Figure 3.

Shows the infection, replication and pathogenesis of TBVs in hosts taking flavivirus as an example. Ticks transmit the virus to susceptible host while feeding. TBVs enter the host cell via endocytosis or by fusing E protein to the heparan-sulfate and glycosaminoglycan receptors (found on vertebrates and tick cells). After entering the host cell, the virus fuses with the endosomal membrane and releases its capsid into the cytoplasm. In the infected cell cytoplasm, the viral RNA is unveiled and transcribed into proteases, which cleave the polypeptides into several NSPs, such as NS1, NS3, 2A, 2B, 4A, 4B, etc. RNA-dependent RNA polymerase and helicases work together to produce gRNA and RNAs, which are both required for viral replication and transcription. The newly synthesized viral RNA is translated, producing envelopes, capsids, membrane proteins, and other components that are then transported to the E.R-Golgi body complex for virion assembly. These virions coat the lipid bilayer completely, mature, and are exocytosed from the cytoplasm of the infected cell. Following transmission from an infected tick, the TBVs replicate and induces inflammatory responses in infected hosts, resulting in clinical signs and symptoms. These viruses use a variety of mechanisms to evade host immune responses and colonize host tissues. In some cases, the host immune responses to TBVs, particularly pro-inflammatory cytokines, can cause neurological and cardiovascular disorders during persistent infections.