Wow! My following went up literally by like 25% in one day. Please if you could all take a gander at my sticky, that would be great, whereby I am (AFAIK) the only person to do off-the-cuff math illustrating how bogus a 100% natural #furincleavagesite is in #SARSCoV2origins
Additionally, as our ever-knowledgeable @Daoyu15 has repeatedly pointed out, all decent alignments of "FCS containing" coronaviruses that have been discovered after the pandemic such as #RmYN02 doesn't actually have an FCS...
So let's say it happens piecemeal and occurs over generations of viral replication.But single indels would cause #frameshifts or premature stops (#nonsense mutations). SO it means that 1 entire codon of 3 nucleotides needs to be inserted OR at the very least, 1 insertion needs...
to be compensated by a deletion elsewhere in the #ORF that doesnt cause a frameshift or other deleterious mutation. so either 2 rare mutations or all three (of the exact nts needed to construct a furin cleavage site, barring the even more mathematically impossible....
event of randomly inserting and then transition mutating into the appropriate nt ) need to occur in one transcript and then that transcript needs to turn into virus that eventually gets into a new host and replicates there, undergoing the same processes to fully complete the site
absolutely mathematically not happening in less than 100 years naturally on bat populations less than 10,000 individuals, based on any spike that can bind ACE2
when you put it in context of what actually happened, in each transcript, the more thermodynamically favorable event is 2 insertion mutations to avoid frameshifts/premature stops to just to get 1 out of the 12 nts for the #FCS.
so, not counting where the FCS is NOR the exact..
nt's needed NOR that its all sequential... it's actually ((1*10^-6)/5)^24 (sorry in my sticky i underestimated how rare it is! i wrote 1e-5 previously, that was a typo!)
1.677722e-161 (aka not happening within the lifespan of the universe, probably the most unlikely thing ever)
@JamieMetzl i swear to god you better have included my math in your interview....
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The left: Politicians lie all the time, so we should just ignore Trump and Pompeo's legitimate claims of election fraud, the origins of the coronavirus, and CCP's dire influence.
ALSO THE LEFT: BELIEVE ALL WOMEN, BELIEVE ALL SCIENTISTS, BELIEVE BIDEN, KAMALAH, & CNN
Yes! Politicians DO lie. But they lie about certain things in certain circuitous ways. They might make a campaign promise and then flake. Or they might feign forgetting. Or they might say "that depends on what your definition of 'is' is".
*skillful* plausible deniability is KEY
however... you *cannot* then dismiss everything a politician says or ignore them outright because of that fact. rather, it should be *alarming* that Pompeo is claiming he has proof of #sarscov2origin in a lab in china. if he were lying like this, that would be a bold-faced lie...
1)"The only measurement of a mutation rate in a β-coronavirus suggests that this site will accumulate ~10^–6 mutations in each round of replication. Each replication cycle takes ~10 hr, and so there are 10^3 cycles/year. "
2) but the argument that there are 1000 cycles of replication/year is *only* true if one considers 10^4 being ~8760, *and* only 1 viral mRNA replicates.
there are numerous other issues with this math.
3)if anyone thinks the math on estimating the chances of obtaining a furin cleavage site is simple... its not. the assumptions about the system, entropy of mrna, evolutionary fitness, parallel virion replications and mutations, host attacking virions cutting down #'s are critical
For example, SARS-CoV-2’s genome closely resembles that of a bat coronavirus, but a small section of the
genome called the “polybasic cleavage site,” believed to provide a selective advantage for disease transmission, would have been expected to evolve over time but instead
is present in the earliest sequences of the virus. Investigators can further determine whether the infecting agent’s genome so closely resembles a given reference
strain that a period of limited or no replication is likely. Such socalled “frozen evolution,” when an infecting
agent’s genome lacks the expected accumulation of mutations over time, suggests that alternate origin hypotheses such as a laboratory accident must be explored.