• Toxicological Research
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• v.13 no.1_2
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• pp.157-160
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• 1997

The primary skin and eye irritancy of the combined vaccine (KGCC-95VI) for the prophylaxis against Japanese encephalitis and Hantaan virus infection recently developed by Korea Green Cross Corporation was investigated. The KGCC-95VI was applied to the back skins of the New Zealand White rabbits. The rabbits were observed for 72 hours and did not exhibit erythema, eschar and edema. The eyes of the rabbits were exposed to the KGCC-95VI. The rabbits were observed for 7 days and did not exhibit any ocular findings on cornea, iris and conjuntivae. The KGCC-95VI is considered not to have the primary skin and eye toxicity in rabbits.

• Biomolecules & Therapeutics
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• v.5 no.2
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• pp.174-178
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• 1997

The immnunogenicity of the possible non-essential component of the combined vaccine (KGCC-957) for the prophylaxis against Japanese encephalitis and Hantaan virus infection recently developed by Korea Green Cross Corporation was investigated using the Hartley guinea pigs. The KGCC-95Vl was administered to the guinea pigs subcutaneously to sensitize the animals. The guinea pigs did not induce any anaphylactic immune responses which could be detectable by the active systemic anaphylaxis (ASA), the passive systemic anaphylaxis (PSA), and the passive cutaneous anaphylaxis (PCA) tests. The KGCC-95Vl is considered not to induce any anaphylactic immune responses except the prophylatic immune effects of the vaccine.

• Journal of Microbiology and Biotechnology
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• v.32 no.8
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• pp.955-959
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• 2022

Japanese encephalitis (JE) is a vaccine-preventable mosquito-borne disease caused by infection with the Japanese encephalitis virus (JEV). JEV has five genotypes, including genotype V (GV), which is considered ancestral to the other genotypes. The first GV strain, GV Muar, was isolated from a Malayan patient in 1952 and GV did not reappear for 57 years until GV XZ0934 was isolated from a mosquito sample in China. Since 2010, 21 GV strains have been identified in Republic of Korea (ROK). Both GV Muar and GV XZ0934 are more pathogenic than other GI/GIII strains and are serologically distinct. However, because the ROK's GV strains have not been experimentally tested, their characteristics are not known. Characterization of the ROK's isolates is needed to enable development of effective GV strain-based vaccines to protect against GV infections.

• Toxicological Research
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• v.13 no.3
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• pp.275-279
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• 1997

The acute toxicity of the combined vaccine (KGCC-95VI) for the prophylaxis against Japanese encephalitis and Hantaan virus infection. recently developed by Korea Green Cross Corporation, was investigated. KGCC-95VI was administered to the Balb /c mice in two routes, orally and subcutaneously, and into the New Zealand White rabbits subcutaneously. $LD_{50}$ was not accessible as there were no deaths in the group treated even at a dose 800 times the expected clinical dose in both animal species. Between the treated and control groups there were no statistically significant differences in body weight changes and clinical signs during the 14-day observation period, and no pathological gross findings. Accordingly KGCC-95VI is considered not to have the acute toxicity in mice and rabbits.

• Toxicological Research
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• v.13 no.4
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• pp.353-357
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• 1997

The possibility of the allergic encephalomyelitis caused by the combined vaccine (KGCC95VI) for the prophylaxis against Japanese encephalitis and Hantaan virus infection, recently developed by Korea Green Cross Corporation, was investigated in the Hartley guinea pigs. The KGCC-95VI was administered to the guinea pigs subcutaneously to sensitize the animals three times at one month intervals. There were no clinical signs or gross pathological findings. There were no abnormal histopathological findings at cerebrums, cerebellums, brain stems and the spinal cords. The concentration of myelin basic protein was 1.10 ng/dose quantified by ELISA, which met the guide4ine of below 2 ng/ml/dose recommended by American Society of Health -System Pharmacists(AHPS) Drug Information. Accordingly, the KGCC-95VI is considered not to induce any allergic immune responses which may lead to the experimental allergic encephalomyelitis.

