Figure 8.

Schematic diagrams of spread and release pathways in HaCaT (A) and Vero (B and C) cells infected with wild-type (A and B) or gE-null viruses (C). Thickness of arrows indicates the likely relative usage of pathways based on the effect of mutations that affect each one. In WT virus-infected HaCaT cells (A), virus is trafficked for CCS on a pathway that depends upon both gE and pUL51. Neither gE nor pUL51 participates in virus release to the medium. In WT virus-infected Vero cells (B), gE and pUL51 operate independently in CCS. The pUL51-dependent pathway is evidently more important for CCS (as indicated by the thicker pathway arrow), and pUL51 participates in the virus release pathway as well. We depict the gE and pUL51 pathways with two completely different pathway arrows, but the gE-dependent and pUL51-dependent CCS pathways may share other viral and cellular factors. In Vero cells infected with gE-null virus (C), The gE-dependent CCS pathway is abrogated, diminishing CCS, but the virion release pathway is enhanced.