It　has　been　widely　believed　that　recurrence　of　herpes　simplex　keratitis　(HSK)　is　due　to　the　reactivation　of　herpes　simplex　virus　type　1　(HSV-1)　from　latent　sites　in　trigeminal　ganglion　(TG).　However,　there　are　also　not　effective　vectors　which　could　target　TG　for　therapy.　Replication-defective　HSV-1　vector　(rdHSV-IFN　gamma)　was　established　by　calcium　phosphate　co-transfection　of　complementing　cells.　We　firstly　infected　rdHSV-IFN　gamma　to　SH-SY5Y,　and　detected　IFN　gamma　expression　by　western　blot,　evaluated　50　%　cellular　cytotoxicity　(CC50)　by　ELISA.　Antiviral　activity　of　rdHSV-IFN　gamma　was　examined　by　immunofluorescence　and　antiviral　concentration　of　50　%　effectiveness　(EC50)　assay.　The　rdHSV-IFN　gamma　vector　was　immunized　to　Wistar　rats　to　observe　targeting　function　to　TG.　Kaplan-Meier　survival　analysis　was　utilized　to　assess　security　of　rdHSV-IFN　gamma.　RT-PCR　and　immunohistochemistry　assay　were　employed　to　detect　rdHSV-IFN　gamma　localization　in　TG.　Western　blot　was　employed　to　detect　IFN　gamma　expression.　rdHSV-IFN　gamma　was　successfully　established,　and　performed　an　effective　antiviral　activity　and　higher　security　in　SH-SY5Y.　There　were　no　significant　differences　of　survival　and　corneal　infection　rate　of　rdHSV-IFN　gamma　immunized　rats　among　groups　(P　＞　0.05).　RT-PCR　and　immunohistochemistry　indicated　that　expression　of　glycoprotein　D　(gD)　in　TG　could　target　TG　and　decreased　following　with　times　post　immunization.　Furthermore,　IFN　gamma　was　expressed　effectively　in　TG　tissues.　Our　findings　indicated　that　established　rdHSV-IFN　gamma　vector　effectively　transported　therapeutic　gene　into　TG　tissues.　The　administration　of　replication-defective　vector　carrying　therapeutic　genes　may　become　a　promising　tool　in　inhibition　or　reoccurrence　of　HSK　in　clinical.