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PubMed2005

History of U.S. military contributions to the study of viral encephalitis.

The viral encephalitides represent 15% (9 of 62) of the infectious diseases identified by the Armed Forces Medical Intelligence Center as being of U.S. military operational importance. Japanese encephalitis, tick-borne encephalitis, Venezuelan equine encephalitis, Eastern equine encephalitis, Western equine encephalitis, West Nile fever, rabies, St. Louis encephalitis, and Murray Valley (Australian) encephalitis are included on the Armed Forces Medical Intelligence Center threat list. This article reviews the U.S. military contributions to the prevention and control of the first seven of these.

Biomedical Research↗
PubMed1996

Cytomegalovirus encephalitis.

PURPOSE: To review the pathologic and clinical features of and establish the frequency of cytomegalovirus encephalitis in adults and to review the methods available for diagnosis and treatment. DATA SOURCE: MEDLINE search of all English-language articles from January 1965 to August 1995. STUDY SELECTION: Articles dealing with cytomegalovirus infection of the brain in adults. We also reviewed all unselected autopsies of these populations to establish the frequency of cytomegalovirus encephalitis in recipients of organ transplants and in patients infected with the human immunodeficiency virus (HIV). DATA EXTRACTION: Epidemiologic and pathologic characteristics, clinical manifestations, diagnostic methods, pathogenetic mechanisms, and use of anticytomegalovirus treatments. DATA SYNTHESIS: Of 676 patients receiving a diagnosis of cytomegalovirus encephalitis, 574 (85%) were infected with HIV, 81 (12%) had other causes of immunosuppression, and 21 (3%) were otherwise healthy. Cytomegalovirus encephalitis was confirmed during autopsy in 12% of HIV-infected patients and 2% of transplant recipients. The most common lesion was microglial nodule encephalitis, but the clinical findings corresponding to this pathologic entity are not well defined. In contrast, the pathologic entity of cytomegalovirus ventriculoencephalitis, found almost exclusively in patients with advanced HIV infection, has distinct clinical features that allow recognition even in patients with HIV encephalopathy. Polymerase chain reaction has been shown to be useful for diagnosis of cytomegalovirus encephalitis. CONCLUSIONS: Cytomegalovirus encephalitis is an important opportunistic infection in HIV-infected patients but is rarely recognized in other groups. Cytomegalovirus ventriculoencephalitis has emerged as a unique entity in patients with advanced HIV infection. Recent developments in diagnostic techniques allow early recognition and may make more aggressive approaches to therapy possible.

Antiviral Agents↗
PubMedDate not supplied

[Partial non convulsive epileptic status as initial presentation of limbic encephalitis].

INTRODUCTION: Limbic encephalitis is an unusual presentation of paraneoplastic syndrome, which includes among its symptoms seizures. CLINICAL CASE: We report a case with a rare presentation of limbic encephalitis as initial symptom of small cell lung carcinoma. A 69 year-old woman presented with partial non convulsive status epilepticus and neuropsychiatric disturbances. Chest radiography and computed tomography showed mediastinal lymphadenopathy and lung nodules. Subsequently, small cell lung carcinoma was diagnosed by lymph node biopsy. The cerebrospinal fluid study was normal. The electroencephalography and magnetic resonance imaging (MRI) findings had distinctive features compatible with temporo-limbic dysfunction. The anti-Hu antibodies were negative. The neuropsychiatric symptoms improved significantly after systemic chemotherapy and adjuvant radiotherapy. A serial follow-up MRI of the head showed no evidence of intracranial metastasis three months after the diagnosis of cancer. Limbic encephalitis may be an initial manifestation of lung cancer. Paraneoplastic limbic encephalitis is considered a remote effect of cancer commonly associated with anti-neuronal antibodies (anti-Hu) and small cell lung carcinoma. CONCLUSIONS: Status epilepticus could be an early sign of limbic encephalitis. The absence of anti-Hu antibodies does not rule out the presence of an underlying small cell lung carcinoma in patients with a clinical diagnosis of limbic encephalitis. Greater awareness for diagnosis and early treatment of the primary tumor offers the best chance for improvement in patients with lung cancer presenting with limbic encephalitis.

Aged↗
PubMed2002

[Viral encephalitis caused by biowarfare agents].

