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At least 19 recordsLinked to original sources
PubMed1992

Epidemiology and control of Japanese encephalitis.

Japanese encephalitis (JE) remains endemo-epidemic in several countries in East, South-East and South Asia. The disease has been under control in Japan since the 1970s owing to mass immunization using mouse-brain-derived inactivated vaccine and to reduced vector mosquito populations. The vector density which was once reduced by wide spraying of insecticides in rice fields showed an increasing trend after the 1980s as a result of mosquito resistance. In the Republic of Korea, the number of JE cases showed a significant decrease after 1983 also because of mass immunization using mouse-brain-derived vaccine. On the other hand, large outbreaks of JE continued to occur in China, Viet Nam, Thailand, India, Nepal and Sri Lanka. In China, a hamster-kidney cell-derived vaccine was developed and used for human immunization. Besides human JE, the fatal outcome of equine JE is an economic problem in China. Current JE vaccine derived from mouse brain is highly purified and its safety and efficacy have been proved by field-tests as well as laboratory experiments. In spite of slight antigenic differences among JE virus isolates, JE vaccine produced by a classical Nakayama strain was effective in preventing overt JE in a field study in Thailand. The technology of mouse-brain-derived inactivated JE vaccine production was transferred from Japan to India, Thailand and Viet Nam. The production of JE vaccine in these countries is still on a pilot scale and insufficient for mass-immunization of susceptible target populations.(ABSTRACT TRUNCATED AT 250 WORDS)

Encephalitis Virus, Japanese↗
PubMed1992

Effect of high-dose dexamethasone on the outcome of acute encephalitis due to Japanese encephalitis virus.

Death due to Japanese encephalitis usually occurs in the first 5 days of hospitalization as a result of deepening coma with respiratory arrest. Death may result from edema-induced increases in intracranial pressure that might be reduced by the administration of steroids. Sixty-five patients presenting in Thailand to four hospitals with a diagnosis of acute Japanese encephalitis were randomized in a double-masked fashion and stratified by initial mental status into a placebo group (saline) or a treatment group (dexamethasone 0.6 mg/kg intravenously as a loading dose followed by 0.2 mg/kg every 6 h for 5 days). Fifty-five of the 65 had confirmed Japanese encephalitis as demonstrated by detection of virus or by Japanese encephalitis virus-specific IgM antibody. Important outcome measures included mortality (24%, treatment group; 27%, control group), days to alert mental status (3.9 vs. 6.2), and neurologic status 3 months after discharge (45% abnormal in each group). No statistically significant benefit of high-dose dexamethasone could be detected.

Acute Disease↗
PubMed1975

Virion and soluble antigens of japanese encephalitis virus.

Japanese encephalitis virions contain a 58 X 10-3-molecular-weight envelope glycoprotein antigen that can be solubilized with sodium lauryl sulfate and separated from other virion structural polypeptides and viral ribonucleic acid by gel filtration chromatography. The 58 X 10-3-molecular-weight envelope protein is the major antigen responsible for cross-reactivity of the virion in complement fixation tests with other closely related arboviruses. A naturally occurring soluble complement-fixing antigen is found in Japanese encephalitis mouse brain preparations after removal of particulate antigens. After partial purification by gel filtration and isoelectric focusing, the 53 X 10-3-molecular weight soluble complement-fixing antigen is more type specific than the Japanese encephalitis envelope antigen in complement fixation tests. Further, the Japanese encephalitis soluble complement-fixing antigen is stable to treatment with sodium lauryl sulfate and 2-mercaptoethanol, whereas virion complement-fixing antigens are unstable after this treatment.

Amino Acids↗
PubMed1977

Intracellular distribution of virus-specific RNA in chick embryo cells infected with Japanese encephalitis virus.

Japanese encephalitis virus (JEV) infected chick embryo (CE) cells were treated with 4 mug actinomycin D/ml and 5 mM-D-glucosamine at 2 or 3 h before harvesting. Production of JEV was not affected by the short-time treatment of these drugs. The radioactivity in virus-specific RNA in the glucosamine-treated cells was a-parently higher than in non-treated cells. Nuclear and cytoplasmic extracts were prepared from the JEV-infected cells pulse-labelled with 3H-uridine at 15 h after infection. Analysis of virus RNA in nuclear extracts on sucrose density gradients showed that most of the radioactivity was in 23S RNA, 26S RNA and 8 to 12S RNA. The radioactivity of virus RNA in cytoplasmic extracts was found in 42S RNA and RNA fragments sedimenting at less than 8S.

