A paper out recently shows that the Spike Protein induces inflammation via TLR2-dependent activation of the NF-κB pathway. Biochemical studies revealed that S protein triggers inflammation via activation of the NF-kB pathway in a MyD88-dependent manner. This combined with another recent paper demonstrating that the Spike Protein interacts with and activates TLR4 allow for a most potent signaling cascade for the induction of carcinogenesis. 

This may explain why the virus presents more as a bacterium, as bacteria are more suited to creating this carcinogenic signaling pathway. TLR4 signaling also is involved in the induction/severity of Cancer Cachexia. Once again, I believe the Robust Immune Response created by the mRNA therapies in no way compensate for the (deliberate) carcinogenic effects of the spike protein's intracellular signaling.