Another worrisome coronavirus variant has made its global debut.
Scientists from the Indian state of Maharashtra identified a new strain two weeks ago that’s linked to between 15% and 20% of cases there.
The variant has earned the somewhat ominous nickname “double mutant” because it has an unprecedented combination of two mutations that may help it both attach better to human cells and hide from the immune system.
Just 24 hours after Indian officials reported the variant, it also popped up in northern California. Researchers from the Clinical Virology Lab at Stanford identified this “double mutant” in a sample from a patients in the San Francisco Bay Area. They suspect another seven cases are linked to the variant.
“We don’t know how those two mutations behave when they’re paired together,” Dr. Benjamin Pinsky, a Stanford virologist who helped discover the variant, told the LA Times.
But Dr. Peter Chin-Hong, an infectious-disease expert at the University of California, San Francisco, said panic about the variant is premature – and its nickname is a bit sensational.
“It suggests that it is doubly scary or doubly transmissible even compared to a variant that we know about, but there is no evidence to suggest that,” Chin-Hong told Insider.
Plus, he added, many variants have multiple mutations.
An unprecedented combination of mutations
Scientists keep tabs on the coronavirus’ evolution by genetically sequencing samples on a regular basis. Every variant has a unique genetic code peppered with mutations – that’s how researchers can classify different strains.
Most mutations are innocuous, but sometimes, a combination of genetic tweaks emerge that helps the virus survive or spread better. The “double mutant” brings together two worrisome mutations in the same variant for the first time.
One mutation, known as L452R, helps the virus’ spike protein bind more tightly to cells. That same mutation is also present in a variant first spotted in Los Angeles last fall. The other mutation – called E484Q – bares a “chilling” resemblance to a mutation found in variants from South Africa and Brazil, according to Chin-Hong. That tweak helps the variant evade detection by antibodies the body has developed in response to an infection with the original virus.
“There’s a reasonable amount of information about those individually,” Pinsky said of the two mutations. But he added: “Will it be worse if they’re together?” We don’t really know how they’re going to interact.”
No studies yet have found that this “double mutant” is deadlier than earlier versions of the virus, or that it can evade vaccines.
That said, some “early hallmarks” suggest the variant could be more transmissible, Chin-Hong said. In the last week, Maharashtra saw a 55% increase in infections. The Indian government says there’s not enough evidence to link that surge to this variant, but epidemiology researchers at the Indian Institute of Public Health have suggested that it’s the most likely explanation.
It’s unlikely the new variant will come to dominate in California
While the discovery of yet another worrisome variant is concerning, it’s not the variant that California in particular should be focused on, according to Chin-Hong.
“I do not at this time think that this ‘Indian variant’ will dominate the California viral landscape,” he said, adding, “we already have two svelte and dastardly variants adept at transmission duking it out.”
Those two are the variant found in the UK, which is linked to 851 cases in California, and another variant first spotted in Southern California. The California Department of Public Health reported last week that the latter accounts for more than 6,200 of the state’s cases.
Chin-Hong also thinks the “double mutant” will have a harder time spreading in California because the state’s winter surge of cases, coupled with rising vaccinations, have left fewer residents vulnerable to infection.
“This all acts as a force field – albeit temporary – against these new variants,” he said.
Ever since the species was first discovered in 1935, scientists have been baffled as to why the furry creatures are unable to hop or jump like most other rabbits.
Academics from PLoS Genetics– a peer-reviewed scientific journal – now have an explanation, Gizmodo reported.
The unusual gait can be explained by a genetic mutation, the study found.
This species has a warped RORB gene, BBC Newsround said. “This was the only mutation that stood out as really striking,” Miguel Carneiro, an academic at the University of Porto, told the media outlet.
A mutation in the RORB gene can result in the loss of spinal cord interneurons.
“When you move, these neurons fire all the time, they coordinate muscle contractions and know if the other limbs are in balance,” Leif Andersson, a co-author of the study, told Gizmodo. “This coordination of muscle contraction is not correct in these rabbits.”
In the Sauteur D’Alfort rabbits, these interneurons were either less abundant or totally absent, the study said. This, in turn, results in the loss of saltatorial locomotion – the ability to jump or hop.
The hand-standing is a result of the rabbits working around their inability to travel like other species, the study said.
Baby rabbits of this species learn, after a few months, to walk solely on their front legs to compensate for the genetic mutation and consequent spinal defects, the New Scientist said.
It’s unlikely that the quirky gait causes the animals any pain, Gizmodo reported.
The team of 12 scientists solved the mystery of the hand-standing rabbits after an experiment involving the breeding of a Sauteur d’Alfort rabbit with another species that can hop and jump normally, Slate reported.
Thousands of coronavirus strains circulate all the time.
Each version of the virus is separated by a handful of tiny changes in its genome. To keep tabs on these strains, and identify which ones may be better at infecting humans or evading vaccines, researchers must genetically sequence samples of the virus.
In the last five months, experts in the UK, South Africa, and Brazil have identified more transmissible variants that could exacerbate the pandemic.
The UK sequences 45 out of every 1,000 coronavirus cases – about 15 times the number of cases that are sequenced in the US. These efforts likely helped UK researchers detect the more infectious B.1.1.7 strain outside London in September.