Animals↗
PubMedDate not supplied

Japanese encephalitis surveillance in China (Province of Taiwan) during 1968-1971. II. Age-secific incidence in connection with Japanese encephalitis vaccination program.

A baseline age/morbidity pattern for Japanese encephalitis (JE) epidemic in China (Province of Taiwan) in the 1960s was sought in JE surveillance. The pattern is characterized by: (1) high incidence in age groups 2-4 years, (2) moderately high incidence in age groups 5-7 years, (3) negligible incidence in children under 1 year of age as well as in adults, and (4) the variability of relative height of peak incidence co-incident with the JE-epidemic size in situ. Concurrently with surveillance, a JE-vaccination program was implemented by the Government. The children of target age groups received two doses of vaccine each during April. Vigilant supervision was given to the campaign to achieve a high coverage rate with two-dose vaccination and meticulous record-keeping. During 1969-1972, 2-year olds were the exclusive target; 52.2% (1969), 71.5% (1970), 74.5% (1971), and 83.0% (1972) of the target age group were covered. A considerable change from the baseline age/morbidity pattern seen in 1968 occurred during the above period. The comparison of epidemicity-adjusted incidence by year indications that incidence reduction in the 2- and 3-year old children in 1971 were substantial and suggests the possible impact of vaccination. The total JE incidence for the period 1968-1971 appears to be much lower in vaccinated population (23 reported and 8 confirmed/0.9 million) than in unvaccinated population (1,330 reported and 679 confirmed/2.2 million).

Age Factors↗
PubMed2025

Proteome Profiling in Cerebrospinal Fluid Reveals Increased Levels of Peroxiredoxin 2 Discriminating Japanese Encephalitis Virus and Scrub Typhus Infection.

Japanese encephalitis virus (JEV) and scrub typhus (ST) are major etiological agents of acute encephalitis syndrome (AES) in India and South Asia. The pathophysiological changes at the molecular level caused by JEV and ST have yet to be studied in detail. The cerebrospinal fluid (CSF) proteomic landscape is a critical indicator of CNS pathology. Here, we conducted label-free quantitative proteomics on CSF from AES patients (n = 15) to identify etiology-specific differentially expressed proteins (DEPs) linked to encephalitis. The key DEPs were validated via ELISA in CSF (n = 49) and serum (n = 33). Our findings revealed 50 proteins exhibited differential expression across JEV and ST groups, with a notable subset of three proteins, PRDX2, KLK6, and TTR. PRDX2 and KLK6 were markedly elevated in JEV CSF (AUC: 0.8933 and 0.9689) but not in ST or non-JEV AES, while TTR was reduced in JEV yet elevated in ST (AUC: 0.5619 vs. 0.8238). Further, PRDX2 upregulation was validated in JEV-infected mouse brains and cortical neurons. Overexpression of PRDX2 in human neuroblastoma cells correlated with enhanced antiviral gene expression, p-STAT1, p-AKT (ser473), and viral replication. Thus, our comprehensive proteomic analysis of CSF identifies PRDX2 as an important circulatory protein, differentially expressed between JEV and ST, with high specificity and enhancing viral propagation, underscoring its role in viral propagation and pathogenesis.

Humans↗
PubMed1992

Study of the outbreak of Japanese encephalitis in Lakhimpur district of Assam in 1989.

An outbreak of Japanese encephalitis was reported from Lakhimpur district of Assam in July-August, 1989. The outbreak affected 90 villages of the district, covering a population of approximately 36,000. There were 140 cases and 70 deaths due to the epidemic, giving a case fatality rate of 50%. There were no cases from Gogamukh area of the district, where a pilot Japanese encephalitis vaccination project was conducted in the population between July-August 1987, with Kasauli Japanese encephalitis vaccine. Serological examination of acute and convalescent cases showed Japanese encephalitis specific IgM indicating strong evidence of recent Japanese encephalitis infection.

Disease Outbreaks↗
PubMed2026

Bergamottin, a bioactive component of bergamot: dual inhibition of Japanese encephalitis virus internalization and genome replication.

