Is the coronavirus becoming more contagious, as a new, unpublished study suggests?
Don’t hit the panic button.
The science is complicated, but the evidence does not support that conclusion, according to prominent infectious-disease experts who were not involved with the research.
The study analyzed various mutations that have arisen in the virus since it emerged late last year, identifying one that has now become dominant throughout the world. That mutation, the authors concluded, may have allowed the virus to spread more readily.
Yet by itself, the emergence of a widespread mutation does not necessarily mean much.
Viruses mutate all the time. Some mutations may cause a virus to infect more people, or perhaps cause more serious disease. Other mutations may cause it to die out faster. Many mutations will have no measurable impact.
If a particular strain of a virus becomes more dominant, that does not necessarily mean it is better at spreading. It may simply be more lucky.
One researcher who urged caution was William Hanage, a Harvard University associate professor of public health. A certain strain can become dominant because the person infected with it was at a large gathering where he or she could pass it on to lots of others — a phenomenon called a “founder effect."
”We need to distinguish between selection, in which a variant becomes more common because it leaves more descendants, and founder effects, in which a variant becomes more common because it was fortunate rolling the dice," Hanage wrote on Twitter.
He called the study’s conclusions “suspect, to say the least.”
He warned that the study was a “preprint,” meaning it had not been formally reviewed for publication in a scientific journal. Such types of preliminary results have been shared online for years, typically garnering little attention beyond the scientific community.
But amid the thirst for answers to the global pandemic, preprints concerning the coronavirus increasingly have been seized upon by policymakers and the general public, often at the expense of true understanding.
No one is faulting the details of the careful genetic analysis in the study by authors at Los Alamos National Laboratory, Duke University, and the University of Sheffield. Their conclusion is what has drawn pushback.
The mutation in question was identified on the spike protein — the now-familiar little knobs found on the surface of each coronavirus particle. The virus uses this spike to latch onto cells in the airways, and it did this very well from the outset regardless of any mutations that have arisen.