Studies have shown that B.1.1.7 is between 56% and 70% more contagious than its viral predecessors. UK officials said in January that people infected with B.1.1.7 may face a higher risk of death than those who get other strains, though more data is needed to confirm this hypothesis.
But even the UK’s sequencing efforts pale in comparison to those in Iceland, Australia, and New Zealand. These nations have sequenced 64%, 41%, and 35% of their coronavirus cases, respectively – the most of any countries so far, according to data from GISAID, a global database that collects coronavirus genomes.
The US ranks 30th on that list – behind countries like Canada, China, Papua New Guinea, and the Republic of Congo – an improvement from its 43rd ranking in December.
Jeff Zients, coordinator of President Joe Biden’s COVID-19 task force, called the situation “totally unacceptable” during a White House briefing on January 27. More genetic sequencing, he said, “will allow us to spot variants early, which is the best way to deal with any potential variants.”
Indeed, knowing where a more transmissible variant is spreading could inform public health measures and travel bans, among other mitigation measures. A country lacking proper genetic surveillance has no way of knowing if a strain is spreading silently within its borders – and that “comes back to bite us,” Fauci said during the January conference.
Variants were circulating undetected in the US
To identify which coronavirus strain has infected a patient, scientists need to map out roughly 30,000 genetic letters in a sample of the patient’s blood or saliva.
The process is time-consuming. Samples collected from patients aren’t always sent in for sequencing and a limited number of labs can complete the genetic analysis.
“Part of the challenge of recognizing these variants is a lack of public health laboratory infrastructure in order to do the surveillance,” Dr. Rochelle Walensky, director of the Centers for Disease Control and Prevention, recently told JAMA.
Nearly all of the US’s initial cases of B.1.1.7 and B.1.351 – another more infectious variant first found in South Africa – involved patients with no travel history. This suggests the strains have been spreading undetected for some time.
The US didn’t report its first case involving B.1.1.7 until December 29, at least three weeks after the variant entered the country, according to some disease experts.
The US’s first B.1.351 cases, reported last week in South Carolina, were detected by chance. Researchers had been testing random samples “in order to identify any instances of the variant viruses,” the state health department said in press release.
Preliminary research published last month suggests vaccines might not provide as much protection against B.1.351, and people who have already been infected with a different version of the virus could get reinfected with the new strain.
The more you look, the more you’ll find
According to Fauci, the CDC is working on partnering with the National Institutes of Health to improve the US’s sequencing infrastructure.
The agency launched a consortium in May called SPHERES to coordinate and standardize genomic sequencing in the US. But “poor funding, coordination, and capacity” has resulted in “patchy” data, according to a report from the National Academies of Science.
Fauci said SPHERES is working on consolidating all the sequencing data from independent US labs by “streaming it into one accessible database so that we can do much more than we’re doing.”
Coordinating sequencing efforts is crucial to improving the country’s pandemic response.
The more viral genomes countries sequence, “the more able we are to spot new lineages” like B.1.1.7 and B.1.351, according to Lucy van Dorp, a geneticist at the University of College London Genetics Institute.
This probably won’t be the last time we learn of a new, potentially more infectious strain, she told Insider.
“There may be other similar variants elsewhere which have not been detected in other regions of the world due to less intensive sequencing efforts,” she said.
Dr. Peter Hotez, a vaccine scientist at Baylor College of Medicine in Texas, said on Twitter last month that the US likely had its own “homegrown variants” circulating.
California researchers confirmed Hotez’s prediction in a preliminary study published on January 20: Experts at Cedars-Sinai Medical detected a new variant called CAL.20C, which represented 24% of all coronavirus cases in Southern California in December.
There’s no indication that the variant is more transmissible yet, but the researchers said CAL.20C may have contributed to LA’s record case surge over the last few months.
United Kingdom Prime Minister Boris Johnson announced last week that people infected with the coronavirus variant first reported in the country may face a higher risk of death than those who get the original virus.
“There is some evidence the new variant may be associated with a higher degree of mortality,” he said at a press conference on Friday.
Studies have shown that the variant, known as B.1.1.7, is more contagious than its viral predecessors. But evidence had not suggested the strain was deadlier until now.
“Whereas an average of 10 out of a 1,000 older people died of the old variant in the UK, this appears to have increased to 13 out of 1,000 people with the new variant,” Patrick Vallance, the UK’s chief scientific advisor said on Friday. He stressed, however, that the evidence remained “uncertain.”
Some experts have since pointed out that just because more people infected with this variant are dying doesn’t mean it’s more lethal than other versions. It could be that the UK’s health system is overburdened by the country’s coronavirus case spike, or that the strain’s increased transmissibility enables it to infect more people with underlying health conditions.
After controlling for variables such as a patient’s age, sex, and geographic location, researchers from the London School of Hygiene & Tropical Medicine and Imperial College London found that, on average, people infected with B.1.1.7 had a 30% higher mortality rate.
A follow-up analysis from Public Health England analyzed data collected between November 23 and January 4, and found that B.1.1.7 was 65% deadlier than other strains. Researchers from the University of Exeter, meanwhile, looked at samples collected since October 1 and found that people infected with the variant were almost twice as likely to die.
