Scientific research about the novel coronavirus and the media’s reporting on it are both moving at breakneck speed. We’re all hungry for breakthroughs, cures, new data—anything that might give us insight into how to find our way out of this crisis. In these first few months of the pandemic, viral misinformation has stemmed from several sources: The origin might be a flawed study, or a news article that sensationalizes new findings without properly grounding them in context.
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.”
If Vartabedian’s job was to report on what this new study said, then he has done a fine job. But discussion of new studies requires context and caveats, so best practices in science journalism dictate that reporters contact researchers with subject-specific expertise to give papers a proper once-over. That’s all the more important when writing about preprints like this one, which have not undergone peer review from other experts.
The nuance and uncertainty in these results might have been illuminated by talking with more experts, especially those not involved directly with the work. Vartabedian’s piece includes excerpts from a Facebook post by lead author Bette Korber as well as her co-author Montefiori. When the piece was published Tuesday, the only named outside expert was Alan Wu, a professor of laboratory medicine at the University of California–San Francisco. Wu surely has expertise—he told me that as a lab director, he is responsible for antibody tests—but he’s a strange choice for outside comment on this research study. Typically, science journalists seek expertise from researchers who have specific expertise in the subject of the paper, which in this case would be a virologist, epidemiologist, or geneticist. “COVID has refocused our attention away from our past expertise,” says Wu. “I do not have content expertise on genetics or virology, but we do offer viral genotyping for other viruses and are looking to do some on COVID sooner rather than later.” His perspective is certainly valuable, but so would the perspectives from those who could’ve more closely evaluated the methods and conclusions of Korber and colleagues’ work.
I asked Vartabedian about his choice of sources, and he says it’s a fair question. “How many people do you need to talk to?” he says. “Getting react[ion] to a story about [a] government decision, you go out and you talk to members of the government, units that are affected. This is somewhat less clear.” He went on to say that you might find some virologists who think Korber and colleagues’ study was great while others say it’s inconclusive. “It’s very tough to weed those comments out to the one or two that are going to fit in the story and make sure those fairly represent the broader view.” (It appears the Times realized the value of including more viewpoints; cached versions of the article show that it quietly edited the piece Wednesday to include perspectives from three other researchers.)
Yes, it is tough to get a handle on scientific consensus, and that’s why science journalists sometimes talk to dozens of sources for a single story. Tactics from political reporting—presenting different viewpoints all as having equal weight—do not always work well when reporting on science. This is an ongoing discussion among journalists, especially science journalists, and has recently become more relevant as general reporters delve into science research.
This study shows the dominance of the G614 mutation, but that doesn’t necessarily mean that its prevalence is because it’s more transmissible. It certainly could be the case that the mutation actually did make the virus more transmissible, but scientists believe we won’t know that until we have more research in hand. To investigate whether that happened, researchers can’t just rely on these computer-modeling results. “You would need to do an experiment comparing the virus with the mutation with the virus without,” says Rasmussen. You might use animal models to compare how likely each variant of the virus is to infect cells, and to study how each variant of the virus replicates.
Montefiori tells me their future research will do something similar to investigate whether the G614 mutation changes vaccines’ effectiveness: They’ll use blood samples from vaccinated people and examine any differences between how viruses with certain mutations—say, G614 and D614—infect cells.
Researchers are also looking into biases with the data available for these genomic analyses. Hanage pointed out on Twitter that there are relatively few sequenced coronavirus genomes coming from China later in the pandemic’s spread, which might bias the dataset Montefiori and his colleagues analyzed. In an email, Hanage pointed me to a thread where researchers were discussing potential errors in GISAID, the massive genomic dataset the researchers used for their analysis; in short, some researchers think that analyses identifying mutations could be driven in part by contamination of samples or sequencing errors in particular labs. Those errors could affect analyses, or they may be minor enough that they don’t change big-picture results. But that, too, bears more research.
So, what big-picture lessons might we take away from this? Researchers will continue to post preprints; nonexperts, including journalists, need to be mindful of the limitations when reading those papers. There’s debate within the science journalism community about whether we should report on preprints at all. Often, it’s better to wait until we know more rather than to prematurely report on preliminary findings. If journalists still choose to write about a preprint, they absolutely need to seek outside comment from scientists with expertise in the relevant fields.
We also should not let sensational coverage of a preprint detract from the paper’s contributions. Rasmussen disagrees with the study authors’ conclusions that G614’s prevalence might mean it’s more transmissible, but she believes the link between prevalence and transmissibility needs to be further studied. While scientists and journalists might have extra incentive to spice up coronavirus research results, in reality, most studies will represent incremental progress, not groundbreaking news. “This is an important observation worthy of further study, but not an earth-shattering discovery that ‘explains’ the pandemic or has major implications for drug and vaccine development,” says Rasmussen.