Entimeter or larger and their diameters range from hundreds of nm to the mm scale. A closer SEM view shows (Fig. 1C) that these wires exhibit decorations with very small crystals (50 to 100 nm in diameter) over the entire surface. Figure 1 D) shows an energy dispersive X-ray absorption (EDAX) spectrum which indicates that the synthesized product consists 
25033180 of pure SnO2 nanomicrowires. The Al peak at 1.5 keV originates from the Al2O3 crucible that was used during synthesis. The inset 1 E) in 1 D) depicts the macroscopic view of the SnO2 snowflake type structure which was taken with a standard digital camera.HCE cells were used as a positive control. Entry of HSV-1 was measured 6 hours post infection using an ONPG colorimetric assay [8]. As shown in Figure 3A, SnO2 nanowires inhibited entry in a dosage dependent manner with maximum viral entry occurring at the lowest concentration (31 mg/ml) of SnO2 treatment. At higher concentrations of SnO2 treatment HSV-1 entry was significantly decreased. HSV-1 entry in cells treated at a concentration of 500 mg/ml and 1000 mg/ml was 5 times lower than untreated cell HCE cells. These results, together with results from our cell viability assay, show that we can obtain a maximum inhibition of entry at a concentration of 500 and 1000 mg/ml without compromising the health of the cells. Due to only a 7 difference in viral entry at concentrations of 500 mg/ml and 1000 mg/ml, 500 mg/ml was chosen as the treatment dose for all subsequent experiments. Next an X-gal entry assay was utilized to further confirm the efficacy of SnO2 nanowires against HSV-1 entry. HCE cells were grown in a 6-well plate and treated with SnO2 and a betagalactosidase-encoding recombinant virus, (along with +/2 control wells). In the presence of X-gal substrate, cells that had been virally infected obtained a blue color, allowing visual analysis of infected cells (Figure 
3B). Uninfected cells display no color change (Negative Control). The number of virally infected cells within SnO2 nanowire treated cells was significantly lower than cells that had not undergone SnO2 treatment (Figure 3C). 1081537 The numerical results of Figure 3C were obtained from the average of six samples in each condition, suggesting that the susceptibility of HCE to HSV-1 infection decreases in the presence of SnO2, thus protecting cells from the virus.SnO2 Nanowire Treatment Reduces Viral Replication, Plaque Formation and Plaque SizeSince treatment with SnO2 nanowires resulted in decreased viral entry, we hypothesized that there should be a net reduction in viral replication as well because a significantly low number of virus particles can enter cells in the presence of SnO2. In order to visually analyze how SnO2 treatment effected viral entry which in turn reduced replication, SnO2 treated HCE cells were infected with HSV-1 (KOS)K26RFP virus. Iloprost Fluorescence microscopy was used to visualize the production of virons in cells several days post infection. As seen in Figure 4A, RFP intensity (red color representative of virus production) in SnO2 treated cell was much lower than untreated cells. Under get Teriparatide normal infection conditions, the virus spreads naturally to neighboring cells, however we observed that in SnO2 treated cells many neighboring cells were uninfected black in comparison to mock treated cells which displayed a higher RFP intensity, which is representative of more virus production. To further assess the effect of SnO2 nanowires on entry and its resultant effect on.Entimeter or larger and their diameters range from hundreds of nm to the mm scale. A closer SEM view shows (Fig. 1C) that these wires exhibit decorations with very small crystals (50 to 100 nm in diameter) over the entire surface. Figure 1 D) shows an energy dispersive X-ray absorption (EDAX) spectrum which indicates that the synthesized product consists 25033180 of pure SnO2 nanomicrowires. The Al peak at 1.5 keV originates from the Al2O3 crucible that was used during synthesis. The inset 1 E) in 1 D) depicts the macroscopic view of the SnO2 snowflake type structure which was taken with a standard digital camera.HCE cells were used as a positive control. Entry of HSV-1 was measured 6 hours post infection using an ONPG colorimetric assay [8]. As shown in Figure 3A, SnO2 nanowires inhibited entry in a dosage dependent manner with maximum viral entry occurring at the lowest concentration (31 mg/ml) of SnO2 treatment. At higher concentrations of SnO2 treatment HSV-1 entry was significantly decreased. HSV-1 entry in cells treated at a concentration of 500 mg/ml and 1000 mg/ml was 5 times lower than untreated cell HCE cells. These results, together with results from our cell viability assay, show that we can obtain a maximum inhibition of entry at a concentration of 500 and 1000 mg/ml without compromising the health of the cells. Due to only a 7 difference in viral entry at concentrations of 500 mg/ml and 1000 mg/ml, 500 mg/ml was chosen as the treatment dose for all subsequent experiments. Next an X-gal entry assay was utilized to further confirm the efficacy of SnO2 nanowires against HSV-1 entry. HCE cells were grown in a 6-well plate and treated with SnO2 and a betagalactosidase-encoding recombinant virus, (along with +/2 control wells). In the presence of X-gal substrate, cells that had been virally infected obtained a blue color, allowing visual analysis of infected cells (Figure 3B). Uninfected cells display no color change (Negative Control). The number of virally infected cells within SnO2 nanowire treated cells was significantly lower than cells that had not undergone SnO2 treatment (Figure 3C). 1081537 The numerical results of Figure 3C were obtained from the average of six samples in each condition, suggesting that the susceptibility of HCE to HSV-1 infection decreases in the presence of SnO2, thus protecting cells from the virus.SnO2 Nanowire Treatment Reduces Viral Replication, Plaque Formation and Plaque SizeSince treatment with SnO2 nanowires resulted in decreased viral entry, we hypothesized that there should be a net reduction in viral replication as well because a significantly low number of virus particles can enter cells in the presence of SnO2. In order to visually analyze how SnO2 treatment effected viral entry which in turn reduced replication, SnO2 treated HCE cells were infected with HSV-1 (KOS)K26RFP virus. Fluorescence microscopy was used to visualize the production of virons in cells several days post infection. As seen in Figure 4A, RFP intensity (red color representative of virus production) in SnO2 treated cell was much lower than untreated cells. Under normal infection conditions, the virus spreads naturally to neighboring cells, however we observed that in SnO2 treated cells many neighboring cells were uninfected black in comparison to mock treated cells which displayed a higher RFP intensity, which is representative of more virus production. To further assess the effect of SnO2 nanowires on entry and its resultant effect on.
