Cell–cell fusion induced by reovirus FAST proteins enhances replication and pathogenicity of non-enveloped dsRNA viruses
Fig 5
Cell–cell fusion has heterogeneous effects on replication of different viruses.
(A–D) Effects of cell–cell fusion on replication of non-fusogenic mammalian orthoreovirus (MRV) and group A rotavirus (RVA). (A, B) Vero cells were transfected with pteropine orthoreovirus (PRV) FAST-p10 expression plasmid vectors or empty vector (1 μg/well). (C, D) BSR cells were transfected with Sendai virus (SeV) modified recombinant F (Fc) and HN expression plasmid vectors or empty vector (1 μg each/well). At 2 h post transfection, cells were infected with MRV strain T1L (A, C) or RVA strain SA11 (B, D) at a multiplicity-of-infection (MOI) of 0.001 plaque-forming units (PFU)/cell. Infectious virus titers in cell lysates at 16 h post infection were determined by plaque-formation assay. Data are expressed as means ± SD (n = 3) and were statistically analyzed using the t-test. (E–G) Effects of cell–cell fusion by PRV FAST-p10 on replication of (E) infectious bursal disease virus (IBDV) in DF1 cells, (F) encephalomyocarditis virus (EMCV) in Vero cells, and (G) vaccinia virus (VV) in BSR cells. Monolayers of DF1, Vero, or BSR cells were transfected with FAST-p10 expression plasmid vectors or empty vector 4 h (E) or 2 h (F, G) before viral infection at a MOI of 0.001 PFU/cell (E–F) or 0.001 TCID50/cell (G). At 14 h post infection (IBDV), 12 h post infection (EMCV), and 20 h post infection (VV), infectious virus titers were determined. Data are expressed as means ± SD (n = 3) and were statistically analyzed using the t-test. p < 0.05 was considered statistically significant.