How Kovid-19 mutations are changing the epidemic

At the beginning of its existence, Kovid-19 gained a capability that would prove to be decisive in his relationship with man. The virus saw a small change in its genetic code. This was the possibility of an unfortunate accident – a piece of genetic information from another virus mixed with coronovirus, while they were both infecting a bat.

Although included within this small fragment of the genome, there were instructions that an important part of the virus had been altered – its spike protein. This important protein studs outside the coronavirus and is the part that binds to the outside of the cells, allowing the rest of the virus to enter inside, where it can replicate.

This change in the spike protein of Kovid-19 meant that it could hijack an enzyme found in the human body called ferrin. This enzyme acts like a pair of molecular scissors, normally cutting open hormones and growth factors to activate them. But when the furin is part of the Kovid-19 spike protein, which is usually folded out of the virus in a series of loops, it opens like a hinge.

“It uncovers a new sequence in the spike protein,” says Yohei Yamuchi, a reader of viral cell biology at the University of Bristol, UK, who is studying how this change led Kovid-19 to become more infectious in humans May have been done. “This is one of the changes that make this virus really different from previous coronaviruses that caused Sir and Mers.”

This new mutation meant that Kovid-19 could suddenly latch onto a key molecule scattered outside human respiratory cells called neuropilin. This molecule helps to deliver material deep inside cells and into tissues – the mutation was like the key to Kovid-19 means a new gate in our cells and viruses can replicate in greater numbers in the human airways.

Although this mutation was just one in the short existence of Kovid-19, it proved to be important. Some researchers believe that this may be one of the major mutations that allowed coronaviruses to jump species and cause fast-spreading disease in humans. But almost as soon as it did so, it started picking up other mutations.


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