Colorado made national news when Gov. Jared Polis announced on Dec. 29 that the state health department had found the first case in the U.S. of a coronavirus variant that had been spreading rapidly in Great Britain and several other countries.
Just over two weeks later, on Jan. 13, the state confirmed its fifth case of the variant known as B.1.1.7. State officials continue to test for it, but they’re doing so with just a tiny sample of the thousands of new COVID-19 cases across the state each day.
The coronavirus variant
Mutations are a part of life. Most lead nowhere; some lead to the likes of cheetahs and sharks. For a virus, the coronavirus happens to be a slow mutator, but that trial and error is happening across trillions of viruses replicating away in millions of bodies, and changes that lead to evolutionary advantage – from the SARS-CoV-2 virus’s perspective, not ours – are bound to happen.
So it was with B.1.1.7. The virus doesn’t appear to cause more severe disease. But the changes the mutation brought to the coronavirus’s spike protein that provides entry into human cells probably make it more contagious. Much more contagious, in fact: 56% more transmissible or more, according to one British modeling study awaiting peer review. Separately, the United Kingdom’s testing and tracing program tracked nearly a million contacts of those who had tested positive for COVID-19. Based on the number of contacts who later became ill, they calculated the B.1.1.7 variant to be 35% to 50% more transmissible. That report was published on Jan. 8.
Dr. Eric Poeschla, a UCHealth physician and head of the Division of Infectious Diseases at the University of Colorado School of Medicine, shared that report during a Jan. 13 virtual Town Hall and did not mince words. U.S. coronavirus case counts are at alarmingly high levels even without new, more easily spread viral variants.
“What’s worrisome is, if this is correct, you throw a 50% or 30% more infectious virus and an exhausted population into the mix, what will happen?” Poeschla said.
Massive competitive advantage
From a virus’s point of view, the more transmissible it is, the more competitive it is. The B.1.1.7 variant emerged in southeast England last September. It now represents the majority of cases in greater London. In neighboring Ireland, the B.1.1.7 lineage comprised 9% of those tested on Dec. 20; by Jan. 3, that figure had grown to 25% of those tested, and then to 45% of those tested by Jan. 11. Irish officials believe that this more infectious coronavirus variant, combined with dipping social-distancing compliance around the holidays, have contributed to Ireland having, as of Jan. 13, the highest rate of new COVID-19 cases of anywhere in the world.
What makes this particular coronavirus variant and, perhaps others that have emerged independently in South Africa (B.1.351 lineage), Brazil (P.1 lineage), and perhaps elsewhere, so much more “competitive”? The science is nascent (essentially all the research papers available so far are preprints). But it looks like the enhanced infectiousness boils down to a chance combination of a few genetic changes to the coronavirus’s RNA. Those changes altered the shape of small parts of the coronavirus spike protein that binds with human cells (technically, the most worrisome change is in the S receptor binding domain, from a genetic variation called N501Y and, in the South African and Brazil variants, a combination of N501Y and E484K).
Why these changes may bring about a big difference in infectiousness isn’t yet clear. It could be that the mutated virus binds more firmly to our cells so it takes fewer coronaviruses to attain the critical mass needed to tip into lasting infection. It could be that the mutation leads to higher viral loads in the nose and throat, as one research team suggested – and therefore sends more viruses flying through the air with each infected exhalation. It could be both. It could be something else entirely.
To most of us, it doesn’t really matter. What does matter is what a perhaps 50% increase in competitiveness will sooner than later mean. Consider some analogies from the world of sports. Fifty percent faster than Usain Bolt in his prime is the speed of a galloping thoroughbred racehorse. Fifty percent longer than Mike Powell’s world-record 29 ft 4 ¼-inch long jump is 44 feet, or the distance of a last-second half-court basketball buzzer-beater. A baseball pitcher who threw 50% harder than today’s biggest guns would boast a 150-plus mph fastball.
A 50% performance boost to a coronavirus already so optimized as to have spread with ease globally and to have killed some 2 million people in the process would bequeath an overwhelming reproductive advantage. We’re seeing that unfold in the UK and Ireland. And as Poeschla put it, “There’s no reason to believe that the United States is different than England. It can turn on a dime.”
