FIG. 2.

WRO cells in EMT exhibit increased susceptibility to HSV-1 attachment, infection, and gene expression. (A) There is earlier and increased HSV-1 VP-16-GFP attachment to WRO-E1 and WRO-E2 cells (bottom rows) as compared with WRO and WRO-C cells (top rows), as visualized by time-lapse fluorescence microscopy. Scale bars: 10 μm. (B) HSV-1 infection is enhanced in WRO-E1 and WRO-E2 as compared with WRO after infection with the herpesvirus NV1066 (MOI of 0.5), which expresses GFP. Scale bars: 25 μm. (C) HSV-1 infection is enhanced in WRO-E1 and WRO-E2 as compared with WRO-C and WRO with the herpesvirus NV1023 (MOI of 0.5), which expresses β-galactosidase. Detected by X-Gal histochemical staining. Scale bars: 75 μm. (D) A time course Western blot of the early herpesviral gene products ICP27 (top) and ICP8 (middle), and the late herpesviral gene product gC (bottom) in cells after infection with NV1023 (MOI of 1) over a 48-hr period shows earlier and more robust herpesviral gene expression by WRO-E1 and WRO-E2 as compared with control cells. (E) Quantification of viral β-galactosidase production by cells 6 and 9 hr after infection with the HSV-1 NV1023 (MOI of 5) demonstrates greater sensitivity of WRO-E1 and WRO-E2 to HSV-1 infection. p.i., postinfection. Color images available online at www.liebertpub.com/hum