Fig. 14.15.

TBE virus life cycle (the nucleus is not shown for clarity). The virus attaches to a still unknown receptor on the cytoplasmic membrane, and penetrates the cell by endocytosis. Endosomal acidification induces the fusion of the endosomal membrane with the viral envelope, whereby the capsid is released into the cytoplasm. The viral genome is used as mRNA and is translated into a polyprotein. The polyprotein is embedded in the endoplasmic reticulum (ER) membrane by signal-peptide-like protein domains. All subsequent steps of the infection cycle occur in close proximity to this cell compartment. The signalase, which is associated with the ER, cleaves the precursor protein in the region of structural proteins C, PrM and E. All other cleavage reactions in the region of non-structural proteins are performed by the NS3 protein, which together with the NS2B protein acts as a protease. These processing reactions give rise to the NS5 protein, which carries the RNA-dependent RNA polymerase activity and transcribes the positive-sense genome into negative-sense RNA molecules. In turn, these serve as templates for the synthesis of new viral genomes. Newly synthesized viral genomes accumulate in regions of the ER membrane that contain high concentrations of viral structural proteins. This leads to budding of virus particles into the ER lumen. In the further course, these are transported via Golgi vesicles to the cell surface and released