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Friesein Profile picture
Friesein
@Friesein
Clean air is a human right. SARS2 is a severe pathogen disabling millions. Let's use scientific modeling and engineering to solve both. Listen to patients.
4 subscribers
Jul 3 • 13 tweets • 4 min read
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.

Jun 12 • 7 tweets • 3 min read
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.

Jun 11 • 10 tweets • 5 min read
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
May 29 • 11 tweets • 3 min read
This is NB.1.8.1. So is this.

May 23 • 6 tweets • 5 min read
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).
May 21 • 6 tweets • 3 min read
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…
May 11 • 10 tweets • 4 min read
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
May 8 • 11 tweets • 4 min read
On the Novavax earnings call today, the head of R&D made an interesting claim.

She said that the Novavax COVID vaccine is capable of inducing mucosal antibodies that could protect against infection.

This lines up with previous data that has been published on the vaccine. 🧵 "Additional exploratory data in the context of our COVID vaccine have shown that our technology platform can induce mucosal antibodies. Mucosal protection is important not only for the person receiving the vaccine, but for instance for reducing virus transmission." —Ruxandra Draghia-Akli, MD, PhD, Head of Research & Development at Novavax Multiple non-human primate studies and human studies have supported the finding that Novavax reduces viral load in upper and lower respiratory tracts.

Some of this data was published as early as 2020. I've covered these findings over the last few years.

May 5 • 10 tweets • 5 min read
Take a look at these blood vessels.

Which one do you think was taken from someone who had COVID a year beforehand?

Answer in the next post. Figure 1 from https://rmdopen.bmj.com/content/11/2/e005469 In the photo on the left are what blood vessels near the fingernails are supposed to look like.

In the photo on the right are what blood vessels near the fingernails look like a year after COVID.

The right photo was taken from someone who wasn't diagnosed with long COVID. Figure 1 from https://rmdopen.bmj.com/content/11/2/e005469
Apr 30 • 6 tweets • 3 min read
SARS-CoV-2 hijacks the clotting system of your body for its own purposes.

The spike protein binds to fibrin, rendering it toxic. Those toxic fibrin proteins damage blood vessel walls and drive an inflammatory response.

Other viruses don't do this. 🧵 We've known for a while that fibrin plays a role in acute severe disease and long COVIDbut not how this worked. The SARS-CoV-2 virus "hijacks the clotting system for its own purpose," with recent research showing its spike protein binds to fibrin, turning it into a "toxic form," Professor Crabb says. The activated toxic form of fibrin lays down deposits on blood vessel walls, he explains, driving a "big inflammatory response" that causes the microvascular damage responsible for neurological and cardiovascular symptoms. It also suppresses natural killer cells.... When fibrin builds up in organs, it weakens the blood brain barrier, making it easier for things to pass through that shouldn't.

This includes spike proteins from SARS-CoV-2, which have been found in long COVID patients.

Fibrin deposition is linked to neurodegenerative disease. Increased BBB permeability associated with parenchymal fibrin deposition is a feature of COVID-19 neuropathology. In the brain of some patients with COVID-19, detection of spike and viral RNA suggests potential neuroinvasion. Our data and previous literature support that, while spike can enhance fibrin toxicity, even in the absence of spike, fibrin is deleterious in diseases such as multiple sclerosis, Alzheimer’s disease, rheumatoid arthritis, colitis and periodonditis. Thus, fibrin may be deposited either together with spike when spike is present in the brain45 or through an open BBB afte...
Mar 9 • 9 tweets • 3 min read
Over the last 5 years we've seen weapons-grade disinformation tactics applied to stop people from talking about the damage that COVID is doing to their bodies.

The ensuing "fog of war" allowed libertarian extremists to use government for advancement of COVID denialism policies. A tree stands alone in the fog. And the most interesting thing is that key factions involved in this scheme, self-assured in their own understanding, will not recognize the role they played in perpetuating this state of affairs.

And they don't recognize the role they continue to play.

Feb 17 • 17 tweets • 6 min read
We are clearly in the midst of an anomalously severe flu season.