However, the researchers didn’t find any evidence that people infected with B.1.1.7 were hospitalized at higher rates.
“If there is an increase in the severity of infection,” NERVTAG wrote, “we would also expect to see an increase in the risk of hospitalization.”
However, William Schaffner, an infectious-disease expert at Vanderbilt University, told Insider that it’s possible fewer people were going to hospitals for treatment, especially given reports that UK hospitals were on the verge of being overwhelmed.
‘Deaths will get out of control as your health system comes under pressure’
The World Health Organization said on Friday that it still needed to see the data UK officials were using before confirming whether the B.1.1.7 variant does indeed cause more severe disease.
If the strain is indeed more lethal, one potential reason could be that people infected with B.1.1.7 have higher viral loads, meaning they produce more viral particles when they’re infected. Higher viral loads, multiplestudies show, are associated with a higher risk of death and more severe disease.
“That was the first thing that certainly came to my mind,” Schaffner said. “It would make very good sense.”
That could also explain the increased contagiousness, since the more viral particles a person spews, the more likely they are to infect others.
But it’s also possible that the variant’s increased transmissibility is indirectly causing a higher death rate even though the strain itself isn’t deadlier. B.1.1.7. has several mutations in the code for its spike protein, which the virus uses to invade cells, that make it between 50-70% more contagious than the original.
One such possibility is that because there are so many more cases in the UK, healthcare systems are stressed and resources are scarce. That on its own can lead to higher death rates.
“If your cases get out of control, your deaths will get out of control as your health system comes under pressure,” Mike Ryan, executive director of the WHO’s health emergencies program, said in a press conference on Friday.
It’s also possible that the strain’s increased transmissibility ensures the virus infects more people who are at higher risk of severe illness.
“It may not be because the virus itself is making any individual more likely to get severe COVID,” Schaffner said. “It may simply be a matter of a more contagious virus getting to more vulnerable people who are older or have underlying health problems like diabetes or lung disease.”
A more transmissible strain may result in a higher death toll than a more lethal one
The UK researchers’ conclusions were based on just 8% of the total deaths that happened in the UK during the study period, which is why Vallance still considers the evidence to be “not yet strong.”
“The results of all studies may therefore not be representative of the total population,” NERVTAG concluded.
To determine which strain infected and killed a person, scientists must genetically sequence a sample of the patient’s blood or saliva. The process is time-consuming, and samples collected from patients aren’t always sent in for sequencing.
The data also did not account for any underlying health conditions in the people who died from COVID-19, which could also skew the mortality rates.
Regardless of the quality of the data, however, and regardless of whether or not the new strain is truly more lethal, its spread will almost certainly lead to a higher death toll in total, since infected individuals will spread it to more people.
Assume the original strain of the coronavirus has a reproductive value (meaning the average number of people one sick person infects) of 1.1 and kills 0.8 people out of every 100 who get sick. In a population of 10,000 people, that virus would kill 129 people in a month.
But then say two new strains emerged, one of which is 50% deadlier, while the other is 50% more transmissible. The strain that’s 50% more lethal would kill about 193 of the 10,000 people in a month. But the strain that’s 50% more transmissible would wind up causing 978 of the 10,000 people to die in that time because of its quick spread.
Anna Medaris-Miller contributed reporting to this story.
The global vaccine rollout is racing against the clock: New, more infectious variants of the coronavirus are spreading worldwide, and it’s unclear how well existing vaccines work against these strains.
For now, vaccines seem effective against the strain identified in December in the UK, called B117. But preliminary research suggests vaccines may be less effective against B1351, the strain identified in South Africa.
“It is all the more reason why we should be vaccinating as many people as you possibly can,” Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, said on Thursday. “Viruses don’t mutate unless they replicate, and if you can suppress that by a very good vaccine campaign, then you could actually avoid this deleterious effect that you might get from the mutations.”
But the process of getting shots into arms is off to a slow start in many countries. The US has administered more coronavirus vaccines than any other nation, but it has only given out roughly 19 million doses as of Friday.
Scientists worry that the current pace of vaccinations may allow time for too many new strains to emerge. That could lead to a scenario in which scientists must update vaccines regularly.
Michael Worobey, a viral evolutionary biologist at the University of Arizona, recently told the BBC that the emergence of new coronavirus strains could be “a glimpse into the future where we are going to be in an arms race with this virus, just like we are with flu.”
It’s also possible that a deadlier strain will turn up before most people are vaccinated. In that case, coronavirus shots may be routinely required for young people, similar to polio or measles vaccines.
The coronavirus could eventually resemble the common cold
The coronavirus’ future depends heavily on our ability to control transmission quickly. The more people develop immunity – whether through natural infection or vaccines – the faster the virus will reach an endemic state, meaning it would circulate perpetually but no longer hit pandemic-level peaks.
In a recent study, researchers at Emory University and Pennsylvania State University suggested that the coronavirus could eventually resemble a common cold that infects people during childhood.
