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Friesein Profile picture
@Friesein
Jul 3 • 13 tweets • 4 min read • Read on X
30 staff scientists at the FDA had signed off on approving Novavax for anyone 12 or older.

They had reviewed multiple clinical trials with 30-45K participants, showing no more than 3 total cases of myocarditis.

Then Vinay Prasad overruled them and limited access to 65+. 🧵
Anyone who has seriously followed the research on COVID will tell you that the risk of myocarditis (among numerous other conditions) from COVID is far greater than that of Novavax.

Yes, that includes Omicron and later variants.

Put aside spike protein for a minute.

The 3CL protease, a critical part of the viral machinery that allows SARS-CoV-2 to replicate, binds with hundreds of proteins in the liver and gut alone.

And that's just scratching the surface.

And for anyone that is concerned about spike protein, you should be concerned about the thing that is able to generate on the order of trillions of them in your own body.

Only the virus can do that. Not Novavax. Not even mRNA.

Trillions of spikes? Isn't that bad for your organs?

You'd better believe it. Even the CDC admitted it.

Well, at least they acknowledged it in a guide for coroners, never mind about warning the living.

Viral persistence shouldn't be a controversial idea. There are precedents.

Hep B causes liver cancer through viral persistence.

EBV causes stomach cancer through viral persistence.

HHV-8 causes Kaposi's sarcoma through viral persistence.

Why wouldn't COVID be persistent?
Well, now the technology is finally emerging that will let us detect viral persistence of COVID.

People like Vinay Prasad serve the purpose of stalling society's recognition of COVID's true severity.

It's not that we got better at handling COVID. We got better at ignoring it.

What will it take to shift public perception around COVID?

I think it all starts with a conversation.

There are forces out there that want us bitterly divided. Isolated. Attacking our peers with differing political opinions.

Here's the truth: COVID informed people don't want lockdowns. We don't want to force you to get vaccines.
What do COVID informed people want?

Speaking for myself, I want biosecurity by default. I want far-UVC in public buildings. I want ventilation. I want access to treatments of my choosing.

I don't want people to sleepwalk into decreased quality of life. That's the status quo.
That encompasses why I even bother spending time on X instead of lurking away silently on the sidelines as another invisible, everyday person.

I can't afford not to try making things better. My family can't afford the status quo. Nobody can. Not even billionaires.
So when you see the likes of Vinay Prasad intervening in FDA scientific decisions, recognize that this too will pass.

Eventually, technology will evolve and so too will our demand for non-invasive mitigations.

And until those mitigations are commonplace, I'm not going anywhere.
Correction: I had meant to say liver and kidneys on this post, although viral persistence has been demonstrated in the gut in separate studies.

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More from @Friesein

Friesein Profile picture
Jun 12
Novavax Availability Update 📢

Costco in Little Rock, AR has reportedly confirmed that they'll have Novavax stock in place by September.

My gut feeling is that this is much closer to the timeline we'll end up seeing for most stores instead of July/August.

Here's why. 🧵
In 2024, the first CVS I heard of that had received their stock was in Pittsfield, MA on September 9.

For Costco, it was in Limerick/Sanatoga, PA on September 13.

Prior to that, the national Costco distribution center had received their stock on September 10, and they began shipping to stores shortly afterwards.

Read 7 tweets
Friesein Profile picture
Jun 11
Novavax Availability Update 📢

I've heard several reports that some Costco pharmacies are expecting Novavax supply between July and the end of August.

I recommend checking with Costco via their web app to find out when you'll be getting it in your area (instructions below). 🧵
Here's how to contact Costco corporate for pharmacy inquiries.

I recommend doing this over talking to your local pharmacy because stores are not always in the loop on shipping status.

Doing this also sends a demand signal to Costco for ordering stock.

Image
This will be the first time Novavax is available outside of Emergency Use Authorization.

Getting access to it this year may require a bit of extra effort, since the new license stipulates that most must have an underlying condition to access the vaccine.

Read 10 tweets
Friesein Profile picture
May 29
This is NB.1.8.1.
So is this.

And some of the symptoms like intense throat pain and fatigue seem to kick in a week or so after the first appearance of symptoms.

Read 11 tweets
Friesein Profile picture
May 23
SARS-CoV-2 is known to bind with mitochondrial proteins in humans.

Mitochondrial dysfunction caused by COVID persists past the acute phase.

Evidence of ongoing mitochondrial and metabolic dysfunction has been found in the heart, kidneys, liver, and lymph nodes, for example. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral proteins bind to host mitochondrial proteins, likely inhibiting oxidative phosphorylation (OXPHOS) and stimulating glycolysis.
These data suggest that when the viral titer first peaks, there is a systemic host response followed by viral suppression of mitochondrial gene transcription and induction of glycolysis leading to the deployment of antiviral immune defenses. Even when the virus was cleared and lung mitochondrial function had recovered, mitochondrial function in the heart, kidney, liver, and lymph nodes remained impaired, potentially leading to severe COVID-19 pathology.
In the case of SARS-CoV-2, it was shown that mitochondria appear swollen and damaged in skin biopsies from patients, and that depletion of mtDNA in endothelial cells significantly reduced the type I IFN response62. In SARS-Cov-2 infected cells, viral RNA was found to be associated with mitochondria using fluorescence and electron microscopy31. Several reports have suggested the colocalization of mitochondrial-SARS-CoV-2 RNA in infected human tissue.
According to recent studies, SARS-CoV-2 infection causes prolonged disruptions in mitochondrial function, significantly altering cellular energy metabolism. Our research employed transmission electron microscopy to reveal distinct mitochondrial structural abnormalities in Long COVID patients, notably including significant swelling, disrupted cristae, and an overall irregular morphology, which collectively indicates severe mitochondrial distress.
There seems to be an inverse relationship between viral load and the expression of mitochondrial genes during the acute phase.

