Figure 5.

Schematic of the interactive effect of Cu on the infection cycle of EhV86. (A) Simplified schematic of the normal infection cycle of EhV86 (after Mackinder et al., 2009). The virion particle (blue hexagon) enters the cell and targets the nucleus where it releases the viral genome. Viral genes are transcribed (red) first by host RNA polymerase in the nucleus and then by viral RNA polymerase in the cytoplasm. Virus DNA replication (orange) also takes place in the nucleus, while the capsid is assembled in the cytoplasm and released via a budding mechanism. Cellular glutathione (GSH) increases (green arrow) as a result of reactive oxygen species generation, which occurs during capsid assembly. (B) Copper down-regulates (green arrow) the infection cycle prior to capsid assembly via transcriptional control of specific viral RNA. Cellular phytochelatin concentrations (PCs) increase in response to elevated copper concentrations, but GSH concentrations are similar to those in uninfected cells as capsid assembly is highly reduced. The ultimate result is a reduction in virus production.