Under that study’s most likely scenario, kids would get their first COVID-19 infection, on average, between ages 3 and 5. Almost every kid would get infected by age 15. Since pediatric infections are generally mild, there would be no need to vaccinate children beforehand. Infants might also have a certain degree of immunity at birth.
“For the first six months or so of life, or maybe longer if you’re nursing, kids have maternal antibodies from their mother, both from the umbilical cord and from breast milk, so there’s a chunk of time in the first year or so of life when kids aren’t going to get a primary infection,” Jennie Lavine, the study’s lead author, told Insider.
The researchers estimated that reinfections would be even milder – and might even boost immunity against related coronavirus strains.
If vaccinations proceed quickly, the New York Times reported, the virus could reach this endemic state in as little as six months to a year. Fauci recently estimated that life could return to normal in the fall if 70% to 85% of Americans were vaccinated by the end of summer.
But based on observed patterns of other human coronaviruses, the researchers’ model suggested that the new coronavirus would most likely become endemic within five to 10 years. Without speedy vaccinations, in other words, outbreaks could persist for some time.
Updating vaccines for new variants
Vaccines trigger the production of virus-specific antibodies, so that if people get exposed to the virus after being vaccinated, those same antibodies will recognize the virus and destroy it before it has a chance to replicate widely.
In an ideal scenario, coronavirus vaccines would protect against all strains of the virus for several years.
But scientists worry that new coronavirus variants may be different enough from the original that they could evade the antibodies developed in response to vaccines. If that happens, scientists might need to constantly tweak vaccines’ genetic instructions to vanquish new strains. The process isn’t necessarily difficult, but it would mean people would need follow-up shots.
“If we ever have to modify the vaccine, that is not something that is a very onerous thing,” Fauci said Thursday. “We can do that, given the platforms we have.”
But a scenario in which new strains require people to get revaccinated regularly – as is already the case with flu shots – becomes increasingly likely the longer it takes to get the current shots into arms.
It’s also possible, though, that other layers of immunity may protect people from emerging strains. White blood cells known as T cells and B cells also remember foreign invaders, often for longer periods of time than antibodies. A recent study suggested that recovered coronavirus patients had robust T-cell and B-cell immunity for at least eight months. A study of SARS, which is caused by a genetically similar coronavirus, showed that recovered patients had T-cell immunity 17 years after their infection.
A deadlier strain could make coronavirus shots routine
By vaccinating people quickly, public-health officials hope to avoid the worst-case scenario: the emergence of a deadlier coronavirus strain.
“Things that we need to keep looking for that would prevent this from becoming a very mild, endemic thing that doesn’t require vaccination would be if somehow the virus changed such that infections in childhood became more severe,” Lavine said.
In that case, she added, all young people would need to get shots before they acquired their first coronavirus infection.
There’s already some evidence that the UK coronavirus strain could be deadlier than original. The UK’s chief scientific adviser, Patrick Vallance, said Friday that the new variant could have an up to 30% higher mortality rate among some age groups, though the evidence remained “uncertain.”
The good news, however, is that existing coronavirus shots seem to work against it.
“From what we’ve seen so far, the variants being described do not alter the ability of neutralizing antibodies elicited by vaccination to neutralize the virus,” Moderna’s chief medical officer, Tal Zaks, said at the JP Morgan Healthcare Conference earlier this month.
But that makes the task of vaccinating people all the more urgent.
“Everyone will probably get infected sometime,” Lavine said “Let’s make it an infection after the vaccination so that you don’t get really sick from it.”
At first, there was little evidence to suggest that COVID-19 vaccines wouldn’t work against the mutated, more infectious versions of the virus that have emerged in the last few months.
But preliminary research published this week suggests that a coronavirus variant detected in South Africa in December can partially evade the defenses vaccines build in our bodies’ immune systems.
The research has not yet been peer-reviewed, but it suggests the variant, known as 501Y.V2, can escape antibodies developed in response to vaccination or infection with the original version of the virus. That may mean existing vaccines won’t provide as much protection, and people who have already been infected with the original version of the virus could get reinfected with the new strain.
Penny Moore, a researcher at South Africa’s National Institute for Communicable Diseases and co-author of the new study, said during a webinar on Monday that compelling data shows the mutations in 501.Y.V2 to be “problematic.”
Her group’s research found that in half of samples studied in the lab, antibodies in the blood of people who had recovered from COVID-19 were unable to stop the variant.
“Based on Penny’s data, it’s likely that the vaccine is going to be somewhat less effective, but how much less effective we don’t know,” David Montefiori, a virologist at Duke University Medical Center who was not involved in the study, told CNN.
The variant can dodge our body’s defenses
Antibodies are protective proteins that our immune system generates when it senses a foreign substance, or antigen, in the body. These proteins are generated during an infection, and they’re what a vaccine prompts the body to build in order to prevent illness.
In general, antibodies fight infection by learning to recognize a virus and signaling to the immune system that it should be destroyed. They do that by binding to the invader until it’s wiped out. But if a virus is different enough from others to evade existing antibodies’ search-and-destroy mechanisms, it can continue to wreak havoc.
The South African researchers set out to see whether antibodies developed in response to the original version of the coronavirus work to protect people from the new variant. They used blood samples from 44 patients who’d recovered from COVID-19 before the 501.Y.V2 variant was detected.
