The coronavirus variant that emerged in the UK belongs to the world now, and growing evidence is confirming the first suspicions of some scientists: it is a super spreader capable of turbining the pandemic and driving less transmissible strains of the virus into oblivion.
Now that the new variant has established a bridgehead in the United States and in more than 40 other countries, the race to contain it has begun. The contest pits humans armed with vaccine, masks and hand sanitizer against a viral strain with a handful of genetic changes that have raised fears since the moment they were detected.
There is some good news: the researchers who measured and modeled the UK variant’s powers found no reason to believe that it makes people sicker when it invades their bodies. Nor does it seem to reduce the time it takes for a newly infected person to be able to spread the virus – a development that can generate waves of new patients.
And new research reinforces the case that COVID-19 vaccines administered in the United States and elsewhere must protect against the new variant.
But other findings are more damaging. Using many different methods to track the UK variant and compare it with its predecessors, two groups of researchers concluded that the rapid growth of the new strain in Britain cannot be dismissed as a fluke.
And as fast as the new strain has spread in its homeland, it should perform even better here. Once established in the United States – a perspective that experts consider inevitable -, frustrating it will require stricter public health measures than those adopted so far, a faster launch of the vaccine and a much greater willingness to be immunized.
“We are losing the race with the coronavirus – it is infecting people much faster than we can put the vaccine in people’s arms and it is overcoming our social distance,” said biologist Derek Cummings of the University of Florida, an expert on emerging pathogens. “Now there is this variant that will make the race even more difficult.”
The genetic changes in the new variant appear to have increased its transmissibility by about 56%, according to the new research, although it can be as low as 40% and as high as 70%.
With this competitive advantage, it will quickly become the most commonly found strain in any region where it gains space. In doing so, coronavirus infections – and the resulting increase in illnesses, hospitalizations and deaths – will explode.
“The bottom line is that it will be more difficult to control this new variant if it takes over,” said Ira Longini, an infectious disease modeler at the University of Florida who was not involved in any of the British studies.
And he will take over, he added.
The superpower of the new variant, as evidenced in Britain, is its ability to plow through public health protection grids and spread easily. It had been spreading for at least a month and probably more before it was detected by insightful (and well-funded) geneticists in the UK.
Travel bans were predictably useless to suppress it. The variant, known to scientists as B.1.1.7, has appeared in 47 countries so far, including countries as far away as Australia, Chile and Japan.
Recently, in 2009, disease hunters saw strains of the flu virus with just a few new genetic adjustments to eliminate existing strains within a year, Longini said.
“I don’t see what could prevent that,” he said. “It must spread across the planet.”
What does this improved transmissibility mean? Imagine a group of people without a mask, none of whom has immunity to the SARS-CoV-2 virus. If a single person with a typical strain comes in and mixes for a few hours, two or three additional people are likely to go home infected.
If the same party participant were infected with B.1.1.7, the virus would find 3.5 to 4.3 new victims during the same event.
This difference may seem small, but as new generations become infected, its effect will be amplified. In a month, a single person with the UK variant could generate 150 new infections – almost quadrupling the 39 cases that would result from a person with an older coronavirus strain.
In reality, the United Kingdom variant would probably encounter a little more resistance in the United States. At this point in the pandemic, about 1 in 5 guests has already been infected and has gained some measure of immunity that may be useful. In addition, some social distance is likely to be observed, the party can be held outside and many participants wear masks.
Under these circumstances, someone with a typical SARS-CoV-2 strain would likely find a single person to infect; on a rare lucky night for the virus, two people would come out infected. At this rate, the pandemic is growing at a relatively imposing rate, and after a month, a total of three people have been infected.
B.1.1.7 changes this image. A carrier of the same party would pass his infection to 1.5 to two other victims. After a month, the initial case results in 11 to 16 new infections.
In the dispute between viral strains, this competitive advantage is important. The purpose of a virus is to find and invade new bodies. The variant that manages to capture more of them and, in turn, infect even more bodies, will leap ahead of its competitors and establish its dominance.
In a short time, the most timid tensions are completely eliminated from the landscape, and the bold newcomer is giving orders for the pandemic.
For example, experts warn that increasing the transmissibility of B.1.1.7 will increase the proportion of the population that needs to be vaccinated to achieve collective immunity and stop the pandemic.
To deny a virus enough new victims to keep the pandemic alive and growing, you need to surround more of its carriers with non-infectious people – in other words, vaccinated people – who will get in their way and hinder transmission. The better a virus infects new victims, the more non-infectious people you will need in the population to block your path to a new victim.
Even before the threat of B.1.1.7 was fully understood, US health officials were increasing their estimates of how many Americans would need to be vaccinated to establish herd immunity here. Although his initial estimates were about 70% of the population, experts like Dr. Anthony Fauci, the country’s leading infectious disease specialist, increased his target to 85%.
Still, in a survey completed in early December, the Kaiser Family Foundation found that only 71% of Americans would definitely or probably get the COVID-19 vaccine. Other recent surveys reported that the proportion of willing Americans was just over half.
In Britain, the increased infectivity of the UK strain has been demonstrated by two groups of researchers using various techniques.
The first group, an influential team of infectious disease modelers at Imperial College London, used genetic sequencing techniques that allowed them to record infections and track the virus’s progress in a population. They compared the growth of B.1.1.7 in three distinct regions of England and found similar patterns of growth in all of them.
For further confirmation, they examined hundreds of positive tests for the coronavirus. In rudimentary genetic screening, widely used to confirm an infection, the UK strain triggers a telltale signal, revealing the presence of changes unique to it.
By that measure, too, the location and growth rates of the new genetic variant – and its consistent ability to fend off other strains – allowed researchers to estimate how much it is more transmissible. And he told them that its rapid growth could not be explained by local conditions (such as a particularly vulnerable elderly population) or environmental circumstances (like the colder climate that forced people to spend more time together indoors) that favored the new variant in relation to existing viral strains.
The second group of researchers, from the London School of Hygiene and Tropical Medicine, used many of the same techniques. They adjusted the outbreak data in mathematical models to show the similarity of the B.1.1.7 footprint in different regions and to explore the possible reasons for the consistency they observed.
They concluded that the rapid rise in infections in Britain had to be fueled by one or more of the changes in the genetic code of the new variant, although they are not sure which made the difference.
It is an inference. But experts say it is a good example.
“If you give me evidence of these studies, I would say that I don’t buy at all,” said UC Irvine biostatistician Vladimir Minin, who was not involved in any of the studies. “But the authors provided a lot of evidence that even the most skeptical among us could not rule out. This is quite solid evidence that this is indeed a faster spreading virus. “
In a country that is already struggling for people to wear masks, stay at home and avoid meetings, vaccines seem to be the only way out. And the arrival of B.1.1.7 is a stronger case than ever to prioritize the elderly and those most likely to become seriously ill or die from an infection, said Dr. Marc Lipsitch, director of the Harvard Center for Dynamics of Communicable Diseases. That way, even if Americans can’t stop the spread of a more challenging virus, vaccines can “neutralize” its impact, he said.
But first, said Cummings, they must have time to work. And that will require more draconian public health efforts to prevent additional deaths.
It is a time similar to the early days of the pandemic, when Americans were asked to make sacrifices to “smooth the curve” and give hospitals time for supplies of ventilators, protective equipment and health workers to retrieve them. This time, the curve that must be flattened is steeper.
Still, Cummings said, “We must not raise our hands and say that this is a lost cause. Every week we receive help. We have these public health tools and we can all do something to slow infections and give us more time to get vaccines out. “
This story originally appeared in the Los Angeles Times.