A new coronavirus mutation is taking over the world. Here’s what that means. – Livescience.com

A mutation in the protein that allows SARS-CoV-2 to enter cells might make it easier for the virus to spread or it might not make a difference at all.
That’s the crux of a debate over a mutation known as D614G, which affects the spike protein
on the virus’ surface. The mutation is not new. It appears in low levels in samples taken from COVID-19 patients as far back as February. But this variation of the virus
(nicknamed the “G” variation) seems to show up in more and more of the virus samples taken from people infected recently compared to early in the pandemic.
A new paper, published July 2 in the journalCell
, argues that the rise in the “G” variation of the new coronavirus is due to natural selection. The study finds that virus particles with this mutation have an easier time making their way into cells, suggesting that it is outcompeting other strains of the virus to become the dominant version of SARS-CoV-2. Other, not-yet-published experiments have found similar results. However, some researchers are not yet convinced that the mutation has any real-world impact on coronavirus transmission
at all. Instead, it’s possible that the G variant’s spread is due to chance, said Nathan Grubaugh, an epidemiologist at the Yale School of Medicine who co-authored acommentary
accompanying the paper’s publication.
“The virus could have easily gotten lucky,” Grubaugh told Live Science.
Related: Live updates on COVID-19
G versus D
Original samples of the novel coronavirus
out of Wuhan, China, were a variation that scientists now call the “D” clade. Before March 1, more than 90% of viral samples taken from patients were from this D variation. Over the course of March, G began to predominate. This mutation is caused by the swapping of an adenine (A) nucleotide to a guanine (G) nucleotide at a particular spot in the coronavirus genome. It always appears alongside three other mutations that similarly swap one building block of RNA for another. (The letters in RNA help code for the proteins the virus makes once inside a cell.)
The G variant represented 67% of global samples taken in March, and 78% of those taken between April 1 and May 18. During this time, the locus of the outbreaks shifted away from China into Europe and the United States.
Related: 11 (sometimes) deadly diseases that hopped across species
 
The mutation piqued interest because it seemed to take over even in areas were the D variation had initially held sway, said Bette Korber, the lead author of the new Cell paper and a computational biologist at Los Alamos National Laboratory in New Mexico. She and her colleagues at Duke University and the La Jolla Institute of Immunology in California inserted the G mutation and D mutations into pseudoviruses, which are viruses engineered to display the surface proteins of other viruses. Pseudoviruses are useful, Korber told Live Science, because they can’t spread disease and because they contain molecular tags that researchers can use to track their movement into cells.
The researchers then exposed cell cultures to pseudoviruses with either the G or D variants of the coronavirus spike protein to track which was more infectious. They found that the G variations led to much higher amounts of virus in the cell culture, indicating increased infection and replication. The viral loads found from G variations of the spike protein were 2.6 to 9.3 times larger than from the D variations of the spike protein.
The pseudoviruses and cells used in the experiment were neither real coronavirus nor human lung
cells, but another study that used infectious SARS-CoV-2 virions reached similar findings. That study, which was published July 7 to the preprint server bioRxiv
and has not yet been peer-reviewed, was spearheaded by biologist Neville Sanjana at New York University. He and his colleagues tested the G and D versions of SARS-CoV-2 in cell cultures, including human lung cells, and found that the G variant infected up to eight times more cells than the D variant.
But just because a virus is better at infecting cells in a lab culture doesn’t mean it will be more transmissible in the real world, Grubaugh said. “If it just takes it

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