• Molecules and Cells
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• v.21 no.1
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• pp.112-120
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• 2006

It has been suggested that defective interfering (DI) RNA contributes to the persistence of Japanese encephalitis virus (JEV). In this study, we characterized molecular and biological aspects of the DI RNA and its relation to viral persistence. We identified a homologous DI virus intimately associated with JEV persistence in Vero cells. The production of DI RNA during undiluted serial passages of JEV coincided with the appearance of cells refractory to acute infection with JEV. We also established a Vero cell clone with a persistent JEV infection in which the DI RNA coreplicated efficiently at the expense of helper virus. The infectious virus yield of the clone fluctuated during its growth depending upon the amount of DI RNA accumulated in the previous replication cycle. Identification of the corresponding negative-sense RNA of the DI RNA indicated that the DI RNA functioned as a replication unit. Most of the DI RNA molecules retained their open reading frames despite a large deletion, encompassing most of the prM, the entire E, and the 5' half of the NS1 gene. Taken together, these observations suggest that the generation of homologous DI RNA during successive JEV acute infections in Vero cells probably participates actively in persistent JEV infection.

• Journal of the Korean Society of Food Science and Nutrition
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• v.29 no.1
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• pp.128-133
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• 2000

This study was designed to verify the efficacy of garlic extracts for protecting the infecton of influenza and Japanese B encephalitis virus. Influenza virus (AO/PR8 strain) and Japanese B encephalitis virus (JaGAr O1 strain) were used to attack mouse through nasal route and each vaccines were injected subcutaneously. 0.002 and 0.2 mL/day of garlic extracts were orally administered to mice. The blood and serum samples were taken from the mice to measure LD50, Defense Index (DI), virus-neutralizing antibody for comparing virus influence inhibiting activities. Defense indices of the male and female mice were not significantly different at every experiment. Vaccination effectively inhibited the influence of influenza virus and 0.002 mL/day garlic extract (0.55$\pm$0.05) resulted in significantly higher DI than the control (0$\pm$0.05) (p<0.05). Although 0.002 mL/day garlic extract (0.55$\pm$0.05) resulted in significantly lower DI than the vaccination (1.10$\pm$0.05), 0.2 mL/day garlic extract (2.05$\pm$0.05) resulted in 10 times higher DI than the vaccination (1.10$\pm$0.05). Garlic extract did not affect DI in Japanese B encephalitis virus influence of the vaccinated mouse, but significantly reduced DI of the non-vaccinated mouse (p<0.05). Garlic extracts did not affect the production of the neutralizing antibody against influenza by vaccination. However, neutralizing antibody production of Japanese B encephalitis was accelerated by vaccination. Consequently, the current study proved the efficacy of garlic on inhibition of influenza virus. Finally, it is very hard to show the higher preventing effect on flu through ingestion of garlic as a food than vaccination.

• Journal of Microbiology and Biotechnology
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• v.14 no.1
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• pp.121-127
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• 2004

Amphotericin B (AmB), an amphipathic polyene macrolide, is an antifungal drug produced by Streptomyces nodosus. Recently, AmB has been shown to exert antiviral activity against rubella virus and human immunodeficiency virus by different mechanisms. In this study, we evaluated the antiviral effect of AmB against Japanese encephalitis virus (JEV) and investigated which step of the viral life cycle was inhibited by AmB to understand the mechanism of antiviral action of AmB. AmB reduced both plaque size and number in the infected cells in a dose-dependent manner. In addition, a 200-fold reduction of infectious virus titer was observed by treatment of infected cells with $5\mug/ml$ of AmB. AmB acted at the post virus-infection step, but not during adsorption of virus to host cells. Western blot analysis revealed that the accumulated level of JEV envelope protein dramatically decreased in the infected cells by treatment with $5-10\mug/ml$ of AmB. Our results indicate that AmB inhibits the replication of JEV at the postinfection step by interfering with viral replication and/or by inhibiting the synthesis of viral proteins.