Although H5N1 has not been detected in high numbers among humans, there's a good chance that it's quietly playing a significant role without even infecting humans directly.

How, exactly? Let's lay it all out: 🧵 A graph of influenza specimens tested for influenza in California. 2024/2025 shows a trend peaking above previous 4 years at 27% vs ~22% and lower peaks. If you want the answer up front without having to read through a detailed explanation, you can skip to the summary and conclusion in the last few posts of the thread.

Otherwise, read on! To summarize the hypothesis: Human-transmissible H1/H3 influenza A subtypes may have already acquired genetic material from H5N1 through reassortment, via mammals simultaneously infected with H1/H3 virus and H5N1. This could explain why we're seeing increased clinical severity.
Feb 11 • 15 tweets • 6 min read
There's been a sharp increase in unsubtyped influenza A detected in Canada and beyond over the last few weeks.

Compared to the previous two seasons, influenza only passed the epidemic threshold (5% test positivity) in January compared to a October/November start.

What's up? 🧵 Image
Image By definition, influenza A without a subtype remains unidentified.

However, given that influenza A shares a gene with H5N1, it is still possible that at least some of those positive results are in fact H5N1.

Feb 10 • 7 tweets • 3 min read
If H5N1 were spreading in humans, would conventional tests for influenza A be expected to detect it?

Yes it would, potentially, since influenza A testing typically targets the M gene for detection.

This gene is conserved between seasonal influenza A in humans and H5N1.🧵 Most tests listed below for the detection of seasonal influenza may be capable of detecting influenza A/H5N1, which is a subtype of influenza A. However, only tests specifically designed for subtyping will be able to determine if the person has seasonal flu, or influenza A/H5. The pictured quote above is from a page on the FDA's website where they list out approved medical devices for the detection of influenza.

fda.gov/medical-device…
Feb 3 • 12 tweets • 4 min read
Amid the gloom and doom, I'm excited to share news that gives me hope.

Invivyd has announced positive initial findings from an ongoing clinical trial of a monoclonal antibody to be used as a pre-exposure prophylactic to prevent COVID-19 infections.

Here are the highlights: 🧵 RELEASE DETAILS INVIVYD ANNOUNCES POSITIVE PHASE 1/2 CLINICAL DATA FOR VYD2311, A MONOCLONAL ANTIBODY DESIGNED TO BEA SUPERIOR ALTERNATIVE TO COVID- 19 VACCINATION FOR THE BROAD POPULATION
VYD2311 Serum Concentration (nanogram/mL) over time. Logarithmic scale. From the image, the red dots represent observed serum concentrations of VYD-2311 IM (n=8), with error bars indicating variability. The concentration is plotted on a logarithmic scale (y-axis) ranging from approximately 10 µg/mL to 1000 µg/mL over a time period of 0 to 65 days (x-axis). Range Observed in Red Dots: Lowest Value: Around 10 µg/mL at the earliest time points (Day 0). Highest Value: Around 300-400 µg/mL at peak concentration (around Day 7). Declining Phase: Gradual decrease, staying above 100 µg/mL throu... Invivyd has been developing a monoclonal antibody to prevent COVID infection.

The idea is you'd get it once or twice a year and get better protection against COVID than available vaccines.

This could make it much easier to avoid long COVID, especially combined with respirators.
Jan 16 • 7 tweets • 4 min read
One needs to ask the question: qui bono?

Who benefits from the perception that certain diseases are viewed as psychological when there are clear physiological causes?

Medical diagnoses don't get created in a vacuum. They exist in service of underlying economic interests. 🧵 Image My question was rhetorical. The answer is insurance companies.

Have you heard of the biopsychosocial model?

