There is as newly published scientific paper that gives evidence that the mRNA vaxxes can generate hepatitis. The infamous spike proteins, once mass produced by one’s cells from the gene therapy which the mRNA vax actually is, travel all around the body and do not remain at the injection site. As these cells express a foreign protein, the body’s T-cells attack these cells, destroying once healthy tissue. If the spike proteins have become imbedded in the liver, then, bingo, hepatitis.
“A new paper is out linking the COVID vaccines and hepatitis is now available: SARS-CoV-2 vaccination can elicit a CD8 T-cell dominant hepatitis.
Marc, among others, believes that this is not directly due to the spike protein, but happens indirectly. Here’s how:
- After injection, the lipid nanoparticles (LNP) in the vaccines carry the mRNA instructions to your cells causing them to express spike protein (known as "transfection"). These transfected cells are all over your body and are not limited to the injection site.
- The T-cells in your immune system then attack these cells (since they are expressing a foreign protein) causing the destruction of (formerly) healthy tissue. If the T-cell attacks happen to cells in the liver, you get hepatitis.
If it happens in cells around your heart, you get myocarditis. If it happens in the cells protecting the blood-brain barrier and in your brain, the barrier can be damaged leading to prion disease, Alzheimer's, dementia, autism, stroke, etc.
With respect to the cases of hepatitis being reported in 11 countries across the world, this may not be related as most of the cases are being reported in unvaccinated people. However, in the VAERS database, hepatic failure is elevated 87X normal and hepatic cirrhosis is elevated 125X normal.
https://www.sciencedirect.com/science/article/pii/S0168827822002343
Abstract
Background & Aims
Autoimmune hepatitis episodes have been described following SARS-CoV-2 infection and vaccination but their pathophysiology remains unclear. Here, we report the case of a 52-year-old male, presenting with bimodal episodes of acute hepatitis, each occurring 2-3 weeks after BNT162b2 mRNA vaccination and sought to identify the underlying immune correlates. The patient received first oral budesonide, relapsed, but achieved remission under systemic steroids.
Methods
Imaging mass cytometry for spatial immune profiling was performed on liver biopsy tissue. Flow cytometry was performed to dissect CD8 T cell phenotypes and identify SARS-CoV-2-specific and EBV-specific T cells longitudinally. Vaccine-induced antibodies were determined by ELISA. Data was correlated with clinical labs.
Results
Analysis of the hepatic tissue revealed an immune infiltrate quantitatively dominated by activated cytotoxic CD8 T cells with panlobular distribution. An enrichment of CD4 T cells, B cells, plasma cells and myeloid cells was also observed compared to controls. The intrahepatic infiltrate showed enrichment for CD8 T cells with SARS-CoV-2-specificity compared to the peripheral blood. Notably, hepatitis severity correlated longitudinally with an activated cytotoxic phenotype of peripheral SARS-CoV-2-specific, but not EBV-specific CD8+ T cells or vaccine-induced immunoglobulins.
Conclusions
COVID19 vaccination can elicit a distinct T cell-dominant immune-mediated hepatitis with a unique pathomechanism associated with vaccination induced antigen-specific tissue-resident immunity requiring systemic immunosuppression.
Lay summary
Liver inflammation is observed during SARS-CoV-2 infection but can also occur in some individuals after vaccination and shares some typical features with autoimmune liver disease. In this report, we show that highly activated T cells accumulate and are evenly distributed in the different areas of the liver in a patient with liver inflammation following SARS-CoV-2 vaccination. Moreover, within these liver infiltrating T cells, we observed an enrichment of T cells that are reactive to SARS-CoV-2, suggesting that these vaccine-induced cells can contribute to the liver inflammation in this context.