![]() “That’s why we thought would not evolve very fast,” says Ravindra Gupta, a clinical microbiologist at the University of Cambridge.īut the virus quickly proved Gupta and his colleagues wrong. That’s because coronaviruses have proofreading proteins that correct errors introduced into the virus’ genetic material as it replicates. Both SARS-CoV and SARS-CoV-2 accumulate approximately two mutations each month half to one sixth the rate seen in influenza viruses. “It’s the worst-case scenario playing out.” March of the variantsĪdding to the oddities, the SARS-CoV-2 virus acquired genetic mutations much more rapidly than expected.Ĭoronaviruses usually mutate at lower rates than other RNA viruses, like influenza and HIV. “In a way, SARS-CoV-2 has found a way in which it can spread and also cause disease,” Andino says. SARS-CoV-2 is also harder to contain because it causes so many asymptomatic cases, people who can then unknowingly spread the virus. It was spreading faster than previous coronaviruses, and one reason, scientists suspect, is its ability to move efficiently from one cell to the next. Still, people weren’t paying as much attention to coronaviruses compared to the “really bad guys” like influenza, HIV, dengue viruses, Andino says. Then the 2012 Middle East Respiratory Syndrome (MERS) outbreak infected more than 2,000 people in 37 countries that virus has so far killed nearly 900. That changed with the 2002-04 Severe Acute Respiratory Syndrome (SARS) outbreak, which infected more than 8,000 people in 29 countries and left 774 dead. A study published in Nature showed that emerging infectious diseases originating in wildlife had increased significantly between 19.īut most experts were worried about influenza viruses and would not necessarily have expected a coronavirus to cause such havoc. As humans expand settlements into wild areas, they raise the odds of a new pathogen jumping from an animal to a person, giving rise to a deadly zoonotic disease. Worst-case scenarioĮxperts had been warning of some kind of looming pandemic for decades. Here’s what scientists have uncovered so far-and the mysteries that continue to tantalize and frustrate coronavirus experts. Two years in, there’s still a lot we don’t know about SARS-CoV-2, says David Wohl, an infectious disease specialist at the University of North Carolina. Scientists are racing to understand the biology of this new and perplexing syndrome called long COVID. Millions of people are grappling with symptoms that linger for weeks to several months after they’d been diagnosed with an infection. Even with the virus’s genetic blueprint in hand and the ability to decode the genomes of new variants within hours, virologists and healthcare professionals struggle to predict how its mutations will alter the virus’s transmissibility and severity. The original SARS-CoV-2 virus rapidly evolved into a string of variants that have hindered a return to pre-pandemic normalcy. The disease has since infected nearly 500 million people in almost 200 countries and killed more than six million people worldwide, and it’s not over yet.Īlong the way, this coronavirus has presented scientists with a bevy of surprises: Many experts are still amazed by how quickly the virus evolves, what it does to the human body, and how it moves in and out of other species. On March 11, 2020-exactly two years ago-the World Health Organization declared COVID-19 to be a pandemic. “It’s similar to an earthquake-you know the earthquake will happen, but normally you don’t think about it.” “The magnitude of it and the implications of it are still hard to comprehend,” Andino says.Īlthough experts in his field suspected a pandemic would occur, “it’s hard to know when,” he says. And yet he never imagined he’d witness a pandemic of this scale in his lifetime. For more than 30 years the University of California, San Francisco researcher has studied RNA viruses, a group that includes the virus that causes COVID-19.
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