The scientists exposed the blood to the new variant and found that the antibodies in half of the samples were impotent against the strain. Antibodies in the other half of the samples mounted a weakened response.
These results “may foreshadow reduced efficacy” of existing vaccines, the team wrote. They also warned that people who’ve gotten the original coronavirus may be at risk of new infections from variants like 501.Y.V2.
Furthermore, Moore’s group found that three types of monoclonal antibodies – laboratory-made antibodies designed to target the coronavirus – were ineffective against the variant. Doctors have been using monoclonal antibodies to treat patients; the Food and Drug Administration has authorized two such treatments.
Still, Moore said more data is needed to draw firm conclusions about how the variant interacts with antibodies inside the body, especially among people who’ve been vaccinated. The research also did not look at other elements of the immune system, like B cells, which play a critical role in developing new antibodies.
Nathan Grubaugh, an epidemiologist from the Yale School of Public Health, said it’s hard to tell how well laboratory tests translate to reality in the body. A 90% reduction in protection during a lab test “may still mean complete protection in a human,” he told Insider.
As the virus mutates, vaccines may need to evolve
The 501Y.V2 variant has one particular mutation in its spike protein – the part the virus uses to invade cells – that has “been shown to reduce antibody recognition” among people who had a prior infection or vaccination, according to Francois Balloux, the director of the University College London Genetics Institute.
Other mutations in the spike protein contribute to 501.Y.V2’s increased infectiousness, the South African researchers said. That could explain why the country has been hit so hard since November. In the last two months, the number of new coronavirus cases per day in South Africa quintupled, from an average of 2,300 to 13,000. It hit a record high of nearly 22,000 cases on January 8, and the country’s test-positivity rate doubled in December. By the end of 2020, 501.Y.V2 had replaced almost all other versions of the coronavirus in South Africa.
It has spread to at least 20 countries.
Other variants like the one found in the UK have similar mutations in their spike protein. But a preliminary study from Pfizer-BioNTech found that the company’s coronavirus vaccine is effective against that variant.
Jesse Bloom, a biochemist a the Fred Hutch Institute in Seattle, said in a statement that he’s “optimistic that current vaccines will remain quite useful,” though he added that as the coronavirus continues to evolve, “eventually it may be necessary to update vaccines.”
An updated vaccine could be ‘rapidly deployed’
All viruses mutate. Most mutations are inconsequential, but occasionally one appears that undermines the immunity people have acquired from a vaccination or prior infection. The flu, for instance, mutates quickly, which is why we have to get a new flu shot every year, and why flu vaccines aren’t 100% effective.
Thee coronavirus mutates slower than the flu. That’s why Trevor Bedford, a virologist at Fred Hutch, predicted in April that “it will take the virus a few years to mutate enough to significantly hinder a vaccine.” But Bedford didn’t know at the time how much the virus would proliferate and how high case numbers would climb; the more chances a virus has to spread (and therefore replicate), the more likely mutations become.
On Wednesday, Bedford tweeted that “the emerging situation can be dealt with through a forthcoming vaccine update.”
BioNTech, Pfizer’s partner, said it could produce a new vaccine for a COVID-19 variant in about six weeks. Tal Zaks, Moderna’s chief medical officer, said his company’s process would be quick, too.
“I think our technology is very well suited to actually rapidly deploy a vaccine based on the new variant,” Zaks said in a recent presentation at the J.P. Morgan Healthcare Conference.
That’s because these mRNA vaccines don’t contain dead versions of virus, but rather genetic instructions for the body to make one of the virus’ signature proteins internally, thereby triggering an immune response. Tweaking those instructions is an easy switch.
The decision to sign off on a modified vaccine would then be up to regulators.
Immunity to a virus isn’t all or nothing
Even if the variant does reduce how well current vaccines work, that doesn’t mean protection from infection disappears completely, experts say.
“We often talk about immunity as sort of an all-or-nothing thing, but it’s not,” Jennie Lavine, a postdoctoral biology researcher at Emory University, told Insider.
The ideal level of protection is sterilizing immunity – when “we have such good immunity in the right places that the virus can’t even replicate if it gets in,” Lavine said.
But there’s plenty of middle ground between that and zero immunity. For example, Lavine said, “the virus might be able to replicate some, maybe causes mild pathology, maybe transmits for a day or two instead of five or six days.”
She added: “The chances that the new variant is getting us all the way from sterilizing immunity to no immunity is really unlikely.”
It also helps that existing vaccines are highly effective against the original virus.
“The Pfizer and Moderna vaccines are 95% effective – that’s an extraordinary level of efficacy,” Montefiori told CNN. “If it reduces to 90, 80, 70% effective, that is still very, very good and likely to have a major impact on the pandemic.”
Catherine Schuster-Bruce and Aria Bendix contributed reporting to this story.
The White House coronavirus task force sent states a report on Sunday warning that there might be a “USA variant” of the coronavirus. The variant could be fueling the unprecedented number of coronavirus cases and deaths in US, the report said, according to mediaoutlets that obtained the document.
The report suggested this USA variant may be more transmissible than the original version of the virus that emerged in China, much like the new strains identified in the UK (B.1.1.7) and in South Africa (B.1.351).
