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Friesein Profile picture
@Friesein
Feb 11 • 15 tweets • 6 min read • Read on X
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…
In the aforementioned article, the same strain found in dairy cows was confirmed to be found in humans.

In addition to the USDA report referenced in the previous article, Dr. Niman points to recent sequencing uploaded to GISAID confirming the findings.

Ohio influenza surveillance shows a significant positivity rate around 40%, which is 3 times higher than the peak of the previous winter.

Reports from on the ground are looking quite concerning.

Meanwhile in TX, significant increases were seen both in terms of COVID-19 and influenza hospitalizations across all age groups.

The flu death numbers stand out at 72%; a number that needs further context/age stratification.

…ess-dashboard-txdshsea.hub.arcgis.com

dshs.texas.gov/sites/default/… Image
Image
On the other hand, H5N1 numbers in wastewater are not universally increasing. Non-rural locations such as Oceanside and Southeast San Francisco show a decrease, for example.

I'll have to dig more into waste water stats later.

data.wastewaterscan.org/tracker/?chart…Image
So what is going on here?

My impression is that there are multiple factors involved. On one hand we have immune dysregulation from previous COVID infections, opening the door to more severe seasonal influenza.

Additionally, we also see H5N1 in a limited subset of human cases.
It is tough to point to a singular cause in this year's influenza A spike, but things are made even more challenging by a reporting blackout from the CDC.

You'll need to rely on state and local health authorities for surveillance data, and GISAID for sequencing. Image
One thing is clear: airborne precautions should continue be taken. If you're COVID-informed, you already know this.

Make sure you adjust your nose wires in a way that improves your fit. Avoid loose-fitting KN95s or KF95s in favor of N95, elasto, PAPR.

Special thanks to @HNimanFC and @Nucleocapsoid for their commentary on the Nevada sequencing.

Feel free to correct me or add anything I'm missing. And please share any relevant graphs from your own regions as well.

Stay safe out there.
Here's the source for the Canadian influenza surveillance from the first post: health-infobase.canada.ca/respiratory-vi…
Correcting myself, H5N1 is a subtype of influenza A. What I meant to say is that there's a shared gene between seasonal influenza A viruses and H5N1—the M1 and M2 matrix genes.

I had also meant to include the legend on the second image in the first post. Note the later start to the 2024-2025 flu season.

By next week we should get a better sense of whether this influenza wave is peaking of continuing to grow past previous waves.

health-infobase.canada.ca/respiratory-vi…Image
I should have worded this post better; it reflects a ~72% increase in influenza deaths over a 1 week period.

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More from @Friesein

Friesein Profile picture
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
Friesein Profile picture
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
Friesein Profile picture
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
Friesein Profile picture
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
Friesein Profile picture
Jan 6
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.
Meanwhile, there's a large crowd of people marching straight towards the quicksand.

You can beg, you can plead, you can show them pictures of the quicksand.

It's no use. They're dead set on marching straight through it anyway.
Read 9 tweets
Friesein Profile picture
Dec 21, 2024
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

To those who think the vaccines solve COVID, that is not the case.

Studies show that neurological manifestations of long COVID are not altered by the mRNA vaccines.

Not getting infected is still the only surefire way to avoid long COVID.

Read 8 tweets

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