Friesein Profile picture
Aug 8, 2024 1 tweets 2 min read Read on X
Cognitive dissonance is hitting people hard with the most recent COVID surges.

They were sold a narrative of "just a cold", but the experiences they're having conflict with that spin.

First they notice that they're experiencing the worst "cold" they can remember... in the summer.

Then they start noticing persistent fatigue after they've supposedly recovered. And a chronic cough. And weird moments where they lose their train of thought mid-sentence. It's a disconcerting situation to be in.

Then they get infected again with digestive symptoms, despite having just had it fairly recently (again, in the summer).

Then they look around and notice everyone around them going through the same thing. They notice hospitals masking again. They notice that more coworkers are off sick all of a sudden.

Not everyone is connecting the dots to COVID just yet, but something still seems off, at least.

The common refrain right now is that there's a lot of illness going around. Some may instinctually call it a cold or the flu, but personal experiences are starting to diverge from the informal definitions assigned to those terms in the zeitgeist.

It's unfortunate that people have been so thoroughly coerced and lulled by authorities into suffering long-term consequences from repeated COVID infections. In a few months, the harsh reality of chronic illness and disability will dawn on large waves of people currently dealing with acute infections. For some, the term "long COVID" will enter their lexicon.

All we can do at this point is continue to inform those willing to listen. Prevention is not futile. Prevention is not synonymous with "lockdown", either. Long-term health outcomes still matter. And just like any other noxious substance, less exposure is better than more.A graph from Walgreens COVID data. National Positivity Trend. Current week: 40.2%

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More from @Friesein

Feb 17
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.
To understand how influenza evolves, you need to trace the progression of the virus from its source.

All mammalian influenza A viruses are thought to originate in birds. They then find their way to certain mammals, where the viruses mutate significantly.

Emergence and transmission of influenza A viruses from aquatic wild bird reservoirs and zoonotic and reverse zoonotic events involving veterinary species. Adapted from Frymus, T., Belák, S., Egberink, H., HofmannLehmann, R., Marsilio, F., Addie, D.D., Boucraut-Baralon, C., Hartmann, K., Lloret, A., Lutz, H., et al. 2021. Influenza Virus Infections in Cats. Viruses 13, 1435. https://doi.org/10.3390/v13081435. Used under the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
Read 17 tweets
Feb 11
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.

There's still uncertainty about the extent of H5N1 transmission in humans, but similar flu A trends are popping up in various places.

One important location to watch is Nevada, where local health authorities reported their first known human infection.

cidrap.umn.edu/nevada-reports…
Read 15 tweets
Feb 10
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…
The M gene (matrix) of influenza A is subdivided into M1 and M2 coding regions.

Between viruses sampled in humans and other species, there was 95% amino acid similarity for M1.

M1 is one of the slowest-evolving proteins encoded in the influenza genome.

pmc.ncbi.nlm.nih.gov/articles/PMC65…In human seasonal influenza viruses, the M gene has been reported to evolve 5- to 10-fold more slowly than the HA gene, although there is a difference in evolutionary rates between the coding regions for M1 and M2, with M2 evolving somewhat more rapidly than M1 (16, 17). Indeed, two recent studies indicate that M1 is one of the slowest-evolving proteins encoded by the influenza virus genome (16, 18). While there are differences in M gene evolutionary rates between viruses infecting different host species, IAV strains sampled globally in humans and across a range of other host species exhibi...
Read 7 tweets
Feb 3
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.
VYD2311 is a monoclonal antibody with neutralization ability against various lineages including XBB.1.5, and it reportedly achieves increased neutralization over pemivibart (pemgarda).

Note: JN.1 neutralization has been confirmed in vitro for pemivibart.

About VYD2311 VYD2311 is a novel monoclonal antibody (mAb) candidate being developed for COVID-19 to continue to address the urgent need for new prophylactic and therapeutic options. The pharmacokinetic profile and antiviral potency of VYD2311 may offer the ability to deliver clinically meaningful titer levels through more patient-friendly means such as an intramuscular route of administration.   VYD2311 was engineered using Invivyd's proprietary integrated technology platform and is the product of serial molecular evolution designed to generate an antibody optimized for neutralizing contem...
Read 12 tweets
Jan 16
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...
I'm not here to suggest that psychology doesn't play a role in the human condition.

Prolonged stress is interpreted by the body as an immune insult, leading to activation of the HPA axis and release of cortisol.

But there's more going on in chronic illness than just psychology.
Read 7 tweets
Jan 6
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…
This increased susceptibility also includes mycoplasma pneumoniae, given the mechanical impairment in mucociliary clearance.

See my earlier thread on this.

Read 9 tweets

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