Three weeks ago, *The Prepared* was among the first in the English-language press to report on a new study suggesting that SARS-CoV-2 had evolved into a more transmissible variant. A more contagious form of the virus would be the second-worst news—only slightly less alarming than a more lethal strain. Given the paper’s strong methodology, we felt confident enough to highlight the findings in our headline and analysis, though we included some cautious reservations.
It turns out those reservations were more significant than we realized. We may have been too quick to accept the original study’s conclusions at face value. A new preprint from an Anglo-Gallic team of statistical geneticists has cast serious doubt on the earlier claim, suggesting that the D614G mutation likely doesn’t make the virus more transmissible after all.
So, this is our *mea culpa*. In the spirit of scientific integrity and journalistic transparency, we want to explain where the original study might have gone off track—and how the new research challenges its findings.
**What the new analysis does and what it shows**
The original study by Korber et al. observed a consistent rise in the prevalence of the D614G mutation over time, which they interpreted as evidence of natural selection rather than random chance. However, the new analysis by Dorp et al. introduces a different approach. It examines whether this pattern holds across multiple independent occurrences of the mutation, and finds that it does not.
In short: D614G probably doesn’t increase the virus’s transmissibility.
The key issue here is distinguishing between **selective pressure**—where a mutation actually gives the virus a fitness advantage—and **founder effects**, where certain mutations spread simply because they happened to be present in early, widely transmitted cases.
Korber’s team argued that the widespread increase in D614G was unlikely to be due to chance alone, citing its consistent rise across multiple regions and time periods. But the new analysis suggests that this pattern could easily be explained by founder effects, especially when looking at independent lineages.
**Different methods**
The new study uses a more refined approach. It looks at recurrent mutations—those that appear independently in different viral lineages—and applies a new metric called the Ratio of Homoplasic Offspring (RoHO). This method compares each mutation with its closest relatives, helping to determine if it's spreading due to actual selection or just random luck.
Instead of comparing all cases with and without the mutation, it focuses on homoplasic strains—those that acquired the same mutation independently—and looks for patterns across these lineages. This can reveal whether a mutation is enriched (more common) or depleted (less common), offering a clearer picture of its true effect.
**New results**
The findings are striking: out of dozens of recurrent mutations, none showed consistent positive enrichment across all their independent origins. In fact, several showed negative enrichment, meaning they emerged frequently but were actually less transmissible. The D614G mutation, in particular, showed no clear advantage—it increased in frequency at the same rate as similar strains without the mutation.
Additionally, the analysis found that many of these mutations involved a specific type of base change—cytosine to uridine—which is unusual and may be linked to human RNA editing systems acting on the virus. This could help explain why some mutations, like D614G, became more common, even if they weren’t inherently more transmissible.
This raises questions about the clinical data from Korber’s study, which found a link between D614G and higher viral loads. While that result could still be valid, it might also be due to chance, temporal bias, or other factors. At this point, it’s hard to say for sure.
**How we (probably) got it wrong**
Science during a pandemic is fast-moving and often messy. Early reports on everything from animal intermediaries to drug treatments have sometimes led to confusion. The idea that D614G increases transmissibility seemed plausible for several reasons:
- A consistent rise in prevalence across geographies
- A change in the spike protein, which is crucial for infection
- A possible mechanism based on protein structure
- Some indirect clinical support
- Endorsement from respected scientists
But the new analysis suggests that these signals may have been misleading. When other outlets picked up the story, they largely attributed the D614G trend to founder effects. We initially dismissed that argument as overly cautious, but now it seems we were wrong.
We’ve reached out to both research teams and other experts for their perspectives. While more studies are needed—especially in-vitro and clinical trials—it now appears far less likely that D614G significantly boosts transmissibility.
We (probably) got it wrong. And we’re sorry.
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