Baculovirus infectivity and the actin cytoskeleton.

Baculovirus infection occurs when susceptible insect larvae ingest viral occlusions and occlusion-derived virus is released in the midgut lumen. Midgut columnar epithelial cells (the sole targets) are penetrated when the viral envelopes fuse with microvillar membranes; subsequently, nucleocapsids are transported basally through the microvilli toward the nucleus where replication ensues. Rapid infection of trachael cells (secondary targets) is under heavy selection because midgut cells are sloughed, an effective defense against systemic infection. The unique multiple nucleocapsid per virion trait acquired by some baculoviruses functions in countering this defense. Systemic infection is amplified after infected tracheal cells transmit infection to hemocytes. Tracheal cells serve as the conduit for virus spread through basal laminal barriers. Discordant susceptibilities to infection of midgut cells, tracheal cells and hemocytes may exist within an individual insect; in fully permissive hosts, all are highly susceptible. Viral manipulation of the actin cytoskeleton both during nucleocapsid transport and after viral gene expression is at the core of successful infection and replication. G-actin, normally cytoplasmic, is efficiently localized within the nucleus during early viral gene expression, and nuclear actin polymerizes during late gene expression, concurrent with shut down of host protein synthesis and early viral gene expression. Nuclear G-actin is now considered essential for cellular transcription and nuclear F-actin can affect transcription by binding chromatin-remodeling complexes. A new hypothesis is offered for how viral manipulation of actin influences timing of viral gene transcription, genome processing and packaging.