Could the same be true of the chronic phase? Could persistent virus be causing ongoing mitochondrial dysfunction? Mitochondrial gene expression was reduced in autopsy tissues from patients admitted to the hospital with high compared with low viral loads, which confirmed that the extent of altered mitochondrial gene expression may be regulated by viral load (fig. S5). Down-regulation of mitochondrial pathways in response to virus in human autopsy samples was most extensive in hearts followed in decreasing order by the kidneys, livers, and lymph nodes (fig. S5). This inhibition of mitochondrial gene expression in visceral autopsy tissues parallels that seen in the nasopharyngeal samples with high viral t...
Overall, autopsy heart tissue from patients with SARS-CoV-2 infection showed a systematic down-regulation of genes involved in multiple mitochondrial functions; this was also found, to a lesser extent, in kidneys and livers and, to the least extent, in nasopharyngeal samples and lymph node autopsy samples. The lung autopsy samples showed down-regulation of CoQ synthesis and mtFASII but up-regulation of genes involved in the TCA cycle and cytosolic protein import (Fig. 3A).
It is clear is that SARS-CoV-2 is capable of causing mitochondrial damage that persists for months or even years.

And we independently know the virus persists in some form, chronically.

For patients, this means that new symptoms can appear after acute COVID infections. Image
We have observed an interesting phenomenon in the mitochondria, the swollen and vacuolated mitochondria, distorted and broken cristae, all indicated severe damage to this important cellular organelle. This damage is highly likely caused by the SARS-CoV-2 Infection, as we have found an almost identical mitochondria disorganization in the mice that were infected with SARS-CoV-2. Our findings are consistent with a recent study in which mitochondrial gene expression was analyzed in autopsy tissues from patients with COVID-19, and core mitochondrial gene expression were suppressed in the hearts,...
Image
Highlights: - SARS-CoV-2 spike protein persists in the skull- meninges-brain axis in COVID-19 patients. - Spike protein is sufficient to induce brain pathological and behavioral changes in mice. - Spike protein enhances brain vulnerability and exacerbates neurological damage in mice. - mRNA vaccines reduce, but do not eliminate, the spike burden
Read 6 tweets
Friesein Profile picture
May 21
I can appreciate skepticism of long COVID as a concept. After all, it may instinctually seem like an epistemological overreach to assign a singular cause to such a heterogeneous disease presentation.

On the other hand, consider the localization of ACE2 throughout your body. Consider the reach of your blood vessels. Couple that with imaging studies that demonstrate spike persistence in areas such as the brain and skull. Consider also that viral persistence has been identified in the gut with replication competent virus.

In the last few years, I've interacted with tons of people on this platform, both vaccinated and unvaccinated, who have lost a significant amount of mobility after having had COVID infections. Healthy and unhealthy, comorbidities or not. People in their 40s are also dying of rare cancers. Athletes and soldiers are having a decrease in functional performance after a single COVID infection, let alone reinfections.

The deeper you look into viral persistence (look at the work Polybio and Erturk Lab are doing on imaging, for example), the more you'll find yourself willing to consider that COVID might play a role in it.

The key is in recognizing that the microvascular changes COVID causes are difficult to detect with off-the-shelf diagnostics. Once research develops more readily commoditized diagnostics, perhaps the condition will gain wider recognition. In the meantime we have a large segment of young, middle-aged, and previously healthy athletes succumbing to unusually debilitating chronic illness after COVID infections. That illness is real despite misgivings some may have. And so too is the underlying damage COVID causes, even if it's not straightforward to detect in all instances. Whatever you want to call the disease, those patients deserve medical treatment despite limitations in the diagnostic tools conventionally available.Image
Where in the body is it found? ACE2 is present in many cell types and tissues including the lungs, heart, blood vessels, kidneys, liver and gastrointestinal tract. It is present in epithelial cells, which line certain tissues and create protective barriers. The exchange of oxygen and carbon dioxide between the lungs and blood vessels occurs across this epithelial lining in the lung. ACE2 is present in epithelium in the nose, mouth and lungs. In the lungs, ACE2 is highly abundant on type 2 pneumocytes, an important cell type present in chambers within the lung called alveoli, where oxygen i...
Image
Image
Long COVID in young Marines.

thelancet.com/journals/lanam…
Evidence of viral persistence from COVID.

ucsf.edu/news/2024/03/4…
Read 6 tweets
Friesein Profile picture
May 11
The NB.1.8.1 variant seems to have originated in Hong Kong, then spread to several other countries in the region (including Singapore & Australia).

It's now spreading to Western US states such as California, which currently has the highest proportion of NB.1.8.1 across the US.🧵 Image
Image
For the month of March, NB.1.8.1 went from having single digit prevalence in Hong Kong to 80%.

It achieved 100% dominance in HK by late April. Image
NB.1.8.1 has also been spreading to Thailand, South Korea, Taiwan, and Japan (which saw a 30% prevalence of the variant at the beginning of April to 70% prevalence by the end of the month).

Read 10 tweets

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