In rabbit kidney (RK13) cells, gG-negative BHV-1 exhibited significant defects in plaque formation and growth compared to that of gG-positive BHV-1. RK13 cells infected with gG-negative BHV-1 exhibited a distinctive CPE and contained a larger number of cells stained with trypan blue dye compared to those infected with gG-positive strains, suggesting that gG-negative BHV-1 inflicted more damage to the infected cells than gG-positive BHV-1. Apoptotic cell death was induced in RK13 cells infected with gG-negative BHV-1 within 8 h. In contrast, the onset of apoptosis in gG-positive BHV-1-infected RK13 cells was around 12-16 h postinfection. In the presence of caspase inhibitor Z-Asp-CH2-DCB, multiplication of gG-negative minus BHV-1 was significantly increased. These results demonstrate that BHV-1 gG is involved in stabilizing the cell structure, postponing apoptotic process, and efficient BHV-1 replication in infected RK13 cells.