Abstract: Objective:To observe the selective killing effect of a recombinant TypeI Herpes simplex virus (HSV-I)-me-diated Gibbon ape leukemia virus membrane fusion glycoprotein (GALV.fus) gene system controlled by UL38and cytomeg -alovirus (CMV) promoters on lung adenocarcinomain vitro . Methods:Lung adenocarcinoma cell line A 549 , human fetal fi -broblast cell line HFL- I GNHu5 and Vero green monkey kidney cells were cultured for study. Recombinant HSV-I plasmids encoding GALV.fus were introduced into Vero cells by liposome to amplify the virus, and then the virus was transfected into A549 and HFL-I GNHu 5 cells. The expression of the recombinant plasmids and antitumor effect in vitro were observed. Recombinant cytomegalovirus (CMV) containing GALV.fus or enhanced green fluorescence protein was used as the con-trol. Total protein was extracted from the transfected A 549 and HFL-I GNHu5 cells, and expression of the GALV.fus gene was detected by Western Blot.Results: Recombinant HSV-I virus was packed successfully. The GALV.fus gene system caused A549 cells to form syncytia in vitro and showed increasing cell death with increasing multiplicity of infection. On the other hand, infection with the control virus induced a typical cytopathic effect, characterized by the cells becoming rounder and swelling. HSV Synco- 2 was tested for loss of its ability to cause syncytial formation in normal non-dividing human cells by infecting primary human fibroblasts in either a quiescent or a cycling state. Infection with recombinant HSV- I mediated GALV.fus gene system caused syncytial formation in these normal human cells when they were cycling. CMV promoter-me-diated cell fusion was only marginally affected in cells whose cycling was either slowed by serum starvation or completely arrested with lovastatin. UL38promoter-mediated cell fusion, on the other hand, was absent in cells whose cycling was decreased or arrested. By Western Blot, the expression of GALV.fus gene could be detected in both A549 cells and embryonic fibroblasts transfected by recombinant HSV- I virus. Conclusion:GALV.fus gene system controlled by the UL38promoter has a powerful selective killing effect against lung adenocarcinoma cells invitro , and this system may be a promising new candidate for gene therapy for lung cancer.