For over a year I have been following the growth of a specific strain of Highly Pathogenic Avian Influenza (HPIA), not only from the angle of global protein security, but as a threat to human health.
Here is a rather large post, linked to a big Twitter thread, going as far as over 18 months back by now.
The African Swine Fever comes, and goes in waves, even though there are now numerous wildlife reservoirs, and is currently laying waste to Africa (heh) pig hordes. From a clinical standpoint, very little is known about the pathophysiology of H6N5 in humans, but the paper below gives us some clues.
Clinical and Immunological Characteristics of Human Infections With H5N6 Avian Influenza Virus
Results
H5N6 patients were found to have higher incidences of lymphopenia and elevated alanine aminotransferase and lactate dehydrogenase levels compared with H5N1 and H7N9 patients. Hypercytokinemia was detected at substantially higher frequencies from H5N6 patients compared to those infected with other AIV subtypes. Evaluation of adaptive immunity showed that both humoral and cellular responses could be detected in the H5N6-infected survivor, but cellular responses were absent in the nonsurvivors. In addition, the surviving patient had lower concentrations of both pro- and anti-inflammatory cytokines/chemokines compared to the nonsurvivors.
Alanine aminotransferase (ALT) is an enzyme used for liver testing, lactate dehydrogenase (LDH) is another enzyme, used to measure the extent of infection (how severe), liver and kidney damage, it is also used to turn sugar into energy by your cells. Compared to other Avian Influenza, this caused more cytokine storm. Similar to Covid, when infection leads to death, there is a substantial immune dysfunction going on.
However, recent studies showed that some H5N6 virus strains also possessed the ability to bind both avian- and human-origin sialic acid receptors and were shown to be more transmissible than H5N1 virus in a ferret model [10, 11], indicating that this pathogen may be of high public health risk.
Ironic enough, the sialic acid receptor on the cell surface is speculated to be used as a co-receptor for SARS-CoV-2.
An H5N6 virus-specific response, as determined by measuring the presence of IFN-γ–secreting cells, was not detected in the nonsurvivors during the course of disease. In contrast, the survivor displayed a substantial increase in the number of IFN-γ–secreting cells, rising from 0.031% at day 7 to 4.15% by day 18, the date of discharge from hospital (Figure 4A). In-depth analysis of the IFN-γ+ T-cell response in the survivor showed a bias toward CD8+ T-cell–mediated immunity
I have covered these extensively already, similar to Covid, you want IFN gamma early, to clear the infection, and CD8 cells to kill everything, a poor CD8 response, or failure for whatever reason to release enough Interferon-gamma, leads to poor outcomes.
This year alone, we had 20 infections, and most of the recent ones, from February to now, ended up being Severe infections, the CFR (Case Fatality Rate/Risk, the chances you have of dying if you get infected) is estimated to be between 30%-40%. This strain is bad enough, and aggressive, but is not the “nightmare” one I have in my mind most of the time. That would be H10N3.
The reason I am worried about H10N3, rather than the one above, is because of this.
Emergence of a novel reassortant avian influenza virus (H10N3) in Eastern China with high pathogenicity and respiratory droplet transmissibility to mammals
The two H10N3 isolates had low pathogenicity in chickens and were transmitted between chickens via direct contact. These viruses were highly pathogenic in mice and could be transmitted between guinea pigs via direct contact and respiratory droplets. More importantly, these viruses can bind to both human-type SAα-2,6-Gal receptors and avian-type SAα-2,3-Gal receptors. Asymptomatic shedding in chickens and good adaptability to mammals of these H10N3 isolates would make it easier to transmit to humans and pose a threat to public health.
Because it doesn’t quite kill birds, rather just spreads through than, and has high pathogenicity in mammals.
Now you have a better understanding of why governments are taking the avian flu so seriously, besides achieving a better hold on food security, or rather, monopolization of such Nation States, given the current growing scarcity around. Doesn’t take many mutations for this any of these strains to get really out of hand, really fast.
Below the surface, in dark places, there are two lines of discussion.
First, we had a twin-demic, a pandemic of both SARS-CoV-2, and Avian Flu, and the avian flu was the one doing most of the damage, and death, the circumstantial evidence for this one is quite extensive, but so is for just SARS-CoV-2 inflicting all the damage. The line of thought is, that they were not testing for it, and testing for flu strains is more difficult.
The second, is viral interference. That we, in fact, avoided losing 30% of the world population, because of SARS-CoV-2 interfering with the flu.
All the current trends in regards to this matter are rather worrisome for me. Governments around the world are using faulty PCR tests to cull massive amounts of chicken, while not paying attention to the actual problem (human adaptation). By my forecasting models and others, we WILL live through another “plague”, but the problem is, no model can show you which type, or from where. Natural, or man-made.
Forecasting is a probabilistic analysis, so it might not even happen =).
Given what I know about these avian flu strains by now, my “Things Hidden”, basically how to minimize, or fix SARS-CoV-2 applies to the same extent to influenza, any strain. In fact, one specific part will be even more effective. The low carbohydrate part.
Glucose: Potential new target for combating annual seasonal flu
N-acetyl-L-cysteine (NAC) inhibits virus replication and expression of pro-inflammatory molecules in A549 cells infected with highly pathogenic H5N1 influenza A virus
Attenuation of influenza-like symptomatology and improvement of cell-mediated immunity with long-term N-acetylcysteine treatment
N-acetylcysteine improves oxidative stress and inflammatory response in patients with community acquired pneumonia
You can buy me a coffee whenever you feel like it.
Deep appreciation for all the supporters!
So stocking up on NAC is good. This would also be a way to make homesteaders look like disease spreaders:(
Really excellent article. Thank you for your assiduous work!
The best substack going... thank John Paul.