hou.

They found that the mutated virus not only replicates about 10 times faster — it’s also much more infectious.

Hamsters were inoculated with one virus or the other. The next day, eight uninfected hamsters were placed into cages next to infected hamsters. There was a divider between them so they could not touch, but air could pass between the cages.

Researchers began looking for replication of the virus in the uninfected animals on day two. Both viruses passed between animals via airborne transmission, but the timing was different.

With the mutant virus, the researchers saw transmission to six out of eight hamsters within two days, and to all the hamsters by day four. With the original virus, they saw no transmission on day two, though all of the exposed animals were infected by day four.

“We saw that the mutant virus transmits better airborne than the [original] virus, which may explain why this virus dominated in humans,” Kawaoka says.

The researchers also examined the pathology of the two coronavirus strains. Once hamsters were infected, they presented essentially the same viral load and symptoms. (The hamsters with the mutated strain lost slightly more weight while sick.) This suggests that while the mutant virus is much better at infecting hosts, it doesn’t cause significantly worse illness.

It’s important to note, the researchers caution, that these pathology results may not hold true in human studies. Hamsters don’t die from COVID-19.

Among the study findings, there was one very bright spot: The D614G strain may spread faster, but Baric says it is also slightly more sensitive to neutralization by antibodies.

The mutation affects the crown-like spikes that give the coronavirus its name. When these spikes latch onto the ACE2 receptors of human cells, infection follows. The D614G mutation causes a flap on the tip of one spike to pop open, allowing the virus to infect cells more efficiently but also creating a pathway to its vulnerable core. With one flap open, it’s easier for antibodies — like the ones in the vaccines currently being tested — to infiltrate and disable the virus.

“SARS-CoV-2 is an entirely new human pathogen and its evolution in human populations is hard to predict,” Baric notes. “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.”

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