But there is no scientific evidence yet that a more contagious version of the coronavirus has originated or started spreading in the US.
In a statement to Business Insider on Friday, the Centers for Disease Control and Prevention said: “To date, neither researchers nor analysts at CDC have seen the emergence of a particular variant in the United States as has been seen with the emergence of B.1.1.7 in the United Kingdom or B.1.351 in South Africa.”
Human behavior has a large effect on transmission rates
The task force’s report, according to CNBC, offered little information about how long the new US strain described might have been circulating, nor what mutations were included in its genetic profile.
Scott Gottlieb, a former commissioner of the Food and Drug Administration, told CNBC’s Closing Bell that the task force’s hypothesis about the existence of a USA variant is in part based on the fact that US and UK’s pandemic growth curves are similar.
According to CNN, the task force’s report said: “This fall/winter surge has been at nearly twice the rate of rise of cases as the spring and summer surges. This acceleration suggests there may be a USA variant that has evolved here, in addition to the UK variant that is already spreading in our communities.”
Given the lack of evidence the task force provided, frustrated officials at the CDC tried to get the statements about the suspected variant removed from the recent report, but they were unsuccessful, according to the New York Times.
Even in the UK, the variant is not the only reason for the steep rise in cases.
“Human behavior has a very large effect on transmission – probably much larger than any biological differences in SARS-CoV-2 variants,” Paul Bieniasz, a virologist at the Howard Hughes Medical Institute, previously told Business Insider.
The variant reported in the UK does have an increased reproductive, or R0, value – the average number of people one sick person infects. The number is 1.5 rather than 1.1, the World Health Organization announced in December, which means that 100 sick people will infect another 150, not 110, on average.
But mitigation measures like social distancing and masking play a big role in how much the virus spreads, regardless of its genetic mutations.
The US isn’t sequencing enough genomes to spot new variants
To monitor the many versions of the coronavirus circulating worldwide – each separated by a handful of tiny changes in its genome – researchers genetically sequence samples of the virus and track the changes over time. UK researchers first pinpointed B.1.1.7 this way in mid-September.
But the US is behind many countries when it comes to keeping tabs on new variants. US researchers have genetically sequenced less than .01% of its coronavirus cases: 2.5 out of every 1,000. In total, the US has only sequenced 51,000 coronavirus samples, the CDC reported. In the UK, labs are sequencing 45 out of every 1,000 cases.
That’s likely the reason the US missed the UK strain’s introduction, and also why it would be difficult to identify a new USA variant. The US didn’t report its first case involving B.1.1.7 until December 29. That was at least three weeks after the strain entered the country, according to Charles Chiu, an infectious-disease expert at the University of California, San Francisco.
So far, more than 50 B.1.1.7 cases have been confirmed across six states, and all but one of those people had no travel history, suggesting the strain has been spreading silently for some time.
Even if a possible new USA variant were indeed responsible for an uptick in cases, pinpointing a connection could take months.
“There is a strong possibility there are variants in the United States; however, it could weeks or months to identify if there is a single variant of the virus that causes COVID-19 fueling the surge in the United States similar to the surge in the United Kingdom,” the CDC told Business Insider in its statement.
Dr. Peter Hotez, a vaccine scientist at Baylor College of Medicine in Texas, said in a tweet on Thursday that “there are likely similar homegrown variants in US as well, it’s just that no one is looking.”
“Like everything else in our national public health response, we’ve come up small on virus genomic sequencing,” he added.
Roughly two weeks after the UK announced that a new coronavirus strain was likely responsible for an uptick in cases in the south of England, the US confirmed its first case of that same strain.
The infected person, a man in his 20s in Colorado, had no recent history of travel outside the US, the office of Colorado Gov. Jared Polis said in a statement. Local authorities are working to identify any potential chains of transmission while the man isolates.
UK researchers first detected the new variant three months ago, as a second wave of infections started to mount at the end of the summer. Government leaders have suggested the new variant may be 70% more infectious than its predecessors. Between mid-November and December 9, the variant jumped from being responsible for 28% of London’s new cases to 62%. But there’s no reason to believe it’s more deadly, and experts think existing vaccines will likely still work.
“There is a lot we don’t know about this new COVID-19 variant, but scientists in the United Kingdom are warning the world that it is significantly more contagious,” Gov. Polis said in a statement. “The health and safety of Coloradans is our top priority and we will closely monitor this case, as well as all COVID-19 indicators, very closely. We are working to prevent spread and contain the virus at all levels.”
Countless versions of the coronavirus are circulating, each separated by a handful of tiny changes in its genetic code. The virus typically accumulates two mutations a month, most of which don’t affect its infectiousness or deadliness.
But every so often, “a mutation, or combination of mutations, can arise which confers an advantage to the virus in some way,” Lucy van Dorp, a researcher at University College London’s Genetics Institute, told Business Insider.
That may be the case with the new UK strain, which geneticists have named B.1.1.7. It collected at least 17 mutations at once. Some of the strain’s mutations affect the virus’ spike protein, which it uses to invade cells. That could make it easier for the virus to infect people. Experts believe the strain could have emerged in a patient who was infected for a long time, allowing the virus to mutate in their body, Science magazine reported.
