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Anyone who gets infected with corona more often runs the risk of developing an incurable immune deficiency. According to Health Minister Lauterbach, this is indicated by various studies that are currently being further researched. As a result, the risk of chronic diseases such as dementia would increase.
According to Federal Minister of Health Karl Lauterbach, several corona infections in one person can have serious consequences for the immune system. "It is worrying what we observe in people who have had several corona infections. Studies now show very clearly that those affected are often dealing with an immune deficiency that can no longer be cured," said Lauterbach of the Düsseldorf "Rheinische Post". .
In addition, in vivo studies have shown that lipid nanoparticles (LNPs) accumulate in the liver, spleen, adrenal glands, and ovaries [6], and that LNP-encapsulated mRNA is highly inflammatory [7]. Newly generated antibodies of the spike protein damage the cells and tissues that are primed to produce spike proteins [8], and vascular endothelial cells are damaged by spike proteins in the bloodstream [9]; this may damage the immune system organs such as the adrenal gland. Additionally, antibody-dependent enhancement may occur, wherein infection-enhancing antibodies attenuate the effect of neutralizing antibodies in preventing infection [10]. The original antigenic sin [11], that is, the residual immune memory of the Wuhan-type vaccine may prevent the vaccine from being sufficiently effective against variant strains. These mechanisms may also be involved in the exacerbation of COVID-19.
Some studies suggest a link between COVID-19 vaccines and reactivation of the virus that causes shingles [12, 13]. This condition is sometimes referred to as vaccine-acquired immunodeficiency syndrome [14]. Since December 2021, besides COVID-19, Department of Cardiovascular Surgery, Okamura Memorial Hospital, Shizuoka, Japan (hereinafter referred to as “the institute”) has encountered cases of infections that are difficult to control. For example, there were several cases of suspected infections due to inflammation after open-heart surgery, which could not be controlled even after several weeks of use of multiple antibiotics. The patients showed signs of being immunocompromised, and there were a few deaths.
As a safety measure, further booster vaccinations should be discontinued. In addition, the date of vaccination and the time since the last vaccination should be recorded in the medical record of patients.
originally posted by: v1rtu0s0
Yep, this is the pivot to blame everything on Covid instead of the vaccine.
That virus is so crafty, doing things no virus has ever done before.
Despite lesser affinity towards COVID-19 virus, as compared to ACE2, this receptor provides a suitable justification behind elevated blood glucose levels in infected patients, retarded COVID-19 risk in women, enhanced susceptibility in geriatrics, greater infection susceptibility of T cells, infection prevalence in non-susceptible human cardiac pericytes and so on. The manuscript invokes the title role and distribution of CD147 in COVID-19 as an entry receptor and mediator of endocytosis-promoted entry of the virus, along with the "catch and clump" hypothesis, thereby presenting its Fundamental significance as a therapeutic target for potential candidates, such as Azithromycin, melatonin, statins, beta adrenergic blockers, ivermectin, Meplazumab etc. Thus, the authors provide a comprehensive review of a different perspective in COVID-19 infection, aiming to aid the researchers and virologists in considering all aspects of viral entry, in order to develop a sustainable and potential cure for the 2019 COVID-19 disease.
originally posted by: infolurker
originally posted by: v1rtu0s0
Yep, this is the pivot to blame everything on Covid instead of the vaccine.
That virus is so crafty, doing things no virus has ever done before.
Hell, it may be both.
We ALL know that Covid was tailor made to infect humans utilizing multiple entry points (ACE2, CD-147, etc)
pubmed.ncbi.nlm.nih.gov...
Despite lesser affinity towards COVID-19 virus, as compared to ACE2, this receptor provides a suitable justification behind elevated blood glucose levels in infected patients, retarded COVID-19 risk in women, enhanced susceptibility in geriatrics, greater infection susceptibility of T cells, infection prevalence in non-susceptible human cardiac pericytes and so on. The manuscript invokes the title role and distribution of CD147 in COVID-19 as an entry receptor and mediator of endocytosis-promoted entry of the virus, along with the "catch and clump" hypothesis, thereby presenting its Fundamental significance as a therapeutic target for potential candidates, such as Azithromycin, melatonin, statins, beta adrenergic blockers, ivermectin, Meplazumab etc. Thus, the authors provide a comprehensive review of a different perspective in COVID-19 infection, aiming to aid the researchers and virologists in considering all aspects of viral entry, in order to develop a sustainable and potential cure for the 2019 COVID-19 disease.
Maybe this is why the Chinese were so TERRIFEIED of covid that they stayed in lockdown hoping it would go away. Could they have known this was an incurable degenerative disease upon repeat infections?
Interesting Hypothesis.
originally posted by: Rich Z
Hmm, I would expect a severely compromised immune system widely spread among the population would be reflected by a notable increase of cancer diagnoses. Both new and recurrences from past cases that were previously considered as being under control.
That other shoe has yet to drop. And it could be a real doozy. Imagine the french revolution on a planetary scale.
If I were a younger, more ambitious, man I would start a business building and selling guillotines.
IMHO.
"We had actually expected that DCs isolated from patients infected with SARS-CoV-2 would activate T cells more potently than DCs obtained from healthy donors," says Krug. "However, we discovered that, in the course of the disease, the proteins present on the surface of the DCs in patients' blood were altered in a way that made them more likely to inhibit T cell responses." In spite of this, by 15 days after diagnosis 90% of these patients had generated antibodies directed against the SARS-CoV-2 spike protein, and many of them had also activated a T cell response. -- these responses are the hallmarks of a robust immune reaction against the virus. "So, the drop in the numbers and reduced functionality of DCs does not seem to have a negative impact on the immune response to the coronavirus itself," Krug says.
"We had actually expected that DCs isolated from patients infected with SARS-CoV-2 would activate T cells more potently than DCs obtained from healthy donors," says Krug. "However, we discovered that, in the course of the disease, the proteins present on the surface of the DCs in patients' blood were altered in a way that made them more likely to inhibit T cell responses." In spite of this, by 15 days after diagnosis 90% of these patients had generated antibodies directed against the SARS-CoV-2 spike protein, and many of them had also activated a T cell response. -- these responses are the hallmarks of a robust immune reaction against the virus. "So, the drop in the numbers and reduced functionality of DCs does not seem to have a negative impact on the immune response to the coronavirus itself," Krug says.
The group found that, in some cases, the immune system mistakenly flagged and q attacked proteins called type I interferons (IFNs) that help regulate immune response. Normally, antibodies attach to foreign invaders, marking them for destruction by other immune cells. But the researchers discovered that some people made “auto-antibodies,” antibodies against their own type I IFNs. Nearly 20% of the people who died from COVID-19 created auto-antibodies.
“Their immune systems mistakenly depleted their IFNs, making them more susceptible to the virus,” Casanova said. These IFN-targeting auto-antibodies are found in uninfected individuals too, suggesting that they may contribute to the development of severe COVID-19. “Critical COVID-19 pneumonia probably results from insufficient type I IFNs in the first days of infection,” Casanova said.