Science‘COVID-19 reporting is supported by the Pulitzer Center and the Haising-Simmons Foundation.
When in December 2020, the number of COVID-19 cases in Manaus, Brazil began to rise again, Nuno Faria was stopped. Virologists at Imperial College London and Associate Professor at Oxford University were co-authors in just one paper Science Estimating that three-quarters of the city’s residents were already infected with SARS-CoV-2, the pandemic coronavirus – this was more than enough, it seemed, to develop herd immunity. The virus should be performed with Manaus. Still hospitals were recuperating. Faria says, “It was difficult to reconcile these two things.” He began hunting for specimens to find out whether changes to the virus could explain the resurgence.
On January 12, Faria and his colleagues posted their preliminary findings on the website virological.org. Thirteen of the 31 samples collected in Manaus in mid-December formed part of a new viral lineage, which they called P.1. Much research is needed, but they say one possibility is that in some people, P.1 triggers a human immune response by the lineage that devastated the city earlier in 2020.
Emerging versions of Coronavirus have been in the news ever since scientists raised an alarm over B.1.1.7, a SARS-CoV-2 variant that first attracted the attention of scientists in England in December and which was already underway The virus is more contagious. But now, they are also focusing on a potential new threat: variants that can make an end run around the human immune response. Such “immune migration” can mean those with COVID-19 who are susceptible to re-formation, and it may be proven that the vaccine may, at some point, require an update.
At the World Health Organization (WHO) meeting on 12 January, hundreds of researchers discussed the most important scientific questions raised by the wave of new mutations. The WHO also convened its COVID-19 Emergency Committee on 14 January to discuss the impact of new variants and travel restrictions that many countries are forcing them to include. The committee called for a global effort to sequence and share more SARS-CoV-2 genomes to help track mutations. It also asked countries to support “global research efforts to understand the significant unknown about SARS-CoV-2 specific mutations and variants”.
The more variable version, B.1.1.7, is already rapidly spreading in the United Kingdom, Ireland and Denmark, and probably in many other countries. The US Centers for Disease Control and Prevention released a modeling study on Friday showing that stress may be highest in the United States in March. But scientists are only concerned about 501Y.V2, a variant has been detected in South Africa. Some mutations carry it, including the names E484K and K417N, alter its surface protein, spike, and have been shown in the lab to show how well monoclonal antibodies counteract the virus. In an impression published earlier this month, Jesse Bloom, an evolutionary biologist at the Fred Hutchinson Cancer Research Center, showed that the E484K also reduced the strength of the entrapped sera from some donors by up to 10-fold – though he called it Not quick to add. This mutation will cause a 10-fold decline in people’s immunity.
P.1 adds to the concerns as it appears to hit a similar constellation of mutations and has emerged at a location with a high degree of immunity. “Whenever you look at the same mutation and begin to spread multiple times across the world to different viral strains, this is really strong evidence that there is some evolutionary benefit to those mutations,” Bloom says.
Like B.1.1.7, the variant identified in Manaus is already in practice. As Faria was completing its analysis of the Brazilian genome, a report was published in the variant, which was found in travelers arriving from Brazil to Japan and it turned out to be P.1.
How these new versions are affecting the course of the epidemic is still unclear. In Manaus, for example, P.1 has nothing to do with the new surge in transition; Oxford Epidemiologist Oliver Pybus states that people’s immunity can be easily reduced. At a press conference today, WHO’s Mike Ryan cautioned that human behavior change is still the major driving force for revival. He said, “It is very easy to just blame the variants and say that it is a virus that has done this. “” Unfortunately, it is also that we did not do this. “
Even if the variant plays an important role, it can promote because it is more easily transmitted like B.1.1.7, not because it can evacuate the immune response. “Of course, it can also be a combination of these factors,” Pybus says. Similarly, in a recent modeling study, researchers at the London School of Hygiene and Tropical Medicine calculated that the 501Y.V2 variant of South Africa may be 50% more transferable, but it is no better in immunity, or Only capable of transmitting as in the previous variant, but able to evade immunity in one in five previously infected people. “Reality can lie between these boundaries,” the authors wrote.
Molecular biologist Esther Sabino of the University of São Paulo, São Paulo, is launching a study to find flaws in Manaus that could help decide between these hypotheses for P1. He has been working to sequence more samples from Manaus since January to follow the spread of variants. “We don’t have data yet, but I estimate, it will be 100% now.” Lab studies investigating variants are also underway. The United Kingdom today launched a new consortium, G2P-UK (“for phenotype-UK”), headed by Wendy Barclay of Imperial College London, to study the effects of emerging mutations in SARS-CoV-2. One idea discussed at the January 12 WHO meeting is to establish a biobank that will aid in the study of housing virus samples, as well as plasma and patients recovered from vaccine recipients.
Interaction between new mutations can make their effects difficult to manipulate. All variants of the United Kingdom, South Africa, and Manaus share a mutation named N501Y, for example, or Nelly, as some researchers call it. But mutations, which affect spike proteins, also occur in some variants that do not spread rapidly, suggesting that N501Y does not work alone, says Christian Anderson of Scripps Research: “Nelly may be innocent, Except when she is hanging out with her bad friends. “
Bloom feels that any changes are unlikely to survive the immune response to the virus completely. “But I would expect those viruses to be of some benefit when a lot of the population has immunity” – which may help explain the surge in the psyche.
So far, the virus has not been resistant to COVID-19 vaccines, says vaccine specialist Philippe Kruse, who chairs a WHO working group on COVID-19 vaccines. “The good news is that the rapid development of these variants suggests that if it is possible for the virus to evolve into a vaccine-resistant phenotype, it may soon be like us,” he said. This possibility, says zoologist Natalie Dean of the University of Florida, calls for an urgent need to have good surveillance for early detection of such escape variants. But it also connects people with the urgency to vaccinate, says Christian Drosten, a virologist at Charité University Hospital in Berlin. He says, “We have to do everything we can to vaccinate as many people as possible now, even if it means the risk of choosing some variants.” ”
If vaccine-resistant SARS-CoV-2 strains emerge, vaccines may need to be updated. Many vaccines can be easily changed to reflect the latest changes, Krause says, but regulators may be bald in authorizing them without looking at updated safety and efficacy data, says Krause. If new variants are transmitted simultaneously with older strains, multi-vaccines are effective against multiple lineages, may even be required. “To be clear: these are drift ideas,” Krause says. “The public should not think it is imminent, and new vaccines will be needed.” But Ravindra Gupta, a researcher at the University of Cambridge, says manufacturers should start producing vaccines designed to induce immunity to mutated versions of spike proteins, as they continue to harvest. “It tells us that we should have these mutations in our vaccines, so that you can close one of the pathways for the virus to go down.”
For now, increased communicability is the biggest concern, says Georgetown University virologist Angela Rasmussen. “I’m surprised why [that] It is not a big part of the conversation, ”she says. The American hospital system, she says, “has capacity in many places and further increases in transmission can tip us over the edge where the system collapses. Then we will begin to see a potentially huge increase in mortality. “