Six people in the UK have tested positive for the P.1 coronavirus variant first detected in Brazil. Five of the six either recently returned from Brazil or had close contact with someone returning from Brazil. Officials are trying to trace a sixth person who tested positive after sending in a home test kit without contact details. The situation has led to fears that this variant could spread more widely.
The P.1 variant seems to have emerged in Brazil in November. It caused a second wave of infections in the city of Manaus, despite up to three-quarters of its population having been infected in the first wave earlier in 2020.
A study by Nuno Faria at Imperial College London and his colleagues suggests that P.1 spread 1.4 to 2.2 times faster than other variants present in Manaus and also reinfected between 25 and 61 per cent of people with immunity to these other variants.
But the researchers stress that the findings are specific to Manaus and don’t necessarily mean that P.1 will spread faster in other places with different existing variants and different levels of immunity. “Our findings from Manaus should not be generalised to other contexts,” says Faria.
Indeed, while P.1 has now been detected in at least 25 countries, local transmission has been reported only in Sweden, Belgium, Mexico and Colombia.
So far, P.1 doesn’t seem to be taking off in the same way as the fast-spreading B.1.1.7 variant first detected in the UK, but Faria cautions that it is too early to draw any conclusions.
While it remains unclear if P.1 is more transmissible outside Brazil, there is good evidence that both P.1 and the similar B.1.351 variant first spotted in South Africa have mutations that enable them to partly evade antibodies from vaccinations or previous infections.
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Thankfully, these variants cannot completely evade immune protection. Our bodies produce both antibodies that prevent the virus from infecting cells in the first place, and T-cells that destroy infected cells to stop the virus making more copies of itself.
To prevent infection, antibodies have to bind to key sites on the spike protein that protrudes from the virus. Mutations in these key sites can reduce antibody effectiveness.
T-cells, by contrast, are effective as long as they recognise any part of the spike protein, so it is much harder for a virus to mutate to evade the T-cell response. “There is no way these variants are escaping T-cell immunity,” Shane Crotty at the La Jolla Institute for Immunology in California told New Scientist in January.
Trials of the Johnson & Johnson vaccine found that it was slightly less effective at preventing symptomatic covid-19 in South America, where P.1 is more common, than in the US. However, the difference was small – 66 per cent instead of 72 per cent – and, crucially, it was still 100 per cent effective at preventing hospitalisations and deaths. These findings are reassuring, as they mean that variants like P.1 will not wipe out all the benefits of vaccination even if they do start spreading widely.
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That said, there are still two big worries. First, if P.1 reaches a number of vulnerable people in the UK who haven’t yet been vaccinated, hospital admissions and death rates could soar again.
Second, the more widely that variants such as P.1 circulate, the more opportunity they have to evolve further. For instance, the fast-spreading B.1.1.7 variant that was first discovered in Kent, and was partly to blame for the recent resurgence of cases in the UK, appears to have now acquired the same E484K mutation that helps P.1 dodge antibodies.
“It is possible that as more and more people get vaccinated, and the selective pressures intensify on the virus, that we will see other mutations,” says Astrid Iversen at the University of Oxford. However, there is a limit to what evolution can achieve.
It is likely that many mutations have “fitness costs” as well as “fitness benefits”, says Iversen. This might explain why other variants with the E484K mutation appeared early in 2020 but died out rather than spreading widely.
This article was updated on 2 March.
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