• IMMUNE NETWORK
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• v.12 no.2
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• pp.48-57
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• 2012

Acute viral encephalitis caused by neurotrophic viruses, such as mosquito-borne flaviviruses, is an emerging and re-emerging disease that represents an immense global health problem. Considerable progression has been made in understanding the pathogenesis of acute viral encephalitis, but the immune-pathological processes occurring during the progression of encephalitis and the roles played by various molecules and cellular components of the innate and adaptive systems still remain undefined. Recent findings reveal the significant contribution of Toll-like receptors (TLRs) and regulatory $CD4^+$ T cells in the outcomes of infectious diseases caused by neurotrophic viruses. In this review, we discuss the ample evidence focused on the roles of TLRs and $CD4^+$ helper T cell subsets on the progression of acute viral encephalitis. Finally, we draw attention to the importance of these molecules and cellular components in defining the pathogenesis of acute viral encephalitis, thereby providing new therapeutic avenues for this disease.

• The Journal of Pediatrics of Korean Medicine
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• v.16 no.1
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• pp.9-19
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• 2002

Viral Encephalitis are a serious meningeal infection occurred by various chemical substance. Chief symptoms are headache. hyperesthesia in child and fretting. irritation in infant. Adolescence complain of a retrobulbar pain, fever, vomiturition, photophobia. Fever can cause choreic movement, mental disorder and seizure. Most of patients have complete recovery, but if there are brain lesions, it is bad prognosis. Occasionally patients complain of continuous headache, mental disorder, ataxia and marasmus. We report on a 4-year-old male patient with viral encephalitis. It has been 40 days since disease. He had disorientation mentality, dysphagia and fever.

• The Journal of the Korean Society for Microbiology
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• v.16 no.1
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• pp.83-89
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• 1981

Japanese encephalitis has been prevalent for long time in the Far East and many patients have been reported in both South East and Mid-West Asia recently. Recently, vaccine was used in prevention of this viral disease of man which was derived from formalin inactivated virus inoculated into mouse brain, but live attenuated active vaccine for human is not developed yet. Author inoculated Japanese encephalitis virus into several cell culture strains for development of live attenuated encephalitis virus strain and the results were as follows: 1. Japanese encephalitis virus was inactivated rapidly in cell free medium at $36^{\circ}C$ and totally inactivated by 72 hours. 2. In growth curve of Japanese encephalitis virus in HeLa cell cultures, maximal multiplication of the virus was occured at 4th day and virus multiplication was continued for at least 12 days. 3. After succeeding passage of the virus in HeLa cell cultures and human esophagus epithelial cell cultures, infectivity of virus for mice was disappeared from 2nd passage in HeLa cell cultures and 3rd passage in esophagus epithelial cell cultures. 4. In inoculation to monkey kidney epithelial cells and chick embryo cell cultures, infectivity of the virus for mice was continued after 10th passages.

• The Journal of Korean Society of Virology
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• v.27 no.2
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• pp.209-216
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• 1997

Three dimensional structures of envelope protein from Korean isolates and Nakayama-NIH strain of Japanese encephalitis virus (JEV) were deduced by a computer program (HyperChem 4.0 Chemplus 1.0) based on the data of the three dimentional structure of Tick-borne encephalitis virus. In the three dimensional structure of envelope protein, neutralizing epitope and T-helper cell recognition site of C-terminal region of Korean isolates were structually similar to those of Nakayama-NIH but the N-terminal region was not. Korean JE isolates were compared with Nakayama-NIH strain by using cross-neutralization antibody test. Neutralizing activities of Korean isolates derived from guinea pigs were higher than those of Nakayama-NIH strain against Korean isolates, although the polyclonal antibody titers of Nakayama-NlH showed 1:160 to 1:640 against Korean isolates. According to the results from three dimentional structures and cross-neutralization analyses, the antigenic difference between Korean JE isolates and Nakayama-NIH strain may be dependent on structural difference of envelope protein.

• Annals of Clinical Neurophysiology
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• v.16 no.1
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• pp.35-38
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• 2014

Japanese-B viral encephalitis (JE) usually has a monophasic illness pattern. A 45-year-old woman in an altered mentality had improved over 1 month. About 1 week after the initial improvement, the patient became comatose with aggravated EEG and MRI findings. Assays of cerebrospinal fluid and serum were positive for the IgM antibody to Japanese-B virus. After intravenous immunoglobulin (IVIG) infusion, the patient recovered. We report a patient with JE who showed a biphasic illness pattern and recovered after IVIG therapy.

