Paxlovid Rebound Infection Cases Continue To Rise
It's Not Enough To Just Hit "Pause" On A Virus, It Has To Be Cleared
Paxlovid has a problem: even Pfizer apologists within the corporate media no longer refrain from using the word “rebound” when discussing Pfizer’s presumed “miracle” COVID-19 drug. Despite Pfizer’s best efforts to argue the “rarity” of the phenomenon, the reality of what the corporate media now has to say about Paxlovid is clear: rebound infection is very much “a thing”.
While the White House announced plans to make the antiviral medicine Paxlovid more accessible across the US, scientists and federal agencies said they are investigating reports of Americans who say they experienced a rebound of COVID-19 soon after finishing the course.
Nasty Taste While Taking Paxlovid, More COVID When Done
It is becoming increasingly apparent even to the corporate media that Paxlovid is ultimately not effective, despite their best efforts to sustain Pfizer’s claims the drug cuts hospitalization and mortality risk by 89%. What’s worse, the drug has a particularly unpleasant side effect: dysgeusia—essentially an unpleasant taste in one’s mouth that lasts apparently for the duration of the Paxlovid regimen.
In Pfizer’s clinical trials, about 5.6 percent of patients reported an “altered sense of taste,” called dysgeusia in the medical literature. A Pfizer spokesperson assured me that “most events were mild” and “very few patients discontinued study as a result”; the outer packaging of the drug doesn’t mention it at all, and the patient fact sheet breezes past it. But Paxlovid-takers told me it’s absolutely dysgeusting.
While Paxlovid mucks up the taste buds while one is taking the drug, the crowning indignity remains the return of positive SARS-CoV-2 tests (as well as COVID symptoms) shortly after ending the Paxlovid regiment.
Some had more serious side-effects as they reported experiencing a second round of symptoms. And when the pills were over they went back to testing positive, a phenomenon that’s become known as “Paxlovid rebound”.
With a foul taste while taking Paxlovid leading to a rebound infection once the Paxlovid regimen is complete, one question has to come to mind: does this drug actually work?
No Data, No Answer
While Pfizer insists the drug is highly effective, everyone else can only take Pfizer’s word on the topic. On Paxlovid, just as on the mRNA inoculations, Pfizer is playing hide-and-seek with the trial data for the drug.
But despite ringing endorsements for Paxlovid, what remains under-discussed is the lack of available data about how well it works in the populations using it. Since the drug costs the government more than $500 per treatment course, this lack of data means that we have no way to evaluate whether Americans are getting a fair deal.
Paxlovid was approved on the basis of good results reported through the EPIC-HR trials, where use of Paxlovid was credited with reducing severe COVID and hospitalization risk from 7% in the placebo arm to 1% in the treatment arm—which is how Pizer was able to make its extravagant “89%” efficacy claim.
Yet there’s an important caveat to the EPIC-HR trials: the participants were required to not have received a COVID inoculation and not have contracted COVID previously.
To participate in EPIC-HR, you had to be unvaccinated and could not have previously had Covid-19. You had to have symptoms and could not have been dealing with Covid-19 for more than five days. Beyond this, you had to have at least one high-risk condition.
This leaves the tens of millions of Americans who have been inoculated (and boosted) in a medical “no man’s land”, as the impact of Paxlovid on inoculated individuals was not closely studied by Pfizer.
This list excludes most Americans. Most Americans do not have high-risk criteria, and 78 percent of Americans have gotten at least one dose of the vaccine. Another 140 million Americans have had Covid-19 already, and this figure is likely an underestimate. Being vaccinated, having had Covid, or both, markedly lower your risk of hospitalization and death after getting Covid (again). Because of when the trial was conducted—between July and early December of 2021—few, if any, subjects were infected with the Omicron variant—also relevant, given that the individual risk of hospitalization with Omicron appears to be lower. The 7 percent figure seen in the trial is not representative of the risk faced by most Americans.
The significance of this cannot be overstated: Paxlovid’s approval was based on a trial population that quite simply does not reflect even a narrow cross-section of COVID patients today. Not only is there no “apples to apples” comparison to be made, there’s not even an “apples to oranges” extrapolation to be made.
The moment we start giving Paxlovid to people who don’t fit EPIC-HR is the moment we can’t be sure of what we will get. Some scientists think that the 89 percent relative reduction would be preserved. Let’s assume they’re right for the moment. With a lower risk of hospitalization in vaccinated people (vaccines still work well for preventing severe disease), let’s assume the risk is 2 percent if you also have high-risk features. Well, instead of 7 percent to 1 percent risk, we might go from 2 percent to 0.2 percent risk—but this is just a guess. The truth is that both the absolute and relative benefits may fall.
