Kai Kupferschmidt
Kai is a contributing correspondent for Science magazine based in Berlin, Germany. He is the author of a book about the color blue, published in 2019.
Posted on 01/19/2021 9:05:57 PM PST by SeekAndFind
When the number of COVID-19 cases began to rise again in Manaus, Brazil, in December 2020, Nuno Faria was stunned. The virologist at Imperial College London and associate professor at the University of Oxford had just co-authored a paper in Science estimating that three-quarters of the city’s inhabitants had already been infected with SARS-CoV-2, the pandemic coronavirus—more than enough, it seemed, for herd immunity to develop. The virus should be done with Manaus. Yet hospitals were filling up again. “It was hard to reconcile these two things,” Faria says. He started to hunt for samples he could sequence to find out whether changes in the virus could explain the resurgence.
On 12 January, Faria and his colleagues posted their initial conclusions on the website virological.org. Thirteen of 31 samples collected in mid-December in Manaus turned out to be part of a new viral lineage they called P.1. Much more research is needed, but they say one possibility is that in some people, P.1 eludes the human immune response triggered by the lineage that ravaged the city earlier in 2020.
Emerging variants of the coronavirus have been in the news ever since scientists raised the alarm over B.1.1.7, a SARS-CoV-2 variant that first caught scientists’ attention in England in December and that is more transmissible than previously circulating viruses. But now, they’re also focusing on a potential new threat: variants that could do an end run around the human immune response. Such “immune escapes” could mean more people who have had COVID-19 remain susceptible to reinfection, and that proven vaccines may, at some point, need an update.
At a World Health Organization (WHO) meeting 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 variants and the travel restrictions that many countries are imposing to contain them. 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 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 on Friday showing the strain could become the predominant variant in the United States in March. But scientists are just as worried about 501Y.V2, a variant detected in South Africa. Some of the mutations it carries, including ones named E484K and K417N, change its surface protein, spike, and have been shown in the lab to reduce how well monoclonal antibodies combat the virus. In a preprint published earlier this month, Jesse Bloom, an evolutionary biologist at the Fred Hutchinson Cancer Research Center, showed that E484K also reduced the potency of convalescent sera from some donors 10-fold—although he is quick to add this does not necessarily mean the mutation would cause people’s immunity to the new strain to drop 10-fold.
P.1 adds to the concerns because it appears to have hit on a similar constellation of mutations and has emerged in a place with a high level of immunity. “Anytime you see the same mutations arising and starting to spread multiple times, in different viral strains across the world, that’s really strong evidence that there’s some evolutionary advantage to those mutations,” Bloom says.
Like B.1.1.7, the variant identified in Manaus is already on the move. Just as Faria was finishing his analysis of the Brazilian genomes, a report was published of a variant detected in travelers arriving in Japan from Brazil—and it turned out to be P.1.
How these new variants are affecting the course of the pandemic is still unclear. In Manaus, for example, P.1 might have nothing to do with the new surge in infections; people’s immunity might simply be waning, says Oxford epidemiologist Oliver Pybus. In a press conference today, WHO’s Mike Ryan cautioned that changes in human behavior are still the major driving force for the resurgence. “It’s too easy to just lay the blame on the variants and say it’s the virus that did it,” he said. “Unfortunately, it’s also what we didn’t do that did it.”
Even if the variant plays a crucial role it might be driving the boost because it is transmitted more easily, like B.1.1.7, not because it can evade the immune response. “Of course it could be a combination of these factors, too,” Pybus says. Similarly, in a recent modeling study, researchers at the London School of Hygiene & Tropical Medicine calculated that South Africa’s 501Y.V2 variant could be 50% more transmissible but no better at evading immunity, or just as transmissible as previous variants but able to evade immunity in one in five people previously infected. “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 working to sequence more samples from Manaus from January to follow the variant’s spread. “We don’t have the data yet, but my guess is, it will be at 100% now,” she says. Lab studies investigating the variants are also underway. The United Kingdom today launched a new consortium, G2P-UK (for “genotype to 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 12 January WHO meeting is to set up a biobank that would aid studies by housing virus samples, as well as plasma from vaccine recipients and recovered patients.
Interactions between the new mutations may make it harder to tease out their effects. The variants from the United Kingdom, South Africa, and Manaus all share a mutation named N501Y, for instance, or Nelly, as some researchers call it. But the mutation, which affects the spike protein, also occurs in some variants that do not spread faster, suggesting N501Y does not operate alone, says Kristian Andersen of Scripps Research: “Nelly might be innocent, except maybe when she’s hanging with her bad friends.”
Bloom thinks none of the changes is likely to let the virus escape the immune response entirely. “But I would expect that those viruses have some advantage when a lot of the population has immunity”—which might help explain the surge in Manaus.
So far, the virus does not appear to have become resistant to COVID-19 vaccines, says vaccinologist 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 evolve into a vaccine-resistant phenotype, this may happen sooner than we like,” he adds. That possibility adds to the urgency of putting good surveillance in place to detect such escape variants early on, says biostatistician Natalie Dean of the University of Florida. But it also adds to the urgency of vaccinating people, says Christian Drosten, a virologist at Charité University Hospital in Berlin. “We have to do everything we can now to vaccinate as many people as fast as possible, even if that means running the risk of selecting for some variants,” he says.
