FIG. 6.

Prolonged BFA treatment results in cytoplasmic accumulations of the fluorescent capsid fusion protein and disruption of the secretory pathway. Dissociated rat SCG neurons were infected with PRV 180 at a high MOI followed by incubation for 12 h (A to C) or treatment with 2 μg of BFA/ml from 2 to 12 h postinfection (D to F) prior to fixation. Autofluorescence of the mRFP-VP26 fusion (red) and indirect immunofluorescence of gE (A and D), TGN38 (B and E), or Mannosidase II (green) (C and F) is shown. Axons containing fluorescent signals are indicated with solid arrowheads (A to C), while examples of nuclei of BFA-treated cells are indicated with hollow arrowheads (D to F). Cytoplasmic accumulations of fluorescent capsid and tegument are indicated with arrows (D to F). For each sample, a region of clustered neuronal cell bodies (white box) is shown at higher magnification.