According to Alexander Greninger, MD, assistant director of the UW Medicine Clinical Virology Laboratory at the University of Washington in Seattle, the mutation enhances the “springiness” of the parts of the virus that anchor onto our cells. In translation? The virus improved its game of infecting our cells when we come in contact with it.
There’s also another theory that the mutation P681R helps the virus to fuse cells together into clumps called syncytia, which basically means it turns into a factory for making viruses. This phenomenon has been seen by scientists before in other viruses, but as they say, no virus ever managed to create such large syncytia.
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