FIG. 4.

Results of cotransfection studies with FIV-PPRchim42 and mutant viruses. (I) Photomicrography on CrFK cells cotransfected with FIV-PPRchim42 and FIV-PPRchim42 (+ control) (A), FIV-PPRchim42 and FIV-PPR (B), FIV-PPRchim42 and the stop construct (which contains the premature truncation of the TM) (C), FIV-PPRchim42 and P¹ (which contains the native threonine in V4) (D), FIV-PPRchim42 and P² (containing the native glutamine in C2) (E), and no-virus β-gal control (F). Note the giant syncytia and viral spread present when constructs containing the truncated TM were used as input virus. This phenotype is disrupted when viruses containing the full-length TM are cotransfected with FIV-PPRchim42. (II) Graphic quantitation of syncytia (more than three nuclei per cell) from multiple fields from each cotransfection. There was a log-fold reduction in the number of syncytia when constructs containing a full-length TM were cotransfected with FIV-PPRchim42. (III) β-Gal assay results, demonstrating that the transfection efficiencies were consistent.