Random variation is an essential component of all living things. It drives diversity, and it is why there are so many different species. Viruses are no exception. Most viruses are experts at changing genomes to adapt to their environment. We now have evidence that the virus that causes Covid, SARS-CoV-2, not only changes, but changes in ways that are significant. This is the first in a series of articles on how the virus changes and what that means for humanity.

In September 2020, a sample of the new coronavirus variant B.1.1.7, also known as the UK variant, was collected and identified for the first time. Within three months, B.1.1.7 would be, at least in Britain, the dominant strain of SARS-CoV-2. Today, its prevalence is estimated to be above 90 percent; its contagiousness, up to 75 percent greater than previous strains; and its viral load, higher too.

B.1.1.7 wasn’t the first variant to successfully overthrow its predecessor. Nor will it be the last, as the 501.v.2 variant, now the dominant strain circulating in South Africa, is already proving. But how do variants form in the first place? The answer goes back to the building blocks of life: the genome. More specifically, single-letter differentiations in viral RNA that may begin as mere errors, but when sufficiently multiplied increase a virus’s chances of survival. These are otherwise known as mutations.

To replicate its genome and thus reproduce itself, SARS-CoV-2 relies on an enzyme called the RNA-dependent RNA polymerase. As the polymerase does the mostly monotonous work of stringing together nucleotides—the organic, protein-coding molecules classified as either adenine (A), thymine (T), cytosine (C), or uracil (U)—a number of mistakes make their way into the mainframe. Many of these point mutations will ultimately be inconsequential. The ones that matter change proteins that impact how the virus functions, such as the spike protein.

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Originally published on Forbes (January 6, 2021)