A Simple Mutation Might Have Accelerated The Infection
70% of the sequences of ~50,000 CoV-2 genomes isolated from infected people around the world carry a simple mutation that might impart an increased ability of the virus to infect human cells. The mutation, first noticed by a researcher at Northwestern University Feinberg School of Medicine, designated D614G or "G" for short, has been found to affect the virus spike protein, which is the surface protein that gives the virus its distinctive “corona” and that binds to ACE-2 molecules on human cells in the lungs, GI tract and vascular endothelium. Lab studies suggest that the mutation in the spike protein enhances its binding to the ACE-2 receptor, thereby enhancing the virus infectability.
The mutation only changes one of about 1300 amino acid building blocks that make up the spike protein. It changes the spike protein amino acid #614 from “D” (aspartic acid) to “G” (glycine). The fact that 70% of viral isolates carry the mutation indicates that the mutation gives the virus variant an infectious advantage that has allowed it to dominate the original virus first identified in China.
The outer parts of the mutated viral spike protein are less likely to break off, which was a weakness of the original CoV-2 virus that originated in China. This weakness made the original virus harder to invade human cells. The “G” mutation makes the virus 10 times more infectious in lab experiments done at the Scripps Institute. Other researchers at the New York Genome Center and New York University, who were studying how the virus binds to and enters cells, but using the original strain isolated in January in China, had a very hard time getting the virus to infect human cells in tissue culture. When they switched to the “G” variant, they found a huge increase in infection, which agreed with what researchers at Scripps found. In human studies done at the Los Alamos National Laboratory, patients with the “G” virus variant typically carried a higher viral load, consistent with the greater infectious nature of the virus. A higher viral load would then make them more likely to spread the virus. In sum, a greater infectious ability and higher viral load, would likely accelerate the spread of the virus.
The mutation does not seem to affect the virulence of the virus. But, all of this points out that as mutations accumulate while the virus spreads, changes in its behavior due to changes in its genome are quite possible.
This is all very preliminary and the research has not been officially published, but it was made available as “preprint” research. The data have been submitted for publication. More research is needed to confirm the observations.
We will see.
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