Spike protein (inc vax) induced immunodeficiency & carcinogenesis megathread #1: SARS-CoV-2 infection causes immunodeficiency in recovered patients by downregulating CD19 expression in B cells
Background
There really shouldn't be this much pathology from one common cause: but we are expressing an agent, spike protein, originally created as a result of whole virus gain of function or vaccine research, an experimental gene therapy transfection treatment that has ongoing emergency use authorisation when there is no emergency and safe, proven alternatives were available all along like Ivermectin, Hydroxychloroquine and so on. It wasn't referred to as âbioweapon researchâ in Fauci's FOI released emails for nothing.
But we are where we are. Let these posts be a warning and to help explain what the medical profession is seeing, what your friends, family, colleagues are suffering from eg Covid âbreakthroughâ reinfection, frequent viral or bacterial infections, more severe colds, relapses of previously controlled cancers, often without knowing why or making the connection.
These posts are but the tip of an iceberg, a highly complex one at that with new research being conducted and released to preprint all the time. (Can you have a complex iceberg? Anyway you get the idea).
The focus of this series is immunology, other systemic pathology is considered separately such as cardiovascular disease & myocarditis, though it's all due to repeat dosing of the same toxic substance (and even the virus itself, it can happen!).
There is a lot of research showing this is harmful to that, but it may be theoretical: the cytotoxin may not reach certain tissues in any significant quantity for any length of time, and our regulatory mechanisms may contain the damage, or the pathology may only occur in severe systemic infections. Perhaps only certain genetic profiles are susceptible?
So I'm far more alarmed if a condition is linked to mild infections, a high percentage of those exposed or after 1, 2 or 3 transfections. That's why repeatable studies are so important and we need widespread monitoring.
We are starting to get datapoints through now that are increasing in significance to where there should be emergency halts and investigations: stroke, thrombosis, myo & pericarditis and immunosuppression. I'm really hoping we don't add carcinogenesis, autoimmune, cardiovascular and neurological diseases to the list.
Thanks to all who are contributing, filling in the gaps where other doctors and researchers are too fearful to speak out, make a stand or just publicly start asking questions as to what is going on?
The last 2 years has been a steep learning curve for us all. Thank you for reading or subscribing and I look forward to your comments.
DC, 15th January 2022.
Hat tip to Nicola Bidoli.
One of the causes is reactive oxygen species mediated damage to mitochondria, something that we know spike protein alone can cause. Distribution studies showed accumulation in the bone marrow & spleen.
The immunodeficiency may persist long enough for you to get re-infected. I'm hoping the immunosuppression isn't cumulative in that case, but its already bad enough.
NAC to the rescue, again.
PBC: Plasma blast cells, the precursor of plasma cells;
BCR: B-cell receptor.
SARS-CoV-2 infection causes immunodeficiency in recovered patients by downregulating CD19 expression in B cells via enhancing B-cell metabolism (2021)
Abstract
The SARS-CoV-2 infection causes severe immune disruption. However, it is unclear if disrupted immune regulation still exists and pertains in recovered COVID-19 patients. In our study, we have characterized the immune phenotype of B cells from 15 recovered COVID-19 patients, and found that healthy controls and recovered patients had similar B-cell populations before and after BCR stimulation, but the frequencies of PBC in patients were significantly increased when compared to healthy controls before stimulation. However, the percentage of unswitched memory B cells was decreased in recovered patients but not changed in healthy controls upon BCR stimulation. Interestingly, we found that CD19 expression was significantly reduced in almost all the B-cell subsets in recovered patients. Moreover, the BCR signaling and early B-cell response were disrupted upon BCR stimulation. Mechanistically, we found that the reduced CD19 expression was caused by the dysregulation of cell metabolism. In conclusion, we found that SARS-CoV-2 infection causes immunodeficiency in recovered patients by downregulating CD19 expression in B cells via enhancing B-cell metabolism, which may provide a new intervention target to cure COVID-19.
Full paper: