It's based on this pre-print, which is strictly a computational analysis of virus sequences. They found a mutation that became dominant over time but didn't do anything to show its functional significance in transmission. https://www.biorxiv.org/content/10.1101/2020.04.29.069054v1 …
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The old adage that correlation does not equal causation applies here. If you are looking at sequence data alone, you can't show effect that this single mutation, spike D614G has on transmission. This means that a mutation at position 614 in spike changed aspartic acid to glycine.
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This happened during the West African Ebola epidemic too. Two groups tested a mutation in Ebola GP (analogous to spike--it's the envelope glycoprotein of Ebola that binds the receptor), called A82V, meaning an alanine was replaced by valine at amino acid #82 in GP.
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Importantly, these studies actually did experiments to show that A82V increased infectivity (the ability to infect cells) in surrogate systems (not actual Ebola virus). Claims about A82V's function in infection and pathogenesis were not made based solely on sequence data.
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This made the news in a big way. The scale and scope of the West African Ebola epidemic was attributed to A82V making the virus not only more transmissible, but also more pathogenic, or "nastier" as this article states.https://www.newscientist.com/article/2111311-ebola-rapidly-evolves-to-be-more-transmissible-and-deadlier/ …
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In cell culture, the A82V mutation did appear to improve viral fitness (the overall ability of the virus to infect cells and replicate), which may explain why this emerged early in the epidemic and there was selection pressure to maintain the A82V change. https://jvi.asm.org/content/91/2/e01913-16 …
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However, when the mutation was tested in animals, it had no effect on pathogenesis or viral shedding. Thus it's a cautionary tale on making broad conclusions about pathogenicity and transmissibility based on in vitro studies w/ surrogate viruses. https://linkinghub.elsevier.com/retrieve/pii/S2211-1247(18)30569-2 …
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And for Ebola GP A82V, these conclusions were based on a number of rigorous, well-controlled experiments conducted by teams of respected virologists. Spike D614G from
#SARSCoV2 has not ever been tested in a single experiment. This is based solely on computational analysis.Show this thread -
The title of the preprint is very misleading. "Spike mutation pipeline reveals the emergence of a more transmissible form of SARS-CoV-2"...NO it does not. It reveals the emergence of a substitution of aspartic acid for glycine at position 614.
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Spike D614G may well have functional importance. It may even increase transmissibility. But we won't know until this is tested experimentally. There's no basis for the breathless OMG
#SARSCoV2 HAS MUTATED TO BE MORE TRANSMISSIBLE WE'RE ALL GONNA DIE tone in the LA Times piece.Show this thread -
Then there's this line: "The report’s authors said they felt an “urgent need for an early warning” so that vaccines and drugs under development around the world will be effective against the mutated strain." Early warning about...what, exactly? Any
#SARSCoV2 transmission is badShow this thread -
If you don't know what a single amino acid change even does, why is there an "urgent need for an early warning"? Warning about what? Are there any vaccines or drugs specifically targeting position 614 in spike? We don't even know if this has any kind of biological effect.
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While it's good to know that this mutation appears to be under positive evolutionary selection, and we should study it to see if it is important for viral fitness or infectivity, it's way too premature to be sounding an "early warning" alarm that OmG tHe ViRuS iS mUtAtInG!!!
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These conclusions about increased transmissibility based on correlation analyses are an overreach. We don't know if the virus is "more transmissible." Experimental evidence or it didn't happen.
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