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. 2021 Sep 13;12:5401. doi: 10.1038/s41467-021-25642-z

Fig. 3. HSV-1 VP16 and gB, but not ICP0, are degraded in an autophagy dependent manner.

Fig. 3

Wildtype cells were infected at 1 MOI with HSV-1 17-strain for 8 h before CHX addition to block protein synthesis. In combination with CHX, either the autophagy inhibitor BafA1, the proteosome inhibitor MG132, or DMSO were added to cells. Cells were sampled at 8 h, and 24 h after infection. a Shown for HeLa cells are immunoblots against the HSV-1 proteins gB, ICP0, VP16, and the internal reference GAPDH, b with band quantification relative to GAPDH (n = 6 replicates). c Shown for HCE cells are immunoblots against the HSV-1 proteins gB, ICP0, VP16, and the internal reference GAPDH, d with band quantification relative to GAPDH (n = 6 replicates). Similarly, LUHMES cells were infected at 2.5 MOI with HSV-1 17-strain for 8 h before CHX addition to block protein synthesis. In combination with CHX, either BafA1, MG132 or DMSO were added to cells. Cells were sampled at 8 h, and 24 h after infection. e Shown for LUHMES cells are immunoblots against the HSV-1 protein gB and the internal reference GAPDH, f with band quantification relative to GAPDH (n = 4 replicates). Data are presented as mean values ± SEM (b, d, f). Two-tailed Student’s t test was performed for statistical analysis (α = 0.05). ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001, ns not significant. Source data are provided as a Source Data file.