Simon Clarke, University of Reading
British health authorities are currently hunting for an unknown person who has tested positive for a variant of the coronavirus known as P1. Sometimes called the Brazil variant, P1 is feared to be more transmissible than earlier forms of the coronavirus. It may also be partially resistant to immunity generated by prior infections or vaccination.
Six people have tested positive with P1 in the UK, but one of them didn’t leave contact details behind when completing their test. This has sparked an urgent effort to find this person and trace their contacts to limit the variant’s spread.
The variant is believed to have originated in Manaus, the capital of Amazonas state in Brazil, and so is also known as the “Manaus variant”. It is a concern because of the mutations it carries.
One of these, called N501Y – which the variant originating in the UK also has – can allow the virus spread more easily. P1 also carries another mutation called E484K, which might allow it to resist antibodies generated against earlier forms of the virus.
However, at this stage, scientists are still researching P1’s capabilities. An early piece of research – yet to be reviewed by other scientists – estimates that P1 is between 1.4 and 2.2 times more transmissible than the variant the UK was dealing with last summer. The same research also suggests that among people who have natural immunity after being infected with an earlier coronavirus strain, P1 may be able to reinfect them between 25% and 61% of the time.
It’s important to stress that the Brazilian variant is highly unlikely to be completely impervious to the immunity raised by a vaccine. However, P1 shares mutations (such as E484K) and behaviours with the South African variant, and evidence suggests this variant has a higher chance of infecting people who’ve had the Oxford/AstraZeneca vaccine than older versions of the virus. Both variants will probably therefore have greater resistance to other vaccines too.
This is because the mutations carried by these variants change the spike protein, a key structure on the virus’s surface that it uses to enter cells and which is also targeted by the immune system. The mutations have reshaped the spike protein sufficiently so that antibodies are unable to bind to it well – which is what allows the virus to get around immunity generated by previous infections or vaccines – but not so much that the virus can’t use the protein to get into our cells.
Although we don’t definitively know how well the Brazilian variant can escape immunity, there is observational evidence that suggests it does. Last year, many scientists believed that coronavirus infections had been so widespread in Manaus that herd immunity had been reached and that the virus would no longer spread there. But since then, cases have spiked again in the city, potentially because of P1’s resistance to previously generated immunity.
Why has P1 appeared?
You may already know that viruses mutate, that this is normal and these small changes to the virus’s genetic code are to be expected. Well, that’s true, but that doesn’t mean they’re always harmless. Many mutations will be irrelevant, and some will make a virus weaker and will die out. But others will make it fitter, giving it an advantage over other variants and allowing it to out-compete them.
As people socially distance, observe stricter personal hygiene and wear masks, it becomes an advantage for the virus to be more transmissible. Similarly, as more people around the world gain immunity through being infected or vaccinated, another advantage would be for the virus to change so that antibodies can no longer attach to it and prevent it from infecting cells.
It’s therefore not surprising to see variants with mutations that provide these advantages now out-competing other forms of the coronavirus. Control measures and rising immunity are pressuring the coronavirus to evolve.
Simon Clarke, Associate Professor in Cellular Microbiology, University of Reading
This article is republished from The Conversation under a Creative Commons license. Read the original article.
