Since 1972 the WHO recommended virologists develop the means to prolong virus/coronavirus infections by impairing immune response to a virus.
The below screenshot was taken from the Bulletin of the World Health Organization, Volume 47, p.259, 1972, Recommendations (3)
Germany included/added SARS-CoV-2’s unique COVID-19 causing viral protein ORF10 to its mRNA vaccines to prolong COVID-19. The disease causing viral protein ORF10 is the reason why Germany’s BioNTech lab uses bioweapons handling protocols for manufacturing Germany’s COVID-19 mRNA vaccines. ORF10 is a biological agent.
A 2021 published study “SARS-CoV-2 ORF10 suppresses the antiviral innate immune response by degrading MAVS through mitophagy” informs you why Germany manufactured its COVID-19 vaccines to include 2 major components of SARS-CoV-2 – it’s spike protein (a modified/variant form of spike protein) and it’s unique COVID-19 causing viral protein, ORF10:
“In this study, we showed that overexpression of ORF10 markedly suppressed the expression of type I interferon (IFN-I) genes and IFN-stimulated genes. Then, mitochondrial antiviral signaling protein (MAVS) was identified as the target via which ORF10 suppresses the IFN-I signaling pathway, and MAVS was found to be degraded through the ORF10-induced autophagy pathway. Furthermore, overexpression of ORF10 promoted the accumulation of LC3 in mitochondria and induced mitophagy. ”
… ORF10 transcripts can be detected in patients infected with SARS-CoV-2 . Moreover, Liu et al. found that the expression level of ORF10 in patients with severe disease was much higher than that in patients with moderate disease; in addition, the expression ratio of ORF10 to nucleocapsid (N) in patients with severe disease was significantly higher than that in patients with moderate disease . Therefore, ORF10 plays a vital role at all stages of SARS-CoV-2 infection. In our study, overexpression of ORF10 promoted the degradation of MAVS and the replication of SARS-CoV-2. Consistent with these results, when ORF10 was knocked down by shRNA, MAVS was not degraded and viral replication was weakened, suggesting that ORF10 facilitates SARS-CoV-2 replication via degradation of MAVS.
A 2022 study published in the Journal of Medical Virology, “SARS‐CoV‐2 ORF10 antagonizes STING‐dependent interferon activation and autophagy“
found that SARS-CoV-2 open reading frame 10 (ORF10) targets STING to antagonize IFN activation. Overexpression of ORF10 inhibits cGAS–STING‐induced interferon regulatory factor 3 phosphorylation, translocation, and subsequent IFN induction. Mechanistically, ORF10 interacts with STING, attenuates the STING–TBK1 association, and impairs STING oligomerization and aggregation and STING‐mediated autophagy; ORF10 also prevents the endoplasmic reticulum (ER)‐to‐Golgi trafficking of STING by anchoring STING in the ER. Taken together, these findings suggest that SARS‐CoV‐2 ORF10 impairs the cGAS–STING signaling by blocking the translocation of STING and the interaction between STING and TBK1 to antagonize innate antiviral immunity.