Japanese encephalitis virus (JEV) is associated with high mortality and severe neurological sequelae, and existing prevention and control strategies remain insufficient. Therefore, the development of novel antiviral agents is of critical public health importance. This study systematically evaluated the antiviral activity and underlying mechanism of bergamottin, a natural product. Bergamottin exhibited significant dose-dependent inhibitory effects against JEV in multiple cell lines, including BHK-21, HuH-7, and Vero cells, demonstrating potent antiviral efficacy. Mechanistic investigations revealed that bergamottin primarily targeted the internalization and replication stages of the JEV life cycle, thereby effectively suppressing viral proliferation. Additionally, adaptive mutation screening indicated that the D389G mutation in envelope protein E confers drug resistance by potentially changing E protein conformation or reducing endocytic efficiency. In vivo experiment, bergamottin significantly reduced viral loads in mouse brain tissue and effectively improved the survival rate of infected mice. Our findings indicated that bergamottin exerted antiviral activity by dual targeting of key steps in the viral life cycle, making it a highly promising candidate for anti-JEV therapy. Further exploration of the antiviral properties of bergamottin is expected to facilitate its clinical development as a treatment for JEV infection.

Animals↗
PubMed1992

Use of the computed tomographic scan in Japanese encephalitis.

Fourteen children with laboratory-confirmed Japanese encephalitis were given cranial computed tomographic (CT) scans six to 30 days after the onset of illness. The findings were variable; there was a generalized decrease in attenuation values, three patients showed features of cerebral atrophy, and four others had normal scans. The findings appeared to relate to both the severity and the stage of the illness at the time the scans were made. CT would appear to be of little use in making a specific diagnosis of Japanese encephalitis.

Brain↗
PubMed1977

Experimental double infection of Japanese encephalitis virus and herpes simplex virus in mouse brain.

In our laboratory, 64 autopsy cases of Japanese encephalitis patients were examined by immunofluorescence. Three patients showed some evidences of double infection of Japanese encephalitis virus and herpes simplex virus. Experiments were done to see the mechanisms of double infection. In doubly infected mice, Japanese encephalitis virus antigen was localized in the herpes simplex virus infected areas in the brain. These results suggested that "blood brain barrier" was broken by herpes simplex virus infection and Japanese encephalitis virus gained access to the susceptible cells.

Animals↗
PubMed1978

An epidemiological review of Japanese encephalitis.

Twenty-five years ago, Japanese encephalitis (JE) was known as an endemic, mosquito-borne disease in East Asia. Today, the causative virus is known to be distributed from maritime Siberia to the north, eastern India to the west, the Archipelago of Japan presumably the Philippines to the east, and from Indonesia to the south. Since the late-1960s, the geopathological status of JE epidemics has undergone considerable changes. The sizes of JE epidemics in Japan and China (Province of Taiwan) have steadily declined. In fact the JE virus itself appears to be disappearing from Japan. Long-term prediction of JE epidemics is more difficult for Korean Peninsula, nevertheless, reported JE morbidity rate in the Republic of Korea has remained at a relatively low level since 1969. In contrast to the trend in East Asia, new epidemic foci of JE have been emerging in the northern part of Tropical Eastern South Asia starting in 1969. Of particular importance are the continued high incidence (annual morbidity rate: 8.67-22.04/100 000) of reported JE in the northern part of Viet Nam between 1969 and 1974, and the high incidence (14.7/100 000) recorded in Chiang Mai Valley, Thailand, between 1969 and 1970. Apparently, the epidemic in Chiang Mai Valley spread to the neighbouring Shan State of Burma in 1974. Another JE epidemic broke out in West Bengal State, India in 1973. The occurrence of JE in the endemic zone south of these areas has remained sporadic. An increasing number of pathogens have been shown to cause signs and symptoms clinically indistinguishable from JE. In this review, the quality and international comparability of available JE statistics are also examined. Only a few countries and areas with reasonably developed statistical and laboratory services are able to provide national JE statistics in a form ready for epidemiological analysis. A practical surveillance system for JE needs to be organized in those countries where JE is a newly emerging health problem.

Asia↗
PubMed1976

Persistence of virus-specific IgM and clinical recovery after Japanese encephalitis.

We have searched for evidence of a chronic Japanese encephalitis virus (JEV) infection in six Thai patients convalescing from acute Japanese encephalitis (JE) in whom JEV-specific IgM antibody was last detected 116 to 350 days after their acute illness. These six patients were compared with 94 other JE patients matched for age, sex and serological response and in whom JEV-specific IgM was either short-lived (less than 90 days) or not tested. All patients were evaluated for the presence or absence of seven abnormal neurological signs over a 1- to 2-year period. During the first 30 days of illness the mean numbers (+/- S.E.M.) of abnormal signs per patients for the IgM and control groups were 3.8 +/- 0.3 and 2.3 +/- 0.1, respectively (P less than 0.01). After 1 year the six IgM patients still had significantly more abnormal neurological signs than controls (1.3 +/- 0.3 and 0.6 +/- 0.1, respectively [P less than 0.01]). By 2 years, the IgM group showed no neurological impairment; examination of cerebrospinal fluids revealed no evidence of subclinical viral infections. The recovery of the six IgM patients between 1 and 2 years after their relatively severe acute illness suggests that IgM antibody persistence was related to acute virulence rather than chronicity of the JEV infection.

