Family members are attending a funeral of a COVID-19 in Manaus, Brazil, on January 13.
MICHAEL DANTAS / AFP via Getty Images
By Kai Kupferschmidt
Science‘COVID-19 reporting is supported by the Pulitzer Center and the Heising-Simons Foundation.
When the number of COVID-19 cases started to increase again in December 2020 in Manaus, Brazil, Nuno Faria was stunned. The virologist at Imperial College London and associate professor at Oxford University have just written an article in the article Science it is estimated that three-quarters of the city’s residents were already infected with SARS-CoV-2, the pandemic coronavirus – more than enough it seemed that the herd immunity would develop. The virus must be done with Manaus. Yet hospitals were full again. “It was hard to reconcile these two things,” Faria says. He began hunting for samples he could follow to determine if changes in the virus could explain the revival.
On January 12, Faria and his colleagues post their initial conclusions on the website virological.org. Thirteen of 31 samples collected in Manaus in mid-December appear to be part of a new viral offspring they called P.1. Much more research is needed, but according to them, the possibility is that P.1 in some people evades the human immune response caused by the gender line that devastated the city earlier in 2020.
Related
Emerging variants of the coronavirus have been in the news since scientists sounded the alarm about B.1.1.7, a SARS-CoV-2 variant that caught scientists’ attention for the first time in December and which is more transmissible than viruses which was previously distributed. But now they are also focusing on a potential new threat: variants that could put an end to the human immune response. Such “immune escape” may mean that more people who have had COVID-19 are susceptible to reinfection, and that proven vaccines need an update at some point.
At a meeting of the World Health Organization (WHO) on 12 January, hundreds of researchers discussed the most important scientific questions raised by the wave of new mutations. WHO also convened its COVID-19 emergency committee on 14 January to discuss the impact of the new variant and the travel restrictions that many countries have in place to limit it. The committee called for a global effort to sequence and share more SARS-CoV-2 genomes to detect mutations. It also called on countries to ‘make global research efforts to better understand critical unknowns about SARS-CoV-2-specific mutations and variants’.
The more transmissible variant, B.1.1.7, is already spreading rapidly in the United Kingdom, Ireland and Denmark, and probably in many other countries. The U.S. Centers for Disease Control and Prevention released a modeling study Friday that shows the strain could become the predominant variant in the United States in March. But scientists are just as concerned about 501Y.V2, a variant found in South Africa. Some of the mutations it carries, including those named E484K and K417N, alter the surface protein, peak and have been shown in the laboratory to reduce how well monoclonal antibodies fight the virus. In a preview published earlier this month, Jesse Bloom, an evolutionary biologist at the Fred Hutchinson Cancer Research Center, showed that E484K also reduced the potential for restorative sera from some donors tenfold – although he adds quickly, it does not mean not necessarily the mutation would cause people’s immunity against the new tribe to decrease tenfold.
P.1 contributes to the concerns because it appears to have struck a similar constellation of mutations and originated in a place with high immunity. “Every time you see the same mutations occur and that start spreading several times in different viral strains around the world, it is strong evidence that these mutations have an evolutionary advantage,” says Bloom.
Like B.1.1.7, the variant identified in Manaus is already on the move. Just as Faria was analyzing the Brazilian genome, a report was published of a variant detected in travelers arriving in Japan from Brazil – and it turned out to be P.1.
Bad friends
How these new variants affect the course of the pandemic is still unclear. In Manaus, for example, P.1 has nothing to do with the new rise in infections; people’s immunity can simply decline, says Oxford epidemiologist Oliver Pybus. At a press conference today, WHO Mike Ryan warned that changes in human behavior are still the biggest driver for the revival. “It’s too easy to just blame the variant and say it’s the virus that did it,” he said. “Unfortunately, that’s also what we did not do.”
Although the variant plays an important role, it can give the boost because it is more easily transmitted, such as B.1.1.7, not because it can evade the immune response. “Of course, it could also be a combination of these factors,” says Pybus. In a recent modeling study, researchers from the London School of Hygiene & Tropical Medicine also calculated that the 501Y.V2 variant of South Africa may be 50% more transmissible, but not better at evading immunity, or just as transmissible. as previous variants, but which it can evade. immunity in one in five people previously infected. “The reality may lie between these extremes,” the authors wrote.
Ester Sabino, a molecular biologist at the University of São Paulo, São Paulo, is launching a study to find reinfections in Manaus that could help decide between these hypotheses for P.1. She is also in the process of sequencing more samples from Manaus from January to track the distribution of the variant. “We do not have the data yet, but I think it will be 100% now,” she says. Lab studies investigating the variants are also underway. The UK today launched a new consortium, G2P-UK (for “genotype to phenotype-UK”), led by Wendy Barclay of Imperial College London, to address the effects of emerging mutations in SARS-CoV-2 study. One idea discussed at the WTO meeting on 12 January is to set up a biobank that will help studies by housing virus samples, as well as plasma from recipients of vaccines and patients recovering.
Interactions between the new mutations may make it more difficult to tease their effects. The variants from the United Kingdom, South Africa and Manaus all share a mutation called N501Y, for example, or Nelly, as some researchers call it. But the mutation, which affects the ear protein, also occurs in some variants that do not spread faster, suggesting that N501Y does not work alone, says Kristian Andersen of Scripps Research: ‘Nelly may be innocent unless she is with her bad friends hang. ”
Bloom believes that none of the changes are likely to cause the virus to completely escape the immune response. “But I would expect the viruses to have some benefit if many have immunity” – which may help explain the increase in Manaus.
Vaccine Updates
So far, the virus does not appear to be resistant to COVID-19 vaccines, says vaccine expert Philip Krause, who chairs a WHO working group on COVID-19 vaccines. “The not-so-good news is that the rapid evolution of these variants suggests that if it is possible for the virus to develop into a vaccine-resistant phenotype, it can happen faster than we want,” he adds. The possibility contributes to the urgency of putting good oversight in place to detect such escape variants early, says University of Florida biostatistician Natalie Dean. But it also contributes to the urgency of vaccinating people, says Christian Drosten, a virologist at the Charité University Hospital in Berlin. “We must now do everything in our power to vaccinate as many people as possible, even if it means you run the risk of opting for some variants,” he says.
If vaccine-resistant SARS-CoV-2 strains emerge, vaccines need to be updated. Several vaccines can be easily modified to reflect the latest changes, but regulators may authorize them without seeing updated safety and efficacy data, Krause said. As new variants circulate along older strains, even multivalent vaccines are needed, which are effective against different sexes. “To be clear: these are downstream considerations,” Krause says. “The public should not think that this is imminent, and that new vaccines will be needed.” But Ravindra Gupta, a researcher at the University of Cambridge, says manufacturers need to start producing vaccines designed to generate immunity to mutated versions of the vein protein, because they are still popping up. “It tells us that we need to have these mutations in our vaccines, so you need to turn off one of the possibilities for shutting down the virus.”
For now, increased portability is the biggest concern, says virologist Angela Rasmussen of Georgetown University. ‘I’m surprised why [that] is not a bigger part of the conversation, ”she says. The U.S. hospital system, she says, “is capable in many places and further increases in transmission could cause us to tip over the edge where the system collapses. Then we will see a huge increase in mortality.”