ABOVE: Merged images illustrate multiple antibodies (green and red) binding to the wildtype SARS-CoV-2 spike protein, which is produced by human cells (DNA in blue, left). In cells (DNA in blue, right) that produce a version of the spike protein with deletions, some antibodies fail to bind (absence of green), while others (red) still attach well.
KEVIN MCCARTHY AND PAUL DUPREX
When SARS-CoV-2, the virus behind the COVID-19 pandemic, first emerged, scientists expected it to evolve slowly because the virus copies its big RNA genome with a polymerase that also corrects errors, thus minimizing the chance for certain types of mutations. This enzyme functionality isn’t present in other RNA viruses such as influenza and HIV, which accumulate single nucleotide polymorphisms, where one nucleotide is substituted for another, much more quickly than SARS-CoV-2 does.
This genomic stability was thought to be good news for vaccine design, but it’s become apparent in recent ...
