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. 2007 Oct 31;82(2):999–1010. doi: 10.1128/JVI.01769-07

FIG. 4.

FIG. 4.

The preferential infection of colon carcinoma tissues by HSV-1 is not due to enhanced viral replication. Colon carcinomas (s.c.) and normal colons of BALB/c mice were prepared for organ culture and infected with HSV-1 as described in Materials and Methods. (A) GFP expression in situ. Organ cultures were infected for 24 h with HSV-1 (2 × 106 IU/well), without acyclovir (II and V) or with acyclovir (20 μM) (III and VI). Acyclovir at 20 μM was found to prevent HSV-1 replication and progeny virus in both Vero cells and colon tissues (data not shown). Green spots represent infected cells and are indicated by arrows. Magnification, ×100. Acyclo., acyclovir. (B) Quantitative analysis of infection. Organ cultures at 24 h postinfection were analyzed for β-Gal enzyme by using the Beta-Glo assay and normalized for protein content as described in Materials and Methods. Data reflect means ± SD (n = 6 replicates). Results are representative of three independent experiments. The asterisk indicates that infection of colon carcinomas treated with acyclovir was significantly enhanced (P < 0.05) compared to that of acyclovir-treated normal colons.