In all likelihood, the variant probably entered the US long before this Colorado case was detected. The US keeps tabs on the genetics of far fewer coronavirus samples than the UK does: Only 51,000 of the 17 million US cases have been genetically sequenced.
“When we start to look for it, we’re going to find it,” he said.
Public health experts say the new strain’s spread is all the more reason to continue wearing masks and social distancing.
“Virus mutations can only accumulate if the virus is allowed to be transmitted,” Nathan Grubaugh, an epidemiologist at the Yale School of Medicine, told Business Insider. “So the longer that we allow uncontrolled transmission to occur, the more chances that the virus will have to adapt to human transmission.”
The surest way to boost the chances of a worrisome coronavirus mutation: let it spread unchecked.
“More infected people means more opportunity for the development of mutations. More movement of people … means new variants can spread faster,” Dr. Shira Dohon, an infectious-disease specialist at Tufts Medical Center, told Business Insider.
When viruses infect a body, they replicate. More spread means more replication, which raises the likelihood of genetic errors. So in places where transmission is high, we are more likely to see a harmful variant emerge, experts say.
UK researchers first detected the variant three months ago, after a second wave of infections started on the heels of a summer of indoor dining, drinking, and exercising. The variant was found just week’s after the UK reported 2,988 cases on September 6 – its highest daily record since late May.
Until just last week, London was in the second-lightest tier of coronavirus lockdowns, which allowed pubs to remain open and limited spectators at sporting events and performances.
“Virus mutations can only accumulate if the virus is allowed to be transmitted. So the longer that we allow uncontrolled transmission to occur, the more chances that the virus will have to adapt to human transmission,” Nathan Grubaugh, an epidemiologist at the Yale School of Medicine, told Business Insider.
Why the UK coronavirus strain is concerning
Countless versions of the coronavirus are circulating, each separated by a handful of tiny changes in its genetic code. The virus typically accumulates two mutations a month, many of which “have no real public-health impact,” Grubaugh said.
Most of the mutations don’t affect the virus’s infectiousness or deadliness, according to Lucy van Dorp, a researcher at University College London’s Genetics Institute.
But every so often, she told Business Insider, “a mutation, or combination of mutations, can arise which confers an advantage to the virus in some way.”
That may be the case with the new UK strain, which geneticists have named B.1.1.7. It collected at least 17 mutations at once. Experts believe the strain could have emerged in a patient who was infected for a long time, allowing the virus to mutate in their body, Science magazine reported.
Some of the strain’s mutations affect the virus’ spike protein, which it uses to invade cells. That could make it easier for the virus to infect people.
Not all scientists agree that the new strain is 70% more infectious, though Grubaugh said existing data suggest it “is associated with increased transmission.”
Indeed, 236,275 people tested positive for COVID-19 in the UK between December 17 and 23 – a 61% increase from the week before. The number of daily new cases has doubled in the last two weeks, to almost 40,000 per day. A couple of hotspots have more than 1,100 cases per 100,000 residents. Between mid-November and December 9, the variant jumped from being responsible for 28% of London’s cases to 62%.
South Africa, too, is dealing with a new coronavirus strain that appears to be more transmissible and shares one mutation related to the spike protein with the UK strain.
‘The more replication, the more opportunities for evolution’
From June to September, the entire UK was put in the middle tier of its COVID alert level system. Restrictions were eased: Bars and gyms opened in July, and more than 100 million discounted meals were served to indoor diners in August via the government’s Eat Out to Help Out plan to stimulate the restaurant sector.
But that reopening may have happened too quickly. One researcher estimated Eat Out to Help Out was linked to almost 20% of all new UK infection clusters in August. London, where new daily cases were in the dozens in July, saw that figure spike to more than 1,000 by the start of October. Summer days with record lows of just 400 to 500 new cases in the UK gave way to daily fall totals of 4,000 to 5,000 new infections.
“The more replication, the more opportunities for evolution and adaptation,” Richard Neher, an epidemiologist tracking coronavirus strains with the Nextstrain project, told Business Insider.
Neher added, though, that since it’s hard to predict what prompts a virus to evolve and when particular mutations will arise, “the chance of this happening might not be exactly proportional to the number of cases.”
The new variant shouldn’t be blamed for all the spread
The new variant has an increased reproductive, or R0, value – the average number of people one sick person infects – of 1.5 rather than 1.1, the World Health Organization announced Monday. That difference of 0.4 means 100 sick people will infect another 150, not 110, on average.
“However, that does not mean that it is responsible for the rising cases in London and the surrounding area,” Dohon said. She and Grubaugh both emphasized that human behavior and mitigation measures play a big role, too.
“If we have a higher proportion of the population that distances and wears masks, it will stop the virus, variant or not,” Grubaugh said.
Indeed, CDC noted that although a variant may dominate a geographic area, “that fact alone does not mean that the variant is more infectious.” A strain could just get lucky, arising by chance in populous areas at the time when a government relaxes restrictions.
