Skip to main content
Fig. 4 | Virology Journal

Fig. 4

From: Mutagenesis of the di-leucine motif in the cytoplasmic tail of newcastle disease virus fusion protein modulates the viral fusion ability and pathogenesis

Fig. 4

The viral budding, replication, protein synthesis, and assembly of LL-motif mutants. A LL-motif mutants caused weakened virus budding. BSR-T7/5 cells were infected with rSG10* or rSG10*-F/L537A. At 36 hpi, the cell supernatants were harvested for ultracentrifugation and the cell lysates and virus particles were analyzed by western blotting. The band intensities were used to calculate budding indices, and all were normalized to rSG10*. B Intracellular and extracellular virus titers of LL-motif mutants. BSR-T7/5 cells were infected with rSG10* or rSG10*-F/L537A at a MOI of 0.1, and cell precipitates and supernatants were collected for TCID50 analysis. Viral replication (C) and translation (D) of LL-motif mutants. BSR-T7/5 cells were infected with rSG10* or rSG10*-F/L537A at an MOI of 3, the total RNA levels of NP fragments were determined by RT-qPCR and the NP expression levels were analyzed by western blotting. The total RNA levels of the NP gene and NP protein expression levels are expressed as percentages of the levels for rSG10*, which were set at 100%. E Interaction between F and NP or HN protein of LL-motif mutants. BSR-T7/5 cells were infected with rSG10* and rSG10*-F/L537A at an MOI of 0.1, the cell lysates were immunoprecipitated with anti-F antibodies, and then the levels of NP and HN protein were detected by western blotting. P values were calculated with a one way or two-way ANOVA; n = 3; *, P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001

Back to article page