title: Effect of G gene-deleted recombinant viral hemorrhagic septicemia virus (rVHSV-ΔG) on the replication of wild type VHSV in a fish cell line and in olive flounder (Paralichthys olivaceus).
abstract: In an earlier study, we generated a replicon viral hemorrhagic septicemia virus (VHSV) particle that was lacking the G gene in the genome (rVHSV-ΔG), and proved the potential of it as a protective vaccine through the immunization of olive flounder (Paralichthys olivaceus) fingerlings. Safety is the most important preconsideration for the development of recombinant live vaccines, and a major concern of propagation-incompetent viral particles would be the possible harmful effect to hosts through the interaction with wild-type viruses. Thus, in the present study, we analyzed the replication of rVHSV-ΔG in the presence of wild-type VHSV and the effect of rVHSV-ΔG on the replication of wild-type VHSV in Epithelioma papulosum cyprini (EPC) cells and in olive flounder fingerlings. The replication of wild-type VHSV in EPC cells was severely suppressed when the MOI of rVHSV-ΔG was 0.1 or 0.01, on the other hand, the titers of rVHSV-ΔG were not increased and stayed in a relatively constant according to time lapse. Furthermore, the replication of other novirhabdoviruses, IHNV and HIRRV, was also inhibited by co-infection with high titers of rVHSV-ΔG. There were no big differences in mortalities between groups infected with wild-type VHSV plus rVHSV-ΔG and groups infected with wild-type VHSV alone, when the challenged wild-type VHSV was more than 10(2) PFU/fish. However, a group of fish infected with 10 PFU/fish of wild-type VHSV plus rVHSV-ΔG showed significantly lower and slowly progressing cumulative mortality than a group of fish infected with 10 PFU/fish of wild-type VHSV alone. This result suggests that rVHSV-ΔG has an ability to attenuate the disease progression caused by wild-type VHSV when co-infected with relatively low titers of wild-type VHSV. These results indicate that the propagation-incompetent rVHSV-ΔG would not worsen but attenuate the progression of a disease caused by wild-type VHSV infection. Therefore, rVHSV-ΔG-based vaccines can provide a safe and effective way to control VHSV.
authors.affiliation: Department of Aquatic Life Medicine, Pukyong National University, Busan, 608-737, South Korea.
authors.forename: Min Sun
authors.initials: MS
authors.lastname: Kim
authors.affiliation: Department of Aquatic Life Medicine, Pukyong National University, Busan, 608-737, South Korea.
authors.forename: Seung Hyuk
authors.initials: SH
authors.lastname: Choi
authors.affiliation: Department of Aquatic Life Medicine, Pukyong National University, Busan, 608-737, South Korea. Electronic address: khkim@pknu.ac.kr.
authors.forename: Ki Hong
authors.initials: KH
authors.lastname: Kim
mesh_terms: D000818:Animals; D002460:Cell Line; D060085:Coinfection / Q000276:immunology / Q000662:veterinary / Q000821:virology; D005393:Fish Diseases / Q000276:immunology / Q000517:prevention & control / Q000821:virology*; D005432:Flounder; D017353:Gene Deletion; D031941:Hemorrhagic Septicemia, Viral / Q000276:immunology* / Q000517:prevention & control / Q000821:virology*; D066298:In Vitro Techniques; D029141:Novirhabdovirus / Q000235:genetics / Q000502:physiology*; D014764:Viral Proteins / Q000235:genetics; D014779:Virus Replication / Q000235:genetics*
chemical_list: D014764:Viral Proteins
keywords: In vivo safety; Replication interaction; VHSV; rVHSV-ΔG