An interesting re-analysis was published today: "Remdesivir treatment does not reduce viral titers in patients with COVID-19"
Basically, remdesivir has no impact on *viral load* in acute COVID!
Here's a summary of the findings—and controversy—for a general audience!
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Initially, remdesivir received emergency FDA approval because in one NIH-sponsored trial, the remdesivir group recovered quicker than the control group. That's ALL.
It was trialed because it does seem to be a great drug in cell cultures in the lab!
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It SEEMED like it would be a great drug, because it does exactly what we want *in cell cultures*. Unfortunately, even in animal models, it seemingly had issues.
In particular, viral load was lower in fluid from the lungs, but not in nose, throat, or rectal swabs.
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In humans, no study has shown a statistically significant decrease in viral load as a result of remdesivir treatment!
Only two studies looked at changes in viral load under remdesivir treatment and both found NO significant differences compared to controls.
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Apparently, one of the studies is criticized for having a small sample size... but that makes it much more likely that they'll have a false POSITIVE result, especially when it seemed to be so effective in preclinical research!
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In a challenge trial in 2022 (dear researchers: NO SC2 CHALLENGE TRIALS, WTF?), they provided remdesivir as a prophylactic against severe COVID, but the data suggested it might not be needed.
Thus, they discontinued administration for the rest of the participants.
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This change in protocol created a quasi-experiment, which is the focus here!
So, even in a study where participants were exposed to a standardized quantity of virus, no differences in viral load were found between the treated-with-remdesivir group and the no-remdesivir group. 7/
Boiling it down:
- It shows a certain level of viral inhibition in the lab
- Some studies have found it may have an impact on OUTCOMES
- But it DOESN'T have an impact on the viral load
The issue seems to be that the dose in the body can't get high enough!
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HOWEVER! Meta-analyses have noted SOME sort of SMALL impact on mortality, for SOME patients, e.g.:
That means a lot more research is needed on the specific factors that lead to severe acute outcomes (and LC!), allowing specific diagnostics, allowing specific treatments.
No clinical trial can be successful if unidentified underlying issues aren't being addressed!
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For the record, this is very different from my first draft of this thread.
After I realized it was written by *current* grad/med students, I rewrote it as an actual critique, instead of my usual incisive schtick
NEW study in the Journal of Hospital Infection has found that, even from a purely economic perspective, the LACK OF MITIGATIONS currently present in healthcare settings MAKES NO SENSE!
Of course, preventative measures save LIVES, too.
Here's a quick analysis...
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This study is out of Australia, where patients who acquire COVID after their admission to the hospital are 50% more likely to die within 90 days.
When over 10% of the patients in the hospital are there BECAUSE of hospital-acquired infections, the problem is obvious.
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They used an established agent-based model—a model which simulates the interactions of individuals in a community—calibrated to actual local data.
Of course, it took a lot of work to get the appropriate data, because data collection was—surprise, surprise!—terrible.
Because the "benefit of the doubt" is often brought up here, I want to make it clear that there is NO DOUBT that, if you willingly stopped masking, you made an empirically-harmful CHOICE.
Let's see what was known and when, starting with a commentary out of Italy in Aug 2021!
Obviously, different countries were going to take different approaches, but right out of the gate, much of the US/Euro response was based on empirically-unfounded dogma.
To begin with, many of the CRITICAL lessons from SARS were ignored by "opinion leaders." 2/
And let's be clear... not a single person who said "vax and relax" had BOTH of these attributes:
- Was informed of the science
- Had your best interest in mind
The fact that a partially-immunized population creates *evolutionary pressure* was already well-known.
A review was published today on an immunostimulator called IMQ. Before reading, I decided I'd only cover it if it hit certain critical points; it hit them all REPEATEDLY.
Wow, wow, WOW. Here's a summary (for everybody)! 1/
This isn't at all a new drug, but for whatever reason, it's been totally ignored by the covid literature (with the exception of a paper from 2020 that is also cited by the current review).
Inexplicably, NOBODY has looked at IMQ yet!
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WARNING: Imiquimod has NOT been CLINICALLY EVALUATED in any way for SARS-CoV-2.
I'm excited about this paper because it matches my mental model of covid pathophysiology almost perfectly, but I'm not a doctor.
This thread is a conceptual explanation. THIS IS NOT ADVICE.
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OOHHHH WOW! New preprint on the host immune response in Long Covid was just posted (few hours ago), and it's more significant than the 3-gene signature!
They found reactivation of viral herpes (EBV/CMV/HSV2) and CONFIRMED PERSISTENT SARS-CoV-2 INFECTIONS! Here's a summary...
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IMO, this is a hugely important study, so I'm going to do my best to explain it in detail, in a way that everybody can understand!
The headline here is that a persistent/reactivated infection of (one or more of) SARS2, EBV, CMV, and/or HSV2 were found in 60% of LC patients!
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Simply put, they looked at the antibodies produced by "Antibody-Secreting Cells" (ASCs), a type of short-lived immune response cells!
The primary types of antibodies stay in the blood. In contrast, ASCs peak *shortly* after infection, then rapidly decline! (see screenshot)
GUESS WHAT?! A new study has shown SARS-CoV-2 infection is DISTINCT from common respiratory viruses!
Unequivocally, COVID is NOT "just a cold."
These findings are HUGELY significant, for multiple reasons! Here's a breakdown of the study (written for a general audience)...
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The paper is fairly complicated, so I'm going to start with the high-level takeaways before explaining everything in more detail.
Overall, they found a 3-gene signature that distinguishes SARS-CoV-2 infections from common viral infections—long before PCR test positivity!
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Because the signature:
1. is SPECIFIC to SARS-CoV-2, 2. is an EARLY indicator of infection, 3. is a DISTINCT pattern from other infections, and 4. even accurately identifies Omicron infections,
this discovery may be useful as a diagnostic tool AND a direction for treatment!
SIGNIFICANT new study has found a potential mechanism of ALS pathogenesis (with broader implications for other unexplained/idiopathic/"functional" neurological conditions?!)
This thread is pretty long, because I try to explain *everything* in a way anyone can understand!
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The short summary is that an endogenous retrovirus (HERV-K) is highly expressed in the brain and spinal cord of ALS patients, and may lead to neuroinflammation which leads to neurodegeneration.
These next several tweets are the background needed to understand the results!
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So, DNA… it's a *language* that encodes the instructions a cell uses to build proteins out of smaller molecules.
Like written language, different symbols are used to indicate when segments start and stop (i.e. capital letters, spaces, punctuation in human language).