Early in its existence, Covid-19 gained an ability that would prove decisive in its relationship with human beings. The virus picked up a seemingly small change in its genetic code. It was likely an unfortunate accident – a fragment of genetic information from another virus got muddled up with that of the coronavirus while they were both infecting a bat.
Included within this tiny piece of genome, however, were the instructions that altered a key part of the virus – its spike protein. This important protein studs the outside of the coronavirus and is the part that attaches to the outside of cells, helping the rest of the virus to sneak inside where it can replicate.
This change to Covid-19’s spike protein meant it could hijack an enzyme found in the human body called furin. This enzyme acts like a pair of molecular scissors, normally cutting open hormones and growth factors to activate them. But when furin snips part of the Covid-19 spike protein, which is normally folded in a series of loops on the outside of the virus, it opens like a hinge.
“This exposes a new sequence in the spike protein,” says Yohei Yamauchi, a reader in viral cell biology at the University of Bristol, UK, who has been studying how this change may have led Covid-19 to become more infective in humans. “It is one of the changes that make this virus really different from previous coronaviruses that caused Sars and Mers.”
This new mutation meant Covid-19 could suddenly latch onto an important molecule found scattered around the outside of human respiratory cells called Neuropilin 1. This molecule helps to transport material inside cells and deeper into tissues – the mutation was like handing Covid-19 the keys to a new door into our cells and meant the virus could replicate in greater numbers in the human airways.
Although this mutation was just one in Covid-19’s short existence, it proved to be important. Some researchers believe it may be one of the key mutations that allowed the coronavirus to jump species and begin causing a rapidly spreading disease in humans. But almost as soon as it did this, it began picking up other mutations.