First, I got locked out of my Twitter account, because sometimes I can’t help myself, lol. The account will be active for 6 days, I will just keep writing here. Half of this article ties with everything else I wrote, but especially with Reverse AIDS Part III, I recommend you to read it.
I usually prefer to write a longer article and link everything together, but given the current circumstances, and events unfolding fast, sometimes I will just write parts of it and link it after awards.
When you completely shift the immune response of something, you are deregulating something else. Death and damage, especially secondary forms of damage, will just lag longer. Maintain your awareness, the government will declare the end of the pandemic, for multiple reasons, but this isn’t over yet. Here is an interesting piece of information from Israel (highly vaccinated population).
The Reverse AIDS posts contain the possible answers to this one. A paper making the rounds the last few days.
The paper refers to spike antigens, not spike protein, but… it…still as bad… lol. How and why ? Well, it’s about to get complex. From this paper, which you will see me referring to a few times in the near future.
The problem of either spike or spike antigen inside you for long, or anywhere inside you, is simple. You are not getting an immune response to one disease (SARS-CoV-2), you are getting an immune response to possibly all the above, and all the sweet implications that carry. It depends on which parts of the spike your cells pickup. Here is one, massive, implication.
SARS-CoV-2 spike protein S1 induces fibrin(ogen) resistant to fibrinolysis: implications for microclot formation in COVID-19
The mere presence of the S1 part of the spike protein is enough to induce, by itself, amyloid-based clots. Amyloid clots are fairly resistant, but that is not the main point here today. Parts of the spike, with antigens of other diseases, will produce specific pathophysiological responses to that pathogen antigen.
Persistence of SARS CoV-2 S1 Protein in CD16+ Monocytes in Post-Acute Sequelae of COVID-19 (PASC) up to 15 Months Post-Infection
In the paper above, the found S1 in monocytes up to 15 MONTHS after infection, and one of the main markers of PASC/Long Covid is high levels of sCD40l, a biomarker for micro clotting, among other things. sCD40l can be derived from both thrombi (clots), but it has a fairly specific immune role.
From this paper.
Mycobacterium tuberculosis (M. tb) antigen-specific IFN-γ, IL-2, and CXCL10 responses were significantly higher in active TB and LTBI compared with controls.
sCD40l has also other immune regulatory roles.
In the post The case for Reverse Marek, I postulated that one of my insane ideas (hypothesis based on interdisciplinary observations) had the possibility of being real. Fragments of the spike protein had toxic effects. A big part of the spike protein, S1 has severe inflammatory implications and long-term impact (micro clotting, cardiovascular damage, muscle weakness, long-term inflammation).
I tried to make it shorter and simpler, especially with the current pathways I am looking at, which need a lot of further research.
Now I leave you, the reader, with both my point and a question. Given all the antigens present in the virus and mainly the S protein. How do you treat 12 immune responses at the same time ?
In the end, all roads still lead to Rome. (Reverse AIDS part IV).
So the narrative change to 'living with the virus' is to cover that omicron is not actually mild? or is it more mild but not to the vaccinated?
1915-1917 worldwide "coronavirus" pandemic (actually, M. avium)
https://academic.oup.com/jtm/advance-article/doi/10.1093/jtm/taaa206/5955501
1918 M. influenzae (Haemophilus influenzae)
https://www.academia.edu/35088077/The_Great_Influenza_Pandemic_What_Really_Happened_in_1918
In the course of a single day, if not in mere hours, M. influenzae became M. africanum (galloping tuberculosis = ebola).
2019-2021 worldwide "coronavirus" pandemic (actually, M. avium)
Dr. Lawrence Broxmeyer did isolate M. avium in patients with Covid-19 back in 2020. Chinese researchers did discover that Sars was a new form of Chlamydia pneumoniae, back in 2003. M. avium can be accompanied by "passenger" mycoplasma.
2022 M. influenzae (patients which had been diagnosed with Mers-Cov also were infected with H. influenzae)
Omicron = Mers-Cov-2
https://lawrencebroxmeyermd.academia.edu/DrLawrenceBroxmeyerMD (M. africanum = ebola and marburg)
Dr. Lawrence Broxmeyer also discovered that M. avium subsp. paratuberculosis and M. bovis are the cause behind prion diseases. These prion diseases are related to heat shock proteins, and thus to G4 quadruplexes and Pseudouridine. These heat shock proteins are latent until they encounter a thermal shock, and then beta sheet prions are formed.