This is the first article in Viral Studies, a Slate series in which we break down recent viral articles and—most importantly—their caveats.
Up first: On Tuesday, the Los Angeles Times published an article about a new analysis from researchers at Los Alamos National Laboratory. The original title was pretty splashy: “A Mutant Coronavirus Has Emerged, Even More Contagious Than the Original, Study Says.” The Times has since changed that headline: “Scientists Say a Now-Dominant Strain of the Coronavirus Appears to Be More Contagious Than Original.”
“Mutant coronavirus” sounds scary! In popular culture, mutants are what arise from chemical spills (Teenage Mutant Ninja Turtles, anyone?), and they often have superpowers (see: the X-Men). In a movie, TV show, or novel about a pandemic, “When a character says, ‘The virus is mutating,’ that usually means all hell is about to break loose,” says virologist Angela Rasmussen. It doesn’t help that this taps into a fear that’s been circulating since the beginning of the virus—that the virus will evolve into something even deadlier.
As a result, people have widely shared this article on social media, expressing surprise or fear that the virus is “getting worse.” In some cases, people point to it as evidence that reopening states is a bad idea. Let’s take a closer look at what the story said, what the study underlying it claims, and what you should actually take away from this.
Yes, the coronavirus has mutated—and it will continue to mutate, as all viruses and animal species do. But those mutations are not fundamentally scary or bad and don’t necessarily change how a virus functions. And viruses like SARS-CoV-2 that have RNA as their genetic material typically mutate faster than DNA viruses, like hepatitis B, or DNA in animal species; when RNA replicates, it lacks some of the crucial “proofreading” abilities used in DNA replication, so there’s a mutation virtually every time the virus copies itself. “Mutations in the genomes of RNA viruses are normal and often unremarkable,” says Rasmussen.
Before we get into what the study says, it’s important to understand where it came from. Typically, scientific research is published in academic research journals, and before it is published, it goes through a process called peer review, where knowledgeable colleagues read over the work and offer critiques. This paper, however, has not yet gone through that peer review process. Rather, it was posted to a website called BioRxiv, a repository of preprints—academic papers that have not yet undergone peer review.
Long before SARS-CoV-2 upended society, scientists posted preprints to sites like BioRxiv because they offered opportunities to discuss findings with others. Researchers might share resources and discuss data with one another; informal discussions via email, in online forums, and on social media can be productive (especially now, as coronavirus researchers are working quickly to understand the virus). But recently, scientific preprints have received more attention than ever from the general public and journalists. And unfortunately, these papers and the conversations scientists have about them aren’t always designed for nonexperts to follow along with. Without the proper background knowledge and context, it’s easy to misinterpret results. (See, for instance, the difference between what a mutation means in pop culture versus what it means to actual virologists.)
Scientists had been talking among themselves about the coronavirus mutation study for days before the Los Angeles Times piece came out. Using a computer model to analyze existing data about the virus’s genome, the researchers identified several mutations. They singled out a mutation on one particular protein called spike and noted that the mutation became popular in Europe in February and then traveled to the U.S., among other places. Their analysis suggested that whenever one particular mutation—known as G614—arrived in new geographic areas, it “became the dominant local form in a matter of only a few weeks.” The authors discuss the possibility that this dominance resulted from the mutation’s transmissibility.
Since the study has not been peer reviewed, an informal version of that process took place on Twitter, where researchers have discussed their thoughts on the methods, and the authors’ conclusions. Harvard epidemiologist Bill Hanage tweeted last week that he thinks claims that G614 is more transmissible “are suspect, to say the least.” For one, the study does not demonstrate that G614 is more popular because it’s more transmissible. “This variant might have been lucky,” Hanage tweeted. Other circumstances besides the mutation’s inherent transmissibility could have helped, like where it happened to travel—in this case, it spread on the U.S.’s East Coast, which was slower to take action in response to the coronavirus than the West Coast, where another variation—known as D614—spread before G614 arrived.
Rasmussen says that the study itself is “fine” and that its overall contributions—identifying that this mutation became prevalent—are important and worth investigating. “If I were reviewing the paper itself for publication in a journal, I’d ask the authors to tone down the certainty of some of their conclusions,” she says. Like Hanage, she emphasizes that the G614 mutation’s prevalence does not mean it’s more transmissible and there are many confounding factors that could account for why G614 became popular: “There are too many variables impacting transmission within large populations of people, such as stay-home orders, testing capacity, case criteria and reporting, isolation and quarantine practices, different cultural and behavioral practices that can modulate exposure risk, genetic factors determining susceptibility, etc.”
The Los Angeles Times piece’s reporting on that study took the most exciting possibility it raises—that this G614 mutation makes the virus more transmissible—and runs with it. The piece’s original title—the one that mentions the “mutant coronavirus”—is eyebrow-raising, and its first line continues in the same tone: “Scientists have identified a new strain of the coronavirus that has become dominant worldwide and appears to be more contagious than the versions that spread in the early days of the COVID-19 pandemic.” While the piece does mention that the study is a preprint that hasn’t undergone peer review, that caveat may be lost on the many readers who aren’t familiar with the process of scientific publishing.
The piece goes on to describe this “new strain,” saying it “quickly infected far more people than the earlier strains that came out of Wuhan” and that “the new strain’s dominance over its predecessors demonstrates that it is more infectious.” (The Times later replaced the word demonstrates with suggests.) This mutation might mean that vaccines “might not be effective against the new [strain].” This reporting conflates prevalence—how widespread that strain is—and transmissibility, says Rasmussen. “It’s very difficult to make conclusions about ‘quickly infecting’ people, much less the impact on drugs and vaccines that haven’t been developed yet.”
But that conflation is made in the study as well. Ralph Vartabedian, the author of the Times’ piece, says, “My story was based on what the report said, so if people want to attack the report, they can attack the story in tandem.” Vartabedian says he was drawn to report on the story because of its potential implications for vaccines; when I reached out to study co-author David Montefiori for comment, he emphasized the same points Vartabedian included in his reporting. “We have little doubt that this new form of the virus is more transmissible,” Montefiori told me in an email. “The vaccines may need to be changed to be effective against both forms of the virus.”
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