These same questions emerged after a different variant of the virus was detected earlier in the pandemic. That strain also has a mutation affecting the spike protein. It’s predominantly the version that spread in Europe and North America last winter, and it’s now more prevalent worldwide than the original virus that emerged in China. Some evidence suggests the strain is more infectious, but it might also have just hit the US and Europe at a moment when testing was limited and lockdowns hadn’t yet been implemented.
‘Variants rarely stay a local problem’
Prime Minister Boris Johnson placed 16 million people in southeastern England under a tier 4 lockdown, the UK’s strictest, on Saturday. Soon after, at least 27 countries have blocked travel from the UK.
But it’s already too late.
“Variants rarely stay a local problem,” Neher said.
Genetics data reveal the strain is present in Scotland and Wales, as well as Denmark, Belgium, Iceland, and the Netherlands. There are a handful of cases in Italy, Australia, Gibraltar, and Singapore, too. Grubaugh said it hasn’t been found in the US yet.
But that may be because US keeps tabs on the genetics of far fewer coronavirus samples than the UK and South Africa do. Only 51,000 of the 17 million US cases have been genetically sequenced, so “the mutation could be more widespread and we just don’t know it,” Grubaugh said.
“When we start to look for it, we’re going to find it,” he said.
That reality leaves only one real option, Grubaugh said: “If a country is worried about the new variant being introduced and causing increased local transmission, a more effective plan is to put measures in place to decrease local transmission.”
He added that his won’t be the last time we learn of a new, potentially more infectious strain.
“Have there been others? Possibly, and maybe they didn’t perpetuate for some reason,” he said. “Will there be others in the future? Likely.”
A new coronavirus strain may be fueling an uptick in spread across the southern UK, according to Health Secretary Matt Hancock.
“Over the last few days, thanks to our world-class genomic capability in the UK, we have identified a new variant of coronavirus, which may be associated with the faster spread in the South of England,” Hancock said Monday, speaking in the House of Commons. He pointed to “very sharp exponential rises in the virus across London, Kent, parts of Essex, and Hertfordshire.”
Hancock added that there’s no evidence to suggest this new strain is more deadly or resistant to vaccines. But it could be more transmissible, he said: “Initial analysis suggests this variant is growing faster than the existing variants.”
Hancock said that at least 60 different local authorities had seen infections from the variant, the World Health Organization had been notified, and UK scientists were doing detailed studies, according to the BBC. He did not publicly provide any further data about the variant, however.
London and large parts of Southern England will be placed into “tier 3,” the strictest level of lockdown, from midnight on Tuesday, Hancock said. That means roughly 34 million British people are now in tier 3 areas, in which pubs and restaurants are closed.
However, scientists are urging calm until more is known about the coronavirus variant Hancock mentioned.
“It is incredibly frustrating to have such a statement made without any associated evidence,” Lucy van Dorp, a geneticist studying the coronavirus’ genome, told Business Insider, adding that it’s unlikely that one mutation would play a big role in changing disease severity for a virus.
‘It’s too early to be worried’ by this new variant
Like all viruses, the coronavirus mutates over time. So scientists have been regularly collecting samples of the coronavirus sine the beginning of the pandemic and genetically sequencing them to track how it changes.
According to Alan McNally, a professor of genomics at the University of Birmingham, testing labs across the UK “picked up” the new variant in the last few weeks.
“It is important to keep a calm and rational perspective on the strain as this is normal virus evolution and we expect new variants to come and go and emerge over time,” he said in a statement to UK’s Science Media Centre. “It’s too early to be worried or not by this new variant, but I am in awe of the surveillance efforts in the UK that allowed this to be picked up so fast.”
The variant includes a mutation in the virus’ spike protein, called N501Y. That spike is what the coronavirus uses to invade our cells, so it’s possible a tweak there could make it easier for the virus to infect our bodies.
“Efforts are under way to confirm whether or not any of these mutations are contributing to increased transmission,” the COVID-19 Genomics UK Consortium, the group that identified the variant, said in a statement.
“There is currently no evidence that this variant (or any other studied to date) has any impact on disease severity, or that it will render vaccines less effective,” it added.
Mutations don’t necessarily impact a virus’ behavior
Other scientists are similarly hesitant to make conclusions based on the news of this new variant.
“There is no evidence that the newly reported variant results in a more severe disease,” Wendy Barclay, head of the Department of Infectious Disease at Imperial College London, said in a Science Media Centre statement on Monday.
Hodcroft said that most mutations her team has seen so far are harmless, and the coronavirus is mutating slowly. There is one variant, called 614G, that might be more transmissible than the original virus, she added, but that question is not settled.
Jonathan Ball, a molecular virologist at the University of Nottingham, struck a cautious tone in his own statement to the Science Media Center.
“The genetic information in many viruses can change very rapidly and sometimes these changes can benefit the virus – by allowing it to transmit more efficiently or to escape from vaccines or treatments – but many changes have no effect at all,” he said.
Ball added: “Even though a new genetic variant of the virus has emerged and is spreading in many parts of the UK and across the world, this can happen purely by chance. Therefore, it is important that we study any genetic changes as they occur, to work out if they are affecting how the virus behaves.”
This story has been updated with additional information. It was originally published on December 14, 2020 at 10:02 a.m.