• The Journal of the Korean Society for Microbiology
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• v.3 no.1
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• pp.51-65
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• 1968

The site of the synthesis of Japanese encephalitis virus(JEV) in the actinomycin-treated and infecter PS Y15 cells(a porcine kidney stable cell line) was observed by the immunofluorescent antibody technique, acridine orange staining, and the autoradiographic analysis. In the parallel studies by immunofluorescent technique and acridine orange staining it the infected cells, Viral protein(as an antigen) and viral RNA were detected at the same site of cytoplasm. In the autoradiographic analysis, the cytoplasmic labeling of $^3H$-uridine was due to the synthesis of JEV-RNA, while the nucleolus and nucleus were not involved. In the autoradiographic studies on the secton of infected cells, the $^3H$-uridine was frequently incorporated around the cytoplasmic vacuoles. This localization of labeling agreed with the site of acridine orange positive granules. The results suggest that the syntheses of the viral RNA and viral protein occurred in the similar site of cytoplasm of the infected cells, and also the virus particles seem to be assembled in the sites of the viral RNA and protein syntheses.

• Korean Journal of Veterinary Research
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• v.62 no.3
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• pp.19.1-19.6
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• 2022

Japanese encephalitis virus (JEV) and Akabane virus (AKAV) are mosquito-borne viruses that cause encephalitis and reproductive disorders in horses and cattle, respectively. There is no treatment for JEV or AKAV infections in animals. Therefore, we evaluated the antiviral activity of 18-mer amphipathic peptides in the 1b-4/21-C series on JEV and AKAV using Vero cells in vitro and evaluated their effects on JEV in mice. Of 6 peptides, 1b-4/21-C12 had the lowest IC₅₀ of 0.313 against JEV and its use as an antiviral against JEV and AKAV was examined. The IC₅₀ of 1b-4/21-C12 against JEV and AKAV was 0.78 and 1.14 µM, respectively. Mice treated with 5 or 2 mg/kg of 1b-4/21-C12 had 32% and 16% survival rates, respectively, and the surviving mice treated with 1b-4/21-C12 began to gain weight beginning 8 days post challenge with the virulent Nakayama strain. Moreover, 20 µM 1b-4/21-C peptide had no cytotoxic effects on Vero cells. Our in vitro and in vivo results indicate that 1b-4/21-C12 has antiviral activity against enveloped JEV and AKAV and might be useful as a therapeutic substance.

• Journal of the korean veterinary medical association
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• v.16 no.8_10
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• pp.297-303
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• 1980

Neuropathological properties of viral diseases affecting the nervous system in swine are described and discussed for the differential diagnosis of the diseases. The virus associated with Viral encephalitis. in swine can be classified into two categories;

• Korean Journal of Veterinary Research
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• v.57 no.1
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• pp.31-36
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• 2017

Japanese encephalitis (JE) is an important zoonosis caused by the mosquito-transmitted JE virus (JEV), which is a causative agent of reproductive failure in pregnant sows. Detection of JEV antibodies in swine is performed by hemagglutination inhibition (HI), virus neutralization (VN), and the plaque reduction neutralization test (PRNT). The most stringent PRNT is the 90% endpoint PRNT ($PRNT_{90}$). These conventional assays are difficult to carry out in diagnostic laboratories with insufficient instruments or cell culture systems. An alternative assay that is easily conducted and time efficient is required. In this study, we improved the indirect enzyme-linked immunosorbent assay (I-ELISA) with clarified antigen for the detection of JEV antibodies. The I-ELISA results obtained from 175 swine serum samples were compared with HI, VN, and $PRNT_{90}$ results. The sensitivity of I-ELISA was 91.8%, 95.0%, and 94.7% compared with HI, VN, and $PRNT_{90}$ results, respectively. The specificity of I-ELISA was 92.2%, 94.7%, and 94.7% compared with HI, VN, and $PRNT_{90}$ results, respectively. Moreover, the I-ELISA results were significantly correlated with the HI (r = 0.93), VN (r = 0.95), and $PRNT_{90}$ (r = 0.92) results. These results suggest that the improved I-ELISA is useful for serosurveillance of JEV in swine.

• 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.