On Jan 9, 2020, about a week after the world first learned of a mysterious cluster of pneumonia cases in central China, authorities announced that scientists had found the culprit: A novel coronavirus.
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It was a sobering announcement and an unnervingly familiar one. Nearly two decades earlier, a different coronavirus had hurdled over the species barrier and sped around the world, causing a lethal new disease called severe acute respiratory syndrome, or SARS. The virus, which became known as SARS-CoV, killed 774 people before health officials contained it.
But even as scientists worried that history might be repeating itself, there was one glimmer of hope. Although all viruses evolve, coronaviruses are known to be relatively stable, changing more slowly than the common flu.
“There was, I think, a sense that would work in our favour and that the nightmare scenario of it being like influenza – constantly changing and needing updated vaccines all the time – would probably not be the case,” said Dr Adam Lauring, a virus expert and infectious disease physician at the University of Michigan.
What many scientists had not counted on was unchecked global spread. During the following weeks, the new virus, SARS-CoV-2, skipped from Wuhan, China, to a cruise ship in Japan, a small town in northern Italy and a biotechnology conference in Boston. Country by country, global coronavirus trackers turned red.
To date, more than 237 million people have been infected with the virus, and 4.8 million have died – 700,000 in the United States alone.
With every infection come new opportunities for the virus to mutate. Now, nearly two years into the pandemic, we are working our way through an alphabet of new viral variants: fast-spreading alpha, immune-evading beta, and on through gamma, delta, lambda and, most recently, mu.