Igor and Brian Mowrey have been posting about Paxlovid for a while. During the Paxlovid trial, only some of the participants were tracked via PCR, and I believe it was around 12% showed a viral spike in the second week. It appears Pfizer came up with the 1-2% number by dividing the number of rebound cases (which were only discovered th…
Igor and Brian Mowrey have been posting about Paxlovid for a while. During the Paxlovid trial, only some of the participants were tracked via PCR, and I believe it was around 12% showed a viral spike in the second week. It appears Pfizer came up with the 1-2% number by dividing the number of rebound cases (which were only discovered through a small sampling of the participants) by the total number of participants.
Viral rebound unquestionably happened during the Paxlovid trials.
Viral rebound also happens naturally. How much it happens with the SARS-CoV-2 virus is hard to pin down. PCR results suggest it happens fairly often--over 10% of the time, but the studies that drive that use high Ct values which are inherently problematic and yield a very high frequency of false positives. Also, a number of earlier studies on the rebound/reactivation phenomenon show a certain skepticism that the "rebound" is actually an artifact of false negative tests.
Because of the false positive potential associated with high Ct values, I am skeptical of the higher estimates of the frequency with which rebound naturally occurs. Thus, I am more willing to accept Pfizer's claim of 1-2% rebound, not so much because I trust Pfizer (I don't), but because that fits with what I believe the natural rate sans inoculation and Paxlovid to be.
In other words, the rebound happens, not because of anything Paxlovid does or does not do, but because it's a natural outgrowth of how some people's immune systems confront the virus.
However, the current focus on viral rebound after Paxlovid would appear to suggest that, currently, the rebound phenomenon is happening with greater frequency, and appears to be happening with greater frequency among inoculated patients.
What we do not have is a reliable metric of how often the rebound happens. If my appraisal of the accuracy of PCR testing is off, and rebound happens more often naturally, then the question is still whether rebound among inoculated patients is higher than the historical rate--and the attention being paid to the phenomenon suggests that it is.
IF that is the case, however, and Paxlovid is not a factor in viral rebound, then the greater frequency of rebound that appears to be happening among inoculated patients MUST be due to inoculated patients having greater difficulty clearing the virus on their own.
If that is NOT the case, then either Paxlovid is a factor in the viral rebound (i.e, the drug is doing something harmful and preventing viral clearance), or it isn't, in which case it isn't doing much of anything at all.
The CDC acknowledges that rebound is an issue for Paxlovid patients. Rochelle Walensky has already drawn that line in the sand.
If the issue is attributable to Paxlovid (always a possibility), then the solution is simple: pull the drug. If the issue is not attributable to Paxlovid, then the rebound cases are absolute proof of lasting immune system damage from the inoculations that not even the CDC and FDA will be able to ignore, since the CDC has already flagged the phenomenon.
Basically, the best case for Paxlovid is that it just doesn't do much of anything overall. However, if that best case is the real world case than the real world case for the mRNA inoculations gets demonstrably worse.
Igor and Brian Mowrey have been posting about Paxlovid for a while. During the Paxlovid trial, only some of the participants were tracked via PCR, and I believe it was around 12% showed a viral spike in the second week. It appears Pfizer came up with the 1-2% number by dividing the number of rebound cases (which were only discovered through a small sampling of the participants) by the total number of participants.
Viral rebound unquestionably happened during the Paxlovid trials.
Viral rebound also happens naturally. How much it happens with the SARS-CoV-2 virus is hard to pin down. PCR results suggest it happens fairly often--over 10% of the time, but the studies that drive that use high Ct values which are inherently problematic and yield a very high frequency of false positives. Also, a number of earlier studies on the rebound/reactivation phenomenon show a certain skepticism that the "rebound" is actually an artifact of false negative tests.
Because of the false positive potential associated with high Ct values, I am skeptical of the higher estimates of the frequency with which rebound naturally occurs. Thus, I am more willing to accept Pfizer's claim of 1-2% rebound, not so much because I trust Pfizer (I don't), but because that fits with what I believe the natural rate sans inoculation and Paxlovid to be.
In other words, the rebound happens, not because of anything Paxlovid does or does not do, but because it's a natural outgrowth of how some people's immune systems confront the virus.
However, the current focus on viral rebound after Paxlovid would appear to suggest that, currently, the rebound phenomenon is happening with greater frequency, and appears to be happening with greater frequency among inoculated patients.
What we do not have is a reliable metric of how often the rebound happens. If my appraisal of the accuracy of PCR testing is off, and rebound happens more often naturally, then the question is still whether rebound among inoculated patients is higher than the historical rate--and the attention being paid to the phenomenon suggests that it is.
IF that is the case, however, and Paxlovid is not a factor in viral rebound, then the greater frequency of rebound that appears to be happening among inoculated patients MUST be due to inoculated patients having greater difficulty clearing the virus on their own.
If that is NOT the case, then either Paxlovid is a factor in the viral rebound (i.e, the drug is doing something harmful and preventing viral clearance), or it isn't, in which case it isn't doing much of anything at all.
The CDC acknowledges that rebound is an issue for Paxlovid patients. Rochelle Walensky has already drawn that line in the sand.
If the issue is attributable to Paxlovid (always a possibility), then the solution is simple: pull the drug. If the issue is not attributable to Paxlovid, then the rebound cases are absolute proof of lasting immune system damage from the inoculations that not even the CDC and FDA will be able to ignore, since the CDC has already flagged the phenomenon.
Basically, the best case for Paxlovid is that it just doesn't do much of anything overall. However, if that best case is the real world case than the real world case for the mRNA inoculations gets demonstrably worse.
Pick your poison? (literally!)