If vaccine-resistant SARS-CoV-2 strains emerge, vaccines might need to be updated. Several vaccines could be easily changed to reflect the latest changes, but regulators might balk at authorizing them without seeing updated safety and efficacy data, Krause says. If new variants circulate alongside older strains, multivalent vaccines, effective against several lineages, might even be needed. “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 should start to produce vaccines designed to generate immunity to mutated versions of the spike protein, because they keep cropping up. “It tells us that we should have these mutations in our vaccines, so that you shut off one of the avenues for the virus to go down.”
For now, increased transmissibility is the biggest worry, says virologist Angela Rasmussen of Georgetown University. “I’m puzzled why [that] isn’t a bigger part of the conversation,” she says. The U.S. hospital system, she says, “is at capacity in many places and further increases in transmission can tip us over the edge where the system collapses. Then we’ll start seeing potentially huge increases in mortality.”
Haven't we heard that somewhere before - as we were being urged, last March, to accept draconian measures "for just a few weeks?"
Regards,
In another 10 years or so, we’re going to have to stay on a vaccine IV.
I’m reminded of Tom Clancy’s book Rainbow Six.🤔
Of course they will - ‘emergency actions’ override all laws ...
OR NOT.
Haven’t quite yet mastered the DNA mutations...
Exactly right. As a PhD scientist I wonder about the capacity of the Dims to understand this article. I think they can’t and won’t...it is not a part of their nature to be logical and demand data to prove or disprove a point.
The vaccine hullaballu is a means for Fauci and others to exert a continuing tightening of control over people everywhere in all groups larger than “2”.
The Covid-19 vaccine is basically as useless as the “flu” vaccine for exactly the same reasons.
i suppose I shouldn’t assume an educated-in-the-most-basic- aspects-of-science population. Sigh.
Deep State continues to feed lies
We have achieved here immunity in our family the natural way.
Got it. Kicked it.
My nephew got it last April, got it again last month. He was much sicker this go around. If it is truly what he had each time, who knows?
Yep - they got the wedge in and now they will apply leverage as needed to make Covid the bug that enslaved the world.
Beware any headline spouting words like “could”, or “might”, or “if”. All that means is that the so-called “experts” don’t know anything more than you do, they’re just trying to sensationalize their own ignorance.
Not discussed in this article is that which is glaringly omitted in spite of subtle clues.
When the B.1.1.7 ‘variant’ was first discovered, it was reported as the UK variant. Same for 501Y.V2 as the South African variant. There was no mention of numbers. Listen carefully to reports; all you’ll hear now are numbers.
Why the sudden change to numbers?
Well, we can’t have the virus referred to by its geographical origin, now can we? /s
(China virus)
“ Except you are only immune for about 3 months, they say.
My nephew got it last April, got it again last month. He was much sicker this go around. If it is truly what he had each time, who knows?”
Then same with the vaccine.
Who is signing up for a quarterly vaccine?
With the high false positive rates on the test, no one knows if they had it unless they test for antibodies.
We continue with our protocol, maintaining our immune system, and with ivermectin in our pocket in case.
It is my understanding tht the current vaccines do not contain the desd or weakened covid virus but rather protein/s that enable the covid virus to attach. Absent the protein, the virus is rendered unable to actually attack the body
If that is so, then a covid mutation would not affect the efficacy of the vaccine?
I tend to think they had the flu.
My sister, much older than me (60s), got very sick and is having residual lung issues.
Ofcourse, I don't know if it is just a lot of it is over thinking and hypervigilance. I had H1N1 about 6-7 years ago. We all did except my daughter who got it two years before.
If I got that today, with Covid, I'd be sure I was dying. It took us all a solid 6 weeks to fully get over it.
Here's a strange one about my family (all in NY, btw). Two sides of the family, two separate infections that started about the same time.
Everyone got sick except my brother-in-law and his brother. Both in their 60s as well.
So, that tells us, if Covid, one of three things:
1. Both didn't come in contact with the virus in their homes and workplace (one has a family business) Seems doubtful.
2. They both had some form of immunity (flu?)
3. There is a genetic component.
Vitamin D levels in blood - differences
RE: It is my understanding tht the current vaccines do not contain the desd or weakened covid virus but rather protein/s that enable the covid virus to attach.
I believe the Chinese Sinovac vaccine does use a dead or inactivated Covid virus. But in Brazil where it was tested on tens of thousands, it was only found to be a little over 50% effective.
Johnson and Johnson also uses the same inactivated/dead virus, but it’s still in its final phases of testing and won’t be available for EUA approval till late February.
The Pfizer and Moderna vaccines in current use are not subject to obsolescence from genetic mutation in the COVID-19 virus. These vaccines target the virus’ “spike proteins”. Spike proteins are COVID-19’s means of accessing cellular ACE-2 receptors to enter cells. Until this virus can mutate specific aspects of the spike proteins it’s doomed.
The hype over mutations is unfounded fear mongering. Thanks to Trump we will climb out of this abyss regardless of the mutations.
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