This lack of pre-approval scrutiny of the drug on inoculated patient cohorts gives the growing number of case studies of Paxlovid among the inoculated increased importance. These case studies are the only study data broadly available on Paxlovid among inoculated individuals.
Case Studies Not Helpful To Paxlovid
The case studies we have are not good news for Paxlovid or an infected patient. A recent case study of Paxlovid on an inoculated and boosted patient resulted in yet another instance of rebound infection—what the study termed “recrudescence”.
We next evaluated the susceptibility of the viral panel to the neutralizing antibody response in the plasma from the patient and two controls. Both controls were fully vaccinated and boosted with the BNT162b2 mRNA vaccine (Pfizer–BioNTech), but one had been infected with and recovered from a SARS-CoV-2infection with symptom onset 3 days prior to the individual who experienced NM/r recrudescence. The average half maximal authentic virus neutralizing antibody concentrations (NT50) against BA.2 PRSD01, BA.1, and parental were, 1668, 1170 and 5239 respectively in the NM/r treated patient. These levels were 8.9, 7.1 and 2.1 times higher than the boosted control but 2.0, 1.7 and 2.6 times lower than the boosted and infected control (Figure 1B).
While this case study ruled out the possibility of drug resistance causing the observed rebound phenomenon, the most optimistic conclusion it was able to reach was that the prescribed dose of Paxlovid was simply insufficient.
This study found that neither development of NM resistance or absence of neutralizing antibody werelikely causes of the recrudescence. Although we were unable to measure T cell responses or drug levels,we feel the most likely possibility for the observed recrudescence is insufficient drug exposure.
How much “insufficient drug exposure” differs from “Paxlovid does not work” I leave for you, the reader, to assess for yourself.
Another study involving three inoculated and boosted patients found that Paxlovid was inadequate to prevent post-acute “long COVID”.
Although this case series is limited by a lack of intensive physiologic and laboratory measurements throughout the disease course, we believe these clinical anecdotes are informative as investigators try to understand the pathophysiology that drives the development and persistence of Long COVID. They suggest that antiviral therapy and/or antigen re-exposure could potentially impact the complex interplay between viral replication and the host immune response that likely underlies this syndrome but raise concern that brief early antiviral therapy alone may be insufficient to prevent the development of Long COVID.
Again, the degree to which “insufficient to prevent the development of Long COVID” differs from “Paxlovid does not work” I leave for you to assess.
While individual cases are hardly conclusive evidence against Paxlovid, they are certainly not helping make the case for Paxlovid. Despite Pfizer’s claimed efficacy rates, the reality of these cases is that Paxlovid was not effective, particularly in inoculated and boosted patients. The EPIC-HR trial might have shown that Paxlovid works “in theory”, but current case studies are a mounting form of evidence that Paxlovid doesn’t work “in reality.”
We’ve Heard This Before
While the corporate media continues to be stymied by such data, elsewhere this information is already widely known. As I have commented before, fellow Substack writer Igor Chudov has scrutinized the available data surrounding the FDA’s EUA announcement and Pfizer’s own initial claims, coupled with a broad survey of social media discussions of individual experiences with Paxlovid. What the corporate media is just now ackowledging Igor documented over a month ago.
It turns out that Paxlovid reduces symptoms, and maybe reduces viral load at day 5, but at the same time it does not clear the virus! Not only that, but the patients cannot clear it for extended periods AFTER paxlovid administration is over:
In other words, Paxlovid really doesn’t work at all.
Nor is Igor alone. Brian Mowrey, author of “Unglossed”, takes the process one step further and outlines a potential theory as to why Paxlovid “rebound” is happening: Paxlovid does little more than hit “pause” on viral replication, and unless the body’s innate immune system is able to clear the virus during that interval, cessation of Paxlovid allows the virus to essentially pick up where it left off.
So, what’s to stop the virus from simply resuming production when this is achieved, either gradually during treatment or after the 5-day course of Paxlovid is complete? Namely, either:
All of the viral RNA in every cell must degrade by then, so that it does not matter if unopened Orf1 polyproteins are opened later.
Failing that, the immune system must locate and destroy every cell that has this assortment of “paused” viral replication elements within.
For both of these guardrails to fail, however, is robustly plausible: Where there’s a Nature, there’s a find-a-way. Even a 1% survival rate for viral RNA after a 5-day course would only set the virus back by about a day’s-worth of replicative progress. And if the innate immune system was not able to keep the virus in check in the first place, then there is no a priori reason to assume that it will be able to snipe all of the “paused” infected cells before the nsp5 box-cutters are released.