Many viruses may cause encephalitis. Three such viruses of the Alpha genus (Venezuelan equine encephalitis (VEE), Western equine encephalitis (WEE) and Eastern equine encephalitis (EEE)) may be used as biological warfare agents. The clinical course of the diseases caused by these viruses is not specific, and resembles a broad range of bacterial and viral diseases. Several attenuated and inactivated vaccines were developed, but their efficacy in the biological warfare scenario is questionable. There is no effective drug therapy for the treatment of these diseases, and treatment is mainly supportive. Several VEE outbreaks were reported in humans and horses in South America and southern United States. This virus usually causes a febrile illness, which might be complicated with encephalitis, mainly in the cases of children and elderly patients. The EEE virus causes the most severe form of disease, with severe encephalitis and high proportion of sequel. It is prevalent mainly in the eastern parts of Northern America. The WEE virus, which is hybridization between the Sindbis virus and the EEE virus, causes encephalitis mainly in children. The severity of the disease caused by WEE and the sequel rate is much lower than that of EEE.

Biological Warfare↗
PubMed2006

Previous infection with West Nile or St. Louis encephalitis viruses provides cross protection during reinfection in house finches.

House finches are competent hosts for both West Nile and St. Louis encephalitis viruses and frequently become infected during outbreaks. In the current study, House finches were infected initially with either West Nile or St. Louis encephalitis viruses and then challenged 6 weeks post infection with either homologous or heterologous viruses. Although mortality rates were high during initial infection with West Nile virus, prior infection with either virus prevented mortality upon challenge with West Nile virus. Prior infection with West Nile virus provided sterilizing immunity against both viruses, whereas prior infection with St. Louis encephalitis virus prevented viremia from St. Louis encephalitis virus, but only reduced West Nile virus viremia titers. Immunologic responses were measured by enzyme immunoassay and plaque reduction neutralization tests. Heterologous challenge with West Nile virus in birds previously infected with St. Louis encephalitis virus produced the greatest immunologic response, markedly boosting antibody levels against St. Louis encephalitis virus. Our data have broad implications for free-ranging avian serological diagnostics and possibly for the recent disappearance of St. Louis encephalitis virus from California.

Animals↗
PubMed1991

A gene(s) within the H-2D region determines the development of toxoplasmic encephalitis in mice.

Studies were performed in a murine model to determine if there is genetic control of the development of toxoplasmic encephalitis. Ten weeks after infection with the ME49 strain of Toxoplasma gondii, mice with the H-2b haplotype (C57BL/6, C57BL/10) and H-2k haplotype (C3H/He, CBA/J) developed remarkable inflammatory changes in their brains, whereas mice with the H-2a haplotype (A/J) and H-2d haplotype (BALB/c, DBA/2) did not. In the area of acute focal inflammation in mice with the H-2b and H-2k haplotypes, tachyzoites and toxoplasma antigens were demonstrated by immunoperoxidase staining, suggesting that the focal inflammation was induced by toxoplasma organisms. B10 congenic mice were used for further analysis of this genetic regulation. Presence of the encephalitis in B10 and B10.BR but not in B10.A and B10.D2 mice at 10 weeks after infection indicated regulation of the inflammation by a gene(s) within the H-2 complex. The encephalitis developed in B10.A (2R) and B10.A (4R) mice but not in B10.A (3R) and B10.A (18R) during infection. These results clearly indicated that the development of toxoplasmic encephalitis was controlled by a gene(s) in the H-2D region. The Qa and Tla genes did not appear to be critical in determining susceptibility to the encephalitis. There was no correlation between serum toxoplasma antibody titres and occurrence of the encephalitis. Injection of a monoclonal antibody to interferon-gamma (IFN-gamma) remarkably augmented the inflammatory changes in the brains of the infected B10 mice. In contrast, the treatment did not induce any inflammatory response in the brains of the infected BALB/c mice. A similar genetic regulation may be operative in determining development of toxoplasmic encephalitis in AIDS and other immunocompromised patients.

Animals↗
PubMed1994

[Encephalitis in adults].

Encephalitis is the result of focal or global inflammation of the brain caused by invasion of the brain parenchyma by viruses, bacteria, parasites or fungi. In addition, postinfectious encephalitis may result from immunological processes as a consequence of preceding viral infections such as measles. For most forms of viral encephalitis no specific therapy is available. Herpes simplex encephalitis may be diagnosed using modern laboratory techniques for detection of viral DNA without the need for brain biopsy. Herpes simplex encephalitis responds well to treatment with acyclovir, as does encephalitis caused by varicella-zoster virus, which typically occurs following cutaneous herpes zoster involving dermatomal distributions of the trigeminal nerve. In immunocompromised hosts many etiologies of encephalitis need to be considered. It is important to arrive at a precise diagnosis in order to choose appropriate therapeutic agents directed toward treatable pathogens such as Toxoplasma gondii and cytomegalovirus.

Adult↗
PubMed1997

Magnetization transfer study of HIV encephalitis and progressive multifocal leukoencephalopathy. Groupe d'Epidémiologie Clinique du SIDA en Aquitaine.