Encephalitis, Japanese↗
PubMed1978

Field experiments on live attenuated Japanese encephalitis virus vaccine for swine.

The efficacy of a live attenuated Japanese encephalitis virus (JEV) vaccine was examined in swine under conditions where natural infection could occur. The pigs immunized with the vaccine produced antibodies within one week after vaccination, and the antibody was retained until the end of the experiment, i.e. 36 days. However, the antibody titers in this group were lower than that in control group naturally infected with JEV. No virus was isolated from the five vaccinated pigs, but virus was isolated from all four untreated control pigs after natural infection, i.e., viremia was detected in all these animals. The duration of viremia in control pigs varied from one to four days. From these findings, it is concluded that immunization of swine with live attentuated JEV vaccine is useful in control of Japanese encephalitis (JE) in humans and some susceptible domestic animals.

Animals↗
PubMed1975

Natural and experimental infections of Japanese tree sparrows with Japanese encephalitis virus.

20 to 37 per cent of wild Japanese tree sparrows had neutralizing antibodies to Japanese encephalitis virus (JEV). Sparrows free of antibodies were inoculated with 10,000 plaque-forming units of JEV. None of the birds became clinically ill. Virus could be detected in blood plasma during the first 3 days after inoculation but not thereafter. Neutralizing antibodies started to appear at 4 days after inoculation and the response was of variable duration, in some cases extending up to 200 days after inoculation.

Animals↗
PubMed1992

Two-way cross-protection between West Nile and Japanese encephalitis viruses in bonnet macaques.

Cross-protection between Japanese encephalitis (JE) and West Nile (WN) viruses was tested in bonnet macaques (Macaca radiata) immunized either with JE virus (JEV) or WN virus (WNV). JEV immunized monkeys were challenged by intranasal (i.n.) route with WNV and vice versa. Four control unimmunized monkeys were similarly infected either with WNV or JEV. Two of three control monkeys infected with WNV, developed paralysis followed by death. Virus was recovered from the central nervous system (CNS) of the both dead control monkeys and the histopathological examination of CNS revealed changes suggestive of viral encephalitis. The control monkey infected with JEV developed encephalitis and the virus was recovered from the blood and CNS. All the 3 JEV-immunized monkeys withstood WNV challenge, whereas only 2 of the 5 WNV immunized monkeys withstood the challenge with JEV. Out of 3 WNV-immunized monkeys surviving challenge with JEV, 2 revealed symptoms suggestive of mild encephalitis followed by complete recovery. The third monkey died on the 60th day post-infection (p.i.) without any symptoms and virus was recovered only from the olfactory lobe. These studies indicate that the immunization with JEV protects the bonnet macaques against WNV, whereas the WNV immunization only reduces the severity of the disease due to JEV.

Animals↗
PubMed1975

Immunization of pigs with the attenuated S- strain of Japanese encephalitis virus.

The attenuated S- strain of Japanese encephalitis virus was produced from a wild strain of this virus by serial cultivation in primary bovine kidney cell cultures at 30 degrees C. Pigs were inoculated with it and examined for ability to produce antibody and protect themselves from infection with a wild strain used for challenge. In pigs inoculated with a single dose of 10(6.5) approximately 10(7.5) TCID50 of the S- strain, the neutralizing antibody titer or hemagglutination-inhibiting antibody (HI) titer increased to 10 approximately 320. An antibody titer exceeding 10 was maintained for 2 approximately 9 weeks. In pigs inoculated twice with 10(6.5) approximately 10(7.0) TCID50 of the S- strain, HI titer increased to 80 approximately 640. In many of these pigs, HI titers of 80 approximately 160 persisted for more than 6 weeks. Pigs inoculated once or twice with 10(7.0) approximately 10(7.5) TCID50 of the S- strain were challenged by inoculation with 10(4.5) approximately 10(5.5) TCID50 of a wild strain and examined for the occurrence of viremia. As a result, an ability to protect from infection was demonstrated in pigs which showed an antibody titer surpassing 10 at the time of challenge. Pregnant sows inoculated with 10(7.0) TCID50 of the S- strain were challenged by inoculation with 10(7.0) TCID50 of a wild strain. Neither death nor infection occurred to any fetus harbored by them. From these results, it is concluded that the S- strain can be used as live virus vaccine for porcine practice.

Animals↗