“It's like people want there to be a novel, severe hepatitis-inducing, globally distributed adenovirus affecting children rather than it being one of the many sequelae of COVID infection. That would absolutely not be a better scenario.” A recent quote from T Ryan Gregory
It is likely that some children will have adverse events due to vaccination and SARS-CoV-2 infection that will result in sequelae including liver damage; however in addition something else is apparently causes serious disease in children. I this the the association with ad41 is weak and that the condition is caused by an as yet known virus, probably Hepatitis X.
Throwback to the pediatric hepatitis surge in India after the delta wave. Seen after mild and asymptomatic infections. It even has a name: CAH-C (covid associated hepatitis in children
Great TWiV. Geez, Google with these terms: virus forest canopy. See what comes up. That question was clearly directed to the question of birds, animals, insects that inhabit the forest canopy. Plant viruses are interesting, very much so, but my sense of this question was that it was about eco-destruction & spillover.
I'm afraid that I wouldn't get too excited about a tetrapeptide-based inhibitor - it's very unlikely to be to orally active. And chances are that if you try to make it smaller, eg a dipeptide analogue then you'll blow out all the specificity and potency for the target enzyme. It would be nice to think that I'm proved wrong here, but it's sadly par for the course for oligopeptide mimetics as drug candidates. It's also a bit odd that an inhibitor with potential covalent binding to the target doesn't just titrate out the TMPRSS2 that is present in the test assay system (ie one might expect an apparent IC50 in the pM range maybe and without the usual sigmoid dose-response curve for a competitive inhibitor, unless there's more TMPRSS2 around than I'm guessing), but that's just a technical observation.
35:18 "Newly discovered peptidometics 385 and 386 are very potent"... how long until something like this can get out to market? Also was Camostat tested as ineffective as a prophylactic or as treatment? TMPRSS2 is one of the explanations for more infections with males so perhaps Camostat in males would be more effective?
NB: *Treyf* (note the correct spelling, although treif is also OK) is not pronounced to rhyme with Jeff, but with Leif, or like 'trey' with a 'f' appended. You probably were misled by the spelling, by a person so misled, they thought a bagel, with any swine flesh, is acceptable.
I'm so thankful that their are experts figuring these things out for us. Thank you for all you do guys!
“It's like people want there to be a novel, severe hepatitis-inducing, globally distributed adenovirus affecting children rather than it being one of the many sequelae of COVID infection. That would absolutely not be a better scenario.” A recent quote from T Ryan Gregory
It is likely that some children will have adverse events due to vaccination and SARS-CoV-2 infection that will result in sequelae including liver damage; however in addition something else is apparently causes serious disease in children.
I this the the association with ad41 is weak and that the condition is caused by an as yet known virus, probably Hepatitis X.
@@christopherrobinson7541 Most of these kids are under 5 so they aren’t even ELIGIBLE for vaccination. So, just no.
Thanks TWiV
Throwback to the pediatric hepatitis surge in India after the delta wave. Seen after mild and asymptomatic infections. It even has a name: CAH-C (covid associated hepatitis in children
Roger Kornberg cites Efraim Racker: "Don't waste clean thinking on dirty enzymes" and admonishes: "purify, purify, purify". "Old school" biochemistry that remains key.
Great TWiV. Geez, Google with these terms: virus forest canopy. See what comes up.
That question was clearly directed to the question of birds, animals, insects that inhabit the forest canopy. Plant viruses are interesting, very much so, but my sense of this question was that it was about eco-destruction & spillover.
I'm afraid that I wouldn't get too excited about a tetrapeptide-based inhibitor - it's very unlikely to be to orally active. And chances are that if you try to make it smaller, eg a dipeptide analogue then you'll blow out all the specificity and potency for the target enzyme. It would be nice to think that I'm proved wrong here, but it's sadly par for the course for oligopeptide mimetics as drug candidates.
It's also a bit odd that an inhibitor with potential covalent binding to the target doesn't just titrate out the TMPRSS2 that is present in the test assay system (ie one might expect an apparent IC50 in the pM range maybe and without the usual sigmoid dose-response curve for a competitive inhibitor, unless there's more TMPRSS2 around than I'm guessing), but that's just a technical observation.
Audio’s fine for me
35:18 "Newly discovered peptidometics 385 and 386 are very potent"... how long until something like this can get out to market? Also was Camostat tested as ineffective as a prophylactic or as treatment? TMPRSS2 is one of the explanations for more infections with males so perhaps Camostat in males would be more effective?
A trial with Camostat was planned, but because of the failure of HCQ, was abandoned.
NB: *Treyf* (note the correct spelling, although treif is also OK) is not pronounced to rhyme with Jeff, but with Leif, or like 'trey' with a 'f' appended. You probably were misled by the spelling, by a person so misled, they thought a bagel, with any swine flesh, is acceptable.
I have audio.
No Audio!!!!
Audio working for me ?
watching you all as this drops watching some guy on Twitter wondering why we aren’t looking into COVID & hepatitis 🤷🏻♀️
And I thought it was just me. Yup, no audio.
I have audio.
I understand nothing tonight. Frustrating.
I have audio.