Share this comment
I think deattenuation happens on a much faster timeframe. For the Sabin live polio vaccine virus, for example, it probably deattenuates by the time it replicates enough in the recipient to be shed back out. This is why Sabin can cause poliomyelitis if caught second-hand by someone who isn't vaccinated - it essentially "is" polio. It does…
I think deattenuation happens on a much faster timeframe. For the Sabin live polio vaccine virus, for example, it probably deattenuates by the time it replicates enough in the recipient to be shed back out. This is why Sabin can cause poliomyelitis if caught second-hand by someone who isn't vaccinated - it essentially "is" polio. It doesn't take years or decades. Just a few cellular passages.
Maybe the timeline is actually slower. The SARS-CoV-2 variant Alpha (and probably Delta) featured amped-up Orf9b production which inproves TOM70 intracellular immunity suppression - https://www.nature.com/articles/s41586-021-04352-y - this is likely a recovered anti-immunity trait that was lost (became clonally "recessive") during cellular passage in the lab, but it still took months to reemerge in real life. But young people still did fine against Alpha / Delta, it wasn't a super-weapon. In the end, a "deattenuated" SARS-CoV-2 just means... a regular coronavirus, with the regular coronavirus intracellular immune evasion toolkit, which is probably really extensive and exquisite and cool. The pathogenicity of SARS-CoV-2 stems from apparent inflammatory or autoimmune responses triggered by weird accessory epitopes on the spike, or maybe weird senescence-alteration effects on monocytes - but not its essential "virulence." So I'm sanguine about potential increases to that virulence. I think they might happen (just as flu sometimes becomes more virulent, defying the trope that viruses "want to get milder"), but they won't dramatically alter our experience of the virus.
I loved this answer. Good points.