Current COVID-19 doses can cause CD8 T-cell dominant hepatitis, according to a recent study led by researchers from the University of Freiburg in Germany.

Although there was never any hepatitis safety signal in the trials of COVID19 shots, multiple studies have lately linked COVID-19 shots to autoimmune hepatitis (AIH)-like diseases.

Both mRNA and vector-based shots caused liver injury, and the duration from shot administration to symptom onset varied from 4 days to 6 weeks.

After being re-exposed to the shot, one patient’s liver injury worsened.

However, it’s unclear if the reported link between COVID-19 jabs and autoimmune hepatitis is coincidental, reflects temporary drug-induced liver harm, or is due to SARS-CoV-2-induced antigen-specific immune activation.

The occurrence of autoimmune hepatitis or AIH-like diseases after SARS-CoV-2 infection, on the other hand, shows that the latter may be a driving element in the sporadic occurrences.

Several cases of autoimmune hepatitis have been reported in the aftermath of SARS-CoV-2 infection and vaccinations, although the pathogenesis is unknown.

The researchers in this new study from Germany looked at the case of a 52-year-old man who had bimodal episodes of acute hepatitis, each happening 2-3 weeks following BNT162b2 mRNA shots, and tried to figure out what was causing it. The patient was given oral budesonide at first but relapsed before achieving remission with systemic steroids.

On liver biopsy tissue, a comprehensive imaging mass cytometry for spatial immune profiling was performed. Flow cytometry was used to dissect CD8 T cell phenotypes to longitudinally identify SARS-CoV-2- and EBV-specific T cells. ELISA was used to determine the antibodies produced by the jab. Clinical labs were used to correlate the data.

According to the findings, a comprehensive examination of the hepatic tissue indicated an immune infiltration dominated by activated cytotoxic CD8 T cells with a panlobular distribution.

In addition, as compared to controls, there was an enrichment of CD4 T cells, B cells, plasma cells, and myeloid cells.

When compared to peripheral blood, the intrahepatic infiltrate had a higher concentration of CD8 T cells with SARS-CoV-2 specificity. Hepatitis severity was found to be linked to an activated cytotoxic phenotype of peripheral SARS-CoV-2-specific CD8+ T cells, but not EBV-specific CD8+ T cells or jab-induced immunoglobulins, over time.

According to the findings, COVID-19 vaccines can cause a different T cell-dominant immune-mediated hepatitis with a discrete patho-mechanism linked to antigen-specific tissue-resident immunity that necessitates systemic immunosuppression.

It is well known that liver inflammation occurs occasionally during SARS-CoV-2 infection.

However, liver inflammation can occur in certain people after receiving COVID-19 vaccines, and it shares some characteristics with autoimmune liver disease.

The findings reveal that after receiving SARS-CoV-2 shots, highly activated T cells aggregate and are uniformly distributed in diverse parts of the liver in a patient with liver inflammation.

Furthermore, there was an enrichment of T cells reactive to SARS-CoV-2 within these liver infiltrating T cells, suggesting that these jab-induced lymphocytes may contribute to hepatic inflammation in this scenario.

The outcomes of the study were published in the Journal of Hepatology, a peer-reviewed journal.

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