Such a tweaking of the vaccines could be done “in minutes,” said Drew Weissman, a professor of medicine at the University of Pennsylvania’s Perelman School of Medicine and one of the inventors of the messenger RNA technology that powers both vaccines.
“It’s very easy,” Weissman added.
This reassurance comes at a jittery moment, when the first two approved vaccines are offering hope that the beginning of the end of this global health emergency is at hand, even as the virus offers disquieting reminders that it is not static.
Authorities in the United Kingdom and South Africa have announced that variants of the coronavirus are spreading in their countries at alarming rates. Some scientists have said it could already be circulating in the United States, though it has not been detected here. The new variants carry mutations detected through genomic sequencing. A paper published Wednesday by scientists at the London School of Hygiene and Tropical Medicine, but not yet peer-reviewed, said that modeling indicates that the variant known as B.1.1.7 is 56 percent more transmissible.
Actually rolling out a recalibrated vaccine would take some time, Weissman acknowledged, perhaps a couple of months, due to manufacturing and regulatory requirements. But he said he doubts the Food and Drug Administration would require the same extensive randomized trials that showed the safety and efficacy of the vaccines developed this year by the pharmaceutical company Moderna and the partnership of Pfizer and BioNTech.
British Health Secretary Matt Hancock said Wednesday that the variant identified in South Africa had turned up in two people in England and is even more transmissible than the mutation-laden variant already circulating at alarming rates in his country. Hancock described the South African variant as having “mutated further” than the United Kingdom variant.
Such dire warnings should not incite panic, scientists say, noting that all viruses mutate and this one doesn’t mutate very quickly. There is zero evidence these mutations have made the virus deadlier, they said. Nor is there any reason to think they will. It is just as likely that mutations would make the virus less deadly, or “pathogenic.”
Research on these variants is in its early stages. In science, extraordinary claims typically require extraordinary evidence, and in this case that would mean far more extensive research, including multiple peer-reviewed studies and numerous laboratory experiments with the variants to see if they truly behave differently.
“What’s the data? Where’s the beef?” said Susan Weiss, a virologist at the University of Pennsylvania who has studied coronaviruses for four decades. “I think, most likely, it’s a tempest in the teapot.”
Still, a number of leading scientists tracking the situation, including Anthony S. Fauci, director of the National Institute of Allergy and Infectious Diseases, have said the variants do appear to be more transmissible.
For now the major pieces of evidence are that they are spreading so rapidly in more than one location and have the kind of mutations that would lead scientists to suspect that natural selection is at play. The variants have genetic mutations that change the structure of the spike protein on the outside of the virus. This could potentially enhance the ability of the virus to bind with receptor cells in the human body, or replicate more readily.
“We know that it has a collection of mutations, some of which we know about, others of which will require more investigation, which can be categorized as looking suspicious,” said William Hanage, an epidemiologist at the Harvard T.H. Chan School of Public Health, referring specifically to B.1.1.7. He said the exact reason for the apparent increase in transmission is unclear, but “it does have a set of mutations that have been previously flagged as worthy of interest and concern.”
There are several scenarios for greater transmissibility of B.1.1.7, said Angela Rasmussen, a virologist at the Georgetown Center for Global Health Science and Security. If the virus binds more easily to receptor cells, a person could become infected through exposure to a lower amount of virus.
Easier replication in the body could lead to higher viral loads, meaning the infected person would shed more virus, facilitating transmission. Or the virus could linger longer in the body and extend the period in which the person is infectious.
But none of this has practical consequences for how people should behave, Rasmussen said. The existing variants of the virus already known to be in circulation in the United States are spreading easily, she noted. The new variants of the virus are contagious in the same way the earlier “wild” types of virus are — and people can protect themselves with the same approaches. Wear a mask, wash your hands — that hasn’t changed.
The greater transmission rate “is not because the virus is suddenly able to seek you out like a heat-seeking missile. It’s just probability,” Rasmussen said. “It’s not an X-Man. It can’t magically melt through a mask if it has eight mutations in the spike protein, or even if it has 50 mutations in the spike protein. That’s like saying you can paint a smiley face on a baseball and suddenly it can travel through a wall.”
The mutations may be signals that the virus is adapting itself to humans and, through natural selection, finding ways to grow and spread. As the virus collides with the human immune system, it is under pressure to evolve. That will continue as the vaccines roll out.
“There’s a lot of pressure on the virus,” Weissman said. “It has to figure out how to infect us better because that’s how it survives.”
But people now have some ingenious tools to counteract mutant viruses. The mRNA vaccines developed by Pfizer-BioNTech and Moderna do not use any coronaviruses or even segments of live or dead viruses. Instead they harness a synthesized piece of messenger RNA, fundamentally no different from what is already in our bodies.
This RNA instructs cells to manufacture a protein that looks like the spike protein that studs the outside of the coronavirus. The body’s immune system then mounts antibodies against it.
Those antibodies are diverse in shape and function and cover the whole waterfront of the spike protein. A mutation here and there, or even eight or 10 or 20 mutations changing the spike protein would still leave vulnerable areas for the antibodies to attack. In effect, the immune system floods the zone.
Nonetheless, the experts agree: This coronavirus is a moving target and needs to be closely monitored, requiring a much greater investment in testing and genomic sequencing in the United States.
“I think you have to remember this virus crossed over into people probably in November or December of last year,” Weissman said. “That was the first time it ever got into humans. It’s a brand new virus. You have to expect that mutations are going to appear that will help the virus grow better.
“I don’t know how long it’ll take the virus to figure out how to grow best in humans. It’s probably years. It could be decades that it keeps mutating,” he said.