Vaccines should work
And because of the nature of exponential growth, the implications could be dire – much worse than if the new strain were no more transmissible, but caused 50% more severe disease among those who got sick. In a back-of-the-envelope hypothetical, mathematician and epidemiologist Adam Kucharski figured that 10,000 infections with the familiar strains of the coronavirus might kill 129 people over the course of a month. A 50% boost in disease severity would lead to 198 deaths. In contrast, with a 50% boost in infectiousness, that figure would jump to 978 people.
Furthermore, there’s clear evidence, as noted, that the chance mutations that happened in Britain last November also happened in South Africa and Brazil. Such mutation may well have happened independently in the United States, too. A team of Ohio State University researchers say they’ve found a homegrown variant with that N501Y mutation in patients in Columbus.
Assuming these coronavirus variants – wherever they emerge from – become dominant, how do we keep a resulting spike in cases and, by extension, hospitalizations and deaths, from triggering renewed lockdowns to avoid swamping health care institutions? As with existing forms of the virus, it will take a combination of vaccination and vigilance.
But will the vaccines thwart the new coronavirus variant? After all, preliminary research indicates that E484K mutation found in the South African and Brazilian variants may repel some of the antibodies vaccines induce the body to produce. At the same time, vaccine makers seem confident that their products will persevere. Pfizer says lab tests showed that their vaccine should be effective against SARS-CoV-2 viruses with the N501Y mutation. Moderna’s vaccine uses the same mRNA strand as Pfizer’s so it should be the same story. With a remarkable 95% effectiveness in preventing COVID-19, the Moderna and Pfizer vaccines can afford a subtle reduction in effectiveness and still be potent, though more people would get sick and the pandemic would take longer to quell.
Dr. Thomas Campbell, the University of Colorado School of Medicine virologist and infectious disease specialist leading the Moderna vaccine study at UCH, shares with Poeschla and other experts the belief that, because these vaccines trigger a cascade of diverse antibody production that target many epitopes – antibody targets – on the spike protein, individual mutations won’t provide much of a hiding place for the coronavirus.
“The worst-case scenario that I would expect would be a reduction in efficacy of the vaccine,” Campbell said. “I don’t think it’s going to eliminate all of the vaccine efficacy because the vaccine will induce a polyclonal response – antibodies that target multiple epitopes in the spike protein. And having a mutation at one or more of those epitopes is unlikely to abolish all of the effects.”
Campbell added that those who have recovered from COVID-19 and have acquired immunity seem to be resistant to the new coronavirus variants.
Regardless, these coronavirus variants introduce further urgency to the race for vaccination-based herd immunity. We’ve started slowly: only about 3.6% of the U.S. population had received a first shot as of Jan. 18, though Colorado is doing a bit better at 4.7% of the population. All the more reason to stay vigilant as far as social distancing, masking up, and staying out of enclosed spaces with those you don’t live with, says Dr. Michelle Barron, UCHealth’s senior medical director of Infection Control and Prevention.
While the vaccine is proven to prevent disease, she adds, only a small minority of us have been vaccinated, and it’s not yet clear if those who have been vaccinated can still transmit the virus or not.
“While these vaccines offer hope, they also terrify me,” Barron said. “I worry that people will get vaccinated and think, ‘I don’t have to wear a mask – we can have that big party.’ In fact, we don’t know whether or not the vaccine stops you from being a carrier.”
Also, she says, the slow pace of vaccination and the immense logistical challenges of inoculating more than 330 million people in the United States alone mean that we’re months away from herd immunity even without the faster spread of new variants.
“Now is not the time to stop wearing a mask or stop social distancing,” Barron said. “The vaccine won’t change that. We’re not out of the woods. I know we want to be. But if we act like ostriches with our heads in the sand and say, ‘We’re good,’ we’re going to end up back where we were.”
Experts worry that these more transmissible coronavirus variants are coming on hard and fast. The variants represent an unwelcome tailwind for the virus in its race against global efforts to innovate and inoculate humanity’s way out of this global pandemic. Now more than ever, our own behavior will dictate where the finish line ends up being – and how grueling the race will be.