Immunologists. Is it possible that COVID-19 is causing you to have an HLA mismatch with yourself?

Modifications in HLA-I expression are found in many viral diseases. They represent one of the immune evasion strategies most widely used by viruses to block antigen presentation and
NK cell response, and SARS-CoV-2 is no exception. These alterations result from a combination of virus-specific factors, genetically encoded mechanisms, and the status of host defences and range from loss or upregulation of HLA-I molecules to selective increases of HLA-I alleles.
In this review, I will first analyse characteristic features of altered HLA-I expression found in SARS-CoV-2.

onlinelibrary.wiley.com/doi/full/10.10…

Is this why COVID mimics GVHD?

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More from @Parsifaler

23 Nov
1) This is a long one. Please bear with it and read to the end of the thread.
SEVERE COVID, MIS-C, MIS-A, MIS-V, LONG COVID AND AUTOIMMUNITY
MOLECULAR MIMICRY OF THE SARS-CoV-2 SPIKE PROTEIN AS “GRAFT,” ITS ACTIONS IN COVID-19 AND GRAFT VS HOST DISEASE: DISEASES OF TARGET TISSUE
2) DESTRUCTION
In my studies, I keep finding a disease which, like an ostinato, is omnipresent in my research results. Interestingly, a parallel with a game I play to unwind led me to a breakthrough.
I play Hearthstone. It is my “mindless” activity to unwind while being able to
3) use my mind, but not in a mind-bending way. I consider myself to be pretty good at the game. I usually make Legend these days. Another Legend player told me that when you are crafting an original deck, and it is not working, look at the cards that are left in your hand when
Read 17 tweets
20 Nov
What I have been saying all along.

I take back my self-questioning in a previous post. I am one of the greatest medical geniuses to ever live. I want to help HUMANITY!

Everything I have said: GIT2 was originally identified as a keystone protein in aging through latent semantic
Indexing (LSI) in the hypothalamus of aging rats. This involvement of GIT2 in the aging process was further demonstrated by the upregulation in both human and primate hypothalamic tissue and in the presence of hydrogen peroxide. Additionally, it was found that GIT2 was strongly
involved in DNA damage repair, through recruitment of ATM to the sites of damage to start the DNA damage repair process. In this age-controlling paradigm it was demonstrated that GIT2 possessed a NEAR IRREVERSIBLE ASSOCIATION with the senescence regulator p53.
Read 4 tweets
17 Nov
1) COVID-19, ACE2 DEPLETION AND RAMPANT ANG II OVEREXPRESSION: A DISEASE OF LOCAL AND SYSTEMIC RAS
The great puzzle of COVID-19 may finally be solved. The immense number of systems involved, and the vast number of symptoms presented can be explained by the implication of Systemic
2) and Local Renin-Angiotensin Aldosterone (RAS) systems.
The RAS systems (both local (non-Renin dependent) and systemic (Renin-dependent) are primarily responsible for fluid homeostasis, most notably blood pressure regulation. However, the RAS system has evolved over time to
3) be responsible for far, far more than just fluid homeostasis. Everything we are seeing in COVID-19, both acute and in its sequelae, can be explained by the overexpression of a single peptide: Angiotensin II. This peptide, necessary to maintain a healthy blood pressure, is kept
Read 20 tweets
17 Nov
1) LESSONS FROM THE PAST INTENTIONALLY SUPPRESSED: PRE SARS-CoV-2 KNOWLEDGE OF ACE2, ITS FUNCTIONS AND THE SARS-CoV SPIKE PROTEIN
To begin with, please read the following paragraph:
To further clarify whether the intraperitoneally injected Spike-Fc protein directly affected lung
2) pathology in mice, we examined the localization of the injected Spike-Fc protein in lung. Spike-Fc was detected in lung homogenates by western blot using human Fc–specific antibody, whereas injected control-Fc was not detected. In addition, using immunohistochemistry, we found
3) that Spike-Fc protein localized to bronchial epithelial cells, inflammatory exudates and alveolar pneumocytes. Notably, Spike-Fc primarily localized to severe lesions. This localization of Spike-Fc protein is similar to Spike antigen staining in SARS-CoV–infected mice.
Read 17 tweets
16 Nov
1) THE LOSS OF ACE2 RESULTS IN THE ULTRA-RAPID DEVELOPMENT AND PROGRESSION OF ACUTE AND CHRONIC AGE-RELATED DISEASES
If one were to be an enemy of humanity and wished to end the lives of as many people as possible and in the stealthiest way possible and could choose only one
2) protein to remove from the body to accomplish this task – that protein would certainly be ACE2.
The loss of ACE2 causes a massive upregulation of Angiotensin II. This hormone is involved in all the pathologies of aging. Microvascular disease, cancer, neurodegeneration, heart
3) disease, sudden death and immune dysfunction.
GROUND GLASS OPACITIES/LUNG INJURY
As an immediate concern, it is thought that the upregulation of ANG II is responsible for the ventilation-perfusion mismatch seen in COVID-19: We hypothesize that hypoperfusion of apparently
Read 19 tweets
15 Nov
1) IS COVID-19 A DISEASE OF INDUCED DNA AND MASSIVE FREE RADICAL DAMAGE WHEREIN CLINICAL SYMPTOMS ARE ACTUALLY A “POST-VIRAL SYNDROME?” THERE IS NO “ASYMPTOMATIC SPREAD” AS THE MAIN PHASE OF “SYMPTOMATIC COVID-19” OCCURS WITHIN THE TRANSCRIPTOME.
Before COVID-19, the medical
2) community spoke of anosmia, in relation to viruses, as post viral olfactory loss.
If we look at lung radiation damage (not in the context of actual radiation, but in context of the massive amounts of free radicals, which it generates) we see a direct parallel to the lung
3) findings of COVID-19. Ionizing radiation produces reactive oxygen species that induce lesions, and not only is tumor tissue damaged, but overwhelming inflammatory lung damage can occur in the alveolar epithelium and capillary endothelium. Is this not COVID-19?
Read 8 tweets

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