PURPOSE: To ascertain whether the use of magnetization transfer (MT) in MR imaging can characterize tissue destruction in human immunodeficiency virus (HIV)-positive patients with presumed progressive multifocal leukoencephalopathy (PML) or HIV encephalitis. METHODS: Brain MR studies that included MT were obtained in three groups: 11 healthy control subjects, 10 HIV-positive patients with clinical and radiologic findings of PML, and 13 HIV-positive patients with HIV encephalitis. MT ratios (MTRs) were calculated in PML and HIV encephalitis lesions and in normal-appearing white matter in the patients and control subjects. RESULTS: PML lesions revealed a dramatic decrease in MTR (22% +/- 2.3). HIV encephalitis lesions had statistically significantly higher MTR values (40% +/- 3.8) than PML lesions. The MTR of normal-appearing white matter was significantly higher in the control subjects (47% +/- 2.3) than in the PML group (46% +/- 3.3) or the HIV encephalitis group (44% +/- 2.6). CONCLUSION: MTR determinations suggest the possibility of distinguishing PML from HIV encephalitis and of indicating whether HIV encephalitis is involved in white matter that appears normal on conventional MR images.

Adult↗
PubMed1984

Serologic evidence for widespread infection with La Crosse and St. Louis encephalitis viruses in the Indiana human population.

The vast under-reporting of La Crosse virus and St. Louis encephalitis virus infections in Indiana residents was evident when numerous inapparent infections were detected retrospectively using serum dilution neutralization analyses of serum obtained in November 1978-April 1979 from 10,208 persons (0.2% of the state's population). An antibody prevalence rate of 3.6% to St. Louis encephalitis virus was detected in the sample population as a whole, with rates as high as 13.2% for residents of individual counties. The estimated average annual rate of infection for the whole population was 0.32%. The antibody prevalence to La Crosse virus in the sample population as a whole was 2.3%, with rates ranging up to 12.5% for residents of individual counties. The estimated average annual rate of infection for the whole population was 0.29%. The epidemiologic behavior of the two viruses was quite different. Age-specific antibody prevalence for St. Louis encephalitis virus indicated a pattern of endemic infection existed in the population as a whole; antibody prevalence rose as the population aged. However, many other infections apparently occurred during the 1975 and earlier epidemics. Age-specific antibody prevalence for La Crosse virus indicated a typical pattern of endemic infection was present. The antibody prevalence to La Crosse virus was best described by the Poisson distribution and that of St. Louis encephalitis virus by the negative binomial distribution. These data support the hypothesis that St. Louis encephalitis virus primarily produces intermittent epidemics in the Midwest while La Crosse virus produces continuous seasonal endemic infections. However, evidence suggestive of a low level of interepidemic St. Louis encephalitis virus infection in the population was also obtained. Computer-drawn synagraphic mapping view "maps" of regional antibody prevalence rates demonstrated the existence of distinct foci of infection for each virus in the human population.

Adolescent↗
PubMed1999

Active HIV-1 redistribution and replication in the brain with HIV encephalitis.

The central nervous system (CNS) is of particular importance in human immunodeficiency virus type 1 (HIV-1) infection. First, the CNS may be difficult to access for anti-retroviral treatment and may become a sanctuary for residual viruses. Second, HIV-1 infection may lead to AIDS dementia complex (ADC) culminating in HIV-1 encephalitis. In order to examine the pattern of drug resistance and the role of encephalitis in enhancing viral redistribution to the CNS, we compared pol gene quasispecies of the spleen and brain in two patients with and two patients without HIV-1 encephalitis, who had been treated with zidovudine (AZT). Although a variable degree of AZT resistance was noted in both the spleen and brain of all patients, phylogenetic analysis indicated that quasispecies developed rather independently in the systemic circulation (spleen) and CNS (brain) of patients without HIV-1 encephalitis, while similar pol gene sequences were obtained from the two compartments of patients with HIV-1 encephalitis. env gene V3 region of patients with HIV-1 encephalitis showed distinct quasispecies in the spleen and brain. Our results suggest that HIV-1 redistribution to CNS is more active in cases with encephalitis and that HIV-1 distributed late to CNS grow actively under certain selective pressure exerted on the V3 region of the env gene.

AIDS Dementia Complex↗
PubMed1986

Partial nucleotide sequence of the Murray Valley encephalitis virus genome. Comparison of the encoded polypeptides with yellow fever virus structural and non-structural proteins.

The sequence of 5400 bases corresponding to the 5'-terminal half of the Murray Valley encephalitis virus genome has been determined. The genome contains a 5' non-coding region of about 97 nucleotides, followed by a single continuous open reading