It is an academic framework that tries to define chronic illness more in terms of personal responsibility and psychological factors vs biology.

tandfonline.com/doi/full/10.10…These harms derive from an empirically unsubstantiated, neoliberal narrative emphasising the role of personal responsibility and effort in ‘recovery’ from ill-health, ignoring socio-structural contributors to chronic illness and disability. Notably, this biopsychosocial model ignores the health-related impact of welfare and disability insurance reforms which the model has been employed to justify.
The model was, however, largely developed through the work of the Centre for Psychosocial and Disability Research at Cardiff University, for some years sponsored by disability insurance giant Unum (then, Unum Provident). The centre was directed by Mansel Aylward, formerly Chief Medical Advisor, Medical Director and Chief Scientist at the Department of Work and Pensions (DWP) with Waddell as honorary professor, whilst some of the centre’s research was commissioned by the DWP (Rutherford 2007a; Stewart 2019). Although Waddell and Aylward were key architects of the BPS model, a number of other...
Jan 6 • 9 tweets • 4 min read
People are starting to take notice of one of COVID's unpleasant effects: increased susceptibility to fungal overgrowth.

This points to the long term effects COVID causes in your immune response. 🧵 Figure 1 from https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2022.1080822/full A graphical summary demonstrating how COVID-19 infection contributes to increased susceptibility to invasive fungal disease. COVID-19 causes significant and immune dysregulation and mucosal damage (e.g., cilia loss).

This can create conditions for invasive fungal diseases such as Aspergillus, Mucorales, and Candida infections.

frontiersin.org/journals/immun…
Jan 6 • 9 tweets • 2 min read
Long COVID is like quicksand.

You could be walking around having a great time until suddenly you're faced with the single most important problem you've ever faced.

Except, nobody is going to even try pulling you out. And most people deny that the quicksand even exists. Need a rope to get out of that quicksand?

Too bad, all we've got is a rubber band. Pull too hard and it will snap back and cause you to sink further.
Dec 21, 2024 • 8 tweets • 3 min read
Polarization kills and leaves people disabled in its wake.

On one extreme: a complete rejection that COVID causes any harm.

On the other end of the ideological spectrum: the idea that vaccines are the final solution even though the virus finds ways to evade it.

Both are wrong. To those operating under the assumption that COVID causes no harm:

I will refer you to the voluminous scientific literature demonstrating the cumulative harm COVID causes physiologically.

This applies both in the acute and chronic phase of the disease

Nov 16, 2024 • 5 tweets • 2 min read
One reason things are so chaotic right now is that there are competing fantasies about what happened with COVID.

Liberals are under the impression that Biden solved COVID and saved the economy.

MAGA is convinced that COVID was a nothingburger, and are acting vindicated. The Gauntlet How COVID Helped Trump Win Biden never ended the pandemic, but he did end government efforts to mitigate its worst impacts JULIA DOUBLEDAY AND WALKER BRAGMAN NOV 15, 2024 They're both wrong, of course.

COVID is still spreading rampantly and shutting down hospital departments.

And people aren't making the connection between new onset cardiovascular damage, walking pneumonia, various other conditions and their past COVID infections. CityNews Overflowing pediatric hospitals in Montreal: parents asked to cooperate Montreal Children's Hospital Montreal Children's Hospital on June 14, 2024. (Johanie Bouffard, CityNews Image) By Katrine Desautels, The Canadian Press Posted November 15, 2024 12:35 pm. Last Updated November 15, 2024 12:43 pm. As Montreal’s two pediatric hospitals experience overflow in their emergency departments, parents are being asked to keep their children home if they don’t require immediate care.
Nov 14, 2024 • 9 tweets • 3 min read
Mass exodus from this site would be a tactical mistake & cause irreparable harm to left-leaning/COVID-informed communities.

When vital information is isolated between platforms, it limits our overall safety and effectiveness.

Right now we desperately need interconnectedness.🧵 Join or Die cartoon, inspired by Benjamin Franklin Copyright Libby Bush https://www.reddit.com/r/Art/comments/ircdci/join_or_die_2020_edition_after_ben_franklin_me/ To create accountability via public pressure, we need a lot of reach.

For example: under Biden's FDA, without any reason provided, Novavax access was limited to those who hadn't had mRNA.

We rallied against that here. The net result? FDA changed course.