Cross Talk between Viruses and Insect Cells Cytoskeleton

Abstract

Viruses are excellent manipulators of host cellular machinery, behavior, and life cycle, with the host cell cytoskeleton being a primordial viral target. Viruses infecting insects generally enter host cells through clathrin-mediated endocytosis or membrane fusion mechanisms followed by transport of the viral particles to the corresponding replication sites. After viral replication, the viral progeny egresses toward adjacent cells and reaches the different target tissues. Throughout all these steps, actin and tubulin re-arrangements are driven by viruses. The mechanisms used by viruses to manipulate the insect host cytoskeleton are well documented in the case of alphabaculoviruses infecting Lepidoptera hosts and plant viruses infecting Hemiptera vectors, but they are not well studied in case of other insect–virus systems such as arboviruses–mosquito vectors. Here, we summarize the available knowledge on how viruses manipulate the insect host cell cytoskeleton, and we emphasize the primordial role of cytoskeleton components in insect virus motility and the need to expand the study of this interaction.

Highly adaptive Phenuiviridae with biomedical importance in multiple fields

“…Enveloped vertebrate-infecting phenuiviruses enter arthropod cells through interaction between virus surface glycoproteins and host cellular factors. They then replicate in a way similar to the process depicted in Figure 3 [108]. Like vertebrate-infecting phenuiviruses, the glycoprotein precursor pc2 encoded by the second segment of RSV is cleaved into pc2-N and pc2-C, which are functional homologs of Gn and Gc, but they are nonstructural.…”

“…Another report suggests that the non-structural protein NS4 (p4) of RSV is also associated with RSV's RNPs and forms inclusion bodies that interact with the microvilli of the host midgut epithelium. NS4 hence aids the virus to enter host cells in midgut visceral muscles, alimentary tract, salivary glands, and reproductive system via microvilli formed by actin [108]. Interaction between virus nucleocapsid protein and certain vector proteins, such as the cuticular protein CPR1 and the lipid transport protein vitellogenin, also aids RSV to enter vector cells [46,110].…”

“…They then replicate in a way similar to the process depicted in Figure 2. 90 Like vertebrate-infecting phenuiviruses, the glycoprotein precursor pc2 encoded by the second segment of RSV is cleaved into pc2-N and pc2-C, which are functional homologs of Gn and Gc, but they are nonstructural. pc2-N and pc2-C are required for RSV entrance into the planthopper midgut cells.…”

“…NS4 hence aids the virus to enter host cells in midgut visceral muscles, alimentary tract, salivary glands, and reproductive system via microvilli formed by actin. 90 Interaction between virus nucleocapsid protein and certain vector proteins, such as the cuticular protein CPR1 and the lipid transport protein vitellogenin, also aids RSV to enter vector cells. 44,92 CPR1 binds to RNPs of RSV in the insect, stabilizes the virus in the hemolymph, and aids the virus to move to the salivary tissues.…”

“…Enveloped vertebrate‐infecting phenuiviruses enter arthropod cells through interaction between virus surface glycoproteins and host cellular factors. They then replicate in a way similar to the process depicted in Figure 2 90 …”