Viruses that encode their genome in RNA, such as SARS-CoV-2, HIV and influenza, tend to pick up mutations quickly as they are copied inside their hosts, because enzymes that copy RNA are prone to making errors. After the severe acute respiratory syndrome (SARS) virus began circulating in humans, for instance, it developed a kind of mutation called a deletion that might have slowed its spread
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Despite the virus’s sluggish mutation rate, researchers have catalogued more than 12,000 mutations in SARS-CoV-2 genomes. But scientists can spot mutations faster than they can make sense of them.
Many mutations will have no consequence for the virus’s ability to spread or cause disease, because they do not alter the shape of a protein, whereas those mutations that do change proteins are more likely to harm the virus than improve it (see ‘A catalogue of coronavirus mutations’). “It’s much easier to break something than it is to fix it,” says Hodcroft, who is part of
Nextstrain, an effort to analyse SARS-CoV-2 genomes in real time.