Why Covid ‘twin variants’ BA.4 and BA.5 spread so fast

7 月 15, 2022World News

Following a relatively quiet Covid period with a gentle decline in the number of infections and hospitalisations, the emergence of the “twin” Omicron BA.4 and BA.5 subvariants is causing figures to go up again around the world.

Experts have stated that a new summer Covid wave has started, although they expect the rise in infections to be “a hill, not a mountain.”




When the Omicron variant emerged last November, it seemed to appear out of nowhere: it was not a mutation from any of the Variants Of Concern (VOC), such as those that were first detected in the UK, South Africa or India – meaning that it lacked some mutations that gave those other variants a clear advantage.




By continuing to mutate, however, BA.4 and BA.5 now also possess the L425R mutation that made the Delta variant circulate much faster. This has resulted in two sub-variants with an unprecedented ability to (re)infect humans, according to Guido Vanham, emeritus professor of virology at the Institute of Tropical Medicine (ITG).

“It is clear that these subvariants are the champions of transmission,” he told De Standaard, explaining that the BA.4 and BA.5 sub-variants evolved from BA.2, which already was highly transmissible. “They only have a few additional mutations but those obviously make a big difference.”

An advantage, not a handicap

Every coronavirus has spike proteins, which allow them to penetrate human cells. The spike looks different for each variant but when researchers examined the BA.4 and BA.5 mutations, the rare F486V mutation stood out.

This mutation is striking because it is usually considered a “handicap” that makes it harder for the virus to bind to human cells. In this case, however, it has been very successful in infecting people as their immune systems do not recognise it as a threat quickly enough.

In practice, that means that the body’s natural defences have a harder time dealing with this “lesser” mutation, making it better at circumventing immunity and replicating more quickly. “In this case, this handicap really is a feature, not a bug for the virus,” Vanham said.


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