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Figurę 1. Viral replication rates of VSV G mutants. L929 cells were infected at an MOI of
(A) 0.1 or (B) 20 At the indicated time points, supematants were harvested and viral titers determined by plaąue assay on Vero cells. Data are the mean ± SEM of three independent experiments.
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Figurę 4. Interferon induction by VSV G mutants. L929 cells were mfected at an MOI of (A) 0.1, (B) 2
Figurę 2. Effect of VSV G mutants on cellular transcription rates. L929 cells were infected at an MO
Figurę 3. Effect of VSV G mutants on cellular protein synthesis rates. L929 cells were infected at a
Viral replication L929 cells were infected at an MOI of 0.1 or 20 in DMEM containing 2% FBS. Forty-f
Figurę 6. Caspase activation by VSV G mutants. (A) L929 and (B) B16 cells were infected at an MOI of
Figurę 6: Expression of PD-1 and PD-L1 on BI6gp33 cells following VSV infection. B16gp33 cells were
Figurę 7: Expression of MHC-I on B16gp33 cells following VSV infection. (a) B16gp33 cells were infec
VSV G mutants replicate efficiently. If VSV G mutants are to be considered for oncolytic virotherapy
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RESULTS Seąuence analysis of VSV G mutants. In order to characterize the potential of VSV G protein
L929 cells with VSV induced a similar mcrease in apoptosis over time for ałl G mutants and for WT VS
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