Readers are highly encouraged to read both Igor’s and Brian’s work on this topic for a full understanding of their research.
Their work warrants especial notice, however, because it underscores the extent to which the corporate media is still “behind the curve” on Paxlovid’s ultimate efficacy. Corporate media types will likely never admit it, but the alternative media sources are considerably farther along in understanding the phenomenon of Paxlovid “rebound”.
Data On Social Media Is Still Data
There is no small irony in the degree to which social media platforms such as Reddit and Twitter have served to advance discussion of Paxlovid “rebound” infection. Even corporate media writers are drawing from social media for their data—even as some almost sound apologetic for doing so!
No researchers have yet published studies measuring the prevalence of rebound, but a good number of clinicians and Paxlovid patients are convinced that it’s higher than 2 percent. “To trust that number would’ve been to not believe my eyes,” Bob Wachter, the chair of medicine at UC San Francisco, told me.
In an attempt to find some clarity, Wachter decided to poll his Twitter connections on whether they’d taken Paxlovid and rebounded. (I’m legally obligated to tell you that Twitter polls are neither scientific nor particularly reliable—which Wachter knows perfectly well.) Of the respondents who said they had taken Paxlovid, 45 percent rebounded; Wachter said he guesses the real proportion is closer to 10 or 20 percent. A few hours after we spoke, Wachter tweeted that his wife, who had recently finished a course of the antiviral and recovered from COVID, just tested positive again.
Two points stand out here: 1) the medical establishment does not believe Pfizer’s claims that rebound is a rare phenomenon, and 2) without independent research from their usual peer-reviewed sources, they are willing to trust anecdotal social media evidence over Pfizer.
Twitter is more trustworthy than Pfizer. Let that sink in.
Even stalwart defenders and advocates for the mRNA inoculations within the medical community are appearing on Twitter to detail their own experiences of Paxlovid rebound:
While social media posts and tweets lack the formal rigor of clinical research, they still represent a growing body of anecdotal and presumably truthful information amounting to a fundamental rejection of Pfizer’s claims and the basis for the FDA’s emergency approval of the drug. For these COVID patients at least, Paxlovid has not worked.
In light of case studies and other clinical data challenging Paxlovid efficacy, while the social media data is anecdotal—and thus would normally be considered “low quality” evidence—the synchronicity between the social media data and the case studies makes the social media data impossible to dismiss.
For the corporate media, a critical mass of such tweets and posts has been reached to where they no longer feel compelled or willing to overlook them, regardless of their presumed evidentiary qualities.
No Escaping Reality
The Achilles Heel of all forms of propaganda, regardless of the agenda it serves, is that there is no denying reality.
No amount of corporate spin or media manipulation will make cases of Paxlovid rebound disappear. No attempt by the corporate media to argue Paxlovid efficacy can hope to prevail against a rising chorus of individual testimonies—many from within the very medical establishment that should be on Paxlovid’s “side”—arguing the opposite.
That rising chorus is exactly what is taking place even now.
The propaganda is failing on the Paxlovid front. Reality is winning.
The reality of COVID anti-virals is that it is not enough merely to suspend viral replication. The body has to end up clear of the virus. When the body does not clear the virus, regardless of the reason why, the anti-viral fails by definition.
The rising chorus of reality is that Paxlovid does not clear the virus, just as Igor Chudov documented over a month ago. The rising chorus of reality is that Paxlovid is not effective, but really does not work at all.
awesome article and I will mention yours in my upcoming paxlovid article
I realize that viruses are not bacteria, but it may be useful to look at bacteria & antibiotics for a moment. Because that's possibly what these goons were thinking.
There are classes of antibiotics (eg tetracycline family) that stop replication & leave it to your immune system & time to eliminate the bacteria. A few decades ago, when I had a raging infection (presumptive septicemia) I was put on tetracycline for *30 days* prior to wisdom teeth extraction.
Even with a healthy immune system, 5 days is not long enough for your body to clear a major infection. Other than minor, topical infections, I don't know of any infection treated less than 7 days, which presumes 5 days to clear + 2 days to be sure. Usually its 10 days (7 to clear, 3 days insurance) or 14 days.
The "stop replication" antibiotics have the fall back of time, since bacteria do age & die. Whereas in a suitable environment, viruses probably can remain viable for an indefinitely extended period.
So with viruses, & this drug, clearance depends completely on a healthy immune system, which we know the jabs damage.
My guess is that much over a 5-day course leads to major system damage in too many to hide.