• Proceedings of the Microbiological Society of Korea Conference
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• 2000.05a
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• pp.23-36
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• 2000

Japanese encephalitis virus (JEV) is the causative agent of a mosquito-borne encephalitis and is transmitted to human via persistently infected mosquito vectors. Although the virus is known to cause only acute infection, there were reports that showed neurological sequelae, latent infection in peripheral mononuclear cells, and recurrence of the disease after acute encephalitis. Innate resistance of certain cell lines, abnormal SN1 expression of the virus, and anti-apoptotic effect of cullular bcl-2 have been suggested as probable causes of JEV persistence even in the absence of defective interfering (DI) particles. Although possible involvement of DI particles in JEV persistence was suggested, neither has a direct evidence for DI presence nor its molecular characterization been made. Two questions asked in this study are whether the DI virus plays any role in JEV persistent infection if it is associated with and what type of change(s) can be made in persistently infected cells to avoid apoptosis even with the continuous virus replication, DI-free standard stock of JEV was infected in BHK-21, Vero, and SW13 cells and serial high multiplicity passages were performed in order to generate DI particles. There different-sized DI RNA species which were defective in both structural and nonstructural protein coding genes. Rescued ORFs of the DI genome maintained in-frame and the presence of replicative intermediate or replicative form RNA of the DI particles confirmed their replication competence. On the other hand, several clones with JEV persistent infection were established from the cells survived acute infections during the passages. Timing of the DI virus generation during the passages seemed coincide to the appearance of persistently infected cells. The DI RNAs were identified in most of persistently infected cells and were observed throughout the cell maintenance. One of the cloned cell line maintained the viral persistence without DI RNA coreplication. The cells with viral persistence released the reduced but continuous infectious JEV particle for up to 9 months and were refractory to homologous virus superinfection but not to heterologous challenges. Unlike the cells with acute infection these cells were devoid of characteristic DNA fragmentation and JEV-induced apoptosis with or without homologous superinfection. Therefore, the DI RNA generated during JEV undiluted serial passage on mammalian cells was shown to be biologically active and it seemed to be responsible, at least in part, for the establishment and maintenance of the JEV persistence in mammalian cells. Viral persistence without DI RNA coreplication, as in one of the cell clones, supports that JEV persistent infection could be maintained with or without the presence of DI particles. In addition, the fact that the cells with JEV persistence were resistant against homologous virus superinfection, but not against heterologous one, suggests that different viruses have their own and independent pathway for cytopathogenesis even if viral cytopathic effect could be converged to an apoptosis after all.

• Korean Journal of Microbiology
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• v.38 no.3
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• pp.221-229
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• 2002

Japanese encephalitis virus (JEV) persistence was established and maintained in Vero cell culture for over 1 year. Eleven clones of plaque morphology mutant JEV, with large and small plaque sizes, were obtained from the cell culture supernatant. Genomic RNA replication efficiency of the mutants in naive Vero cell appeared to correspond to their different plaque sizes. No significant changes in envelop protein ORF or in non-coding regions at both ends of the RNA genome suggested that there could be an unidentified factor(s) playing role in JEV attenuation. Unlike to the replication of wild-type JEV, the mutants did not induce severe degree of cytopathic effect in Vero cells upon infection. While obvious decrease of Bcl-2 and its mRNA expression and sharp increase of p53 in naive Vero cells infected with either wild-type JEV or the large plaque-forming mutant, those changes were not observed with the small plaque-forming one. Together with these observation, internucleosomal DNA fragmentation and chromosomal DNA profile in the Vero cells infected with the mutants suggest that an overall changes in cytopathic effect in the plaque morphology mutants-infected cells should be primarily due to the reduced genomic RNA replication and the compromised degree of p53-independent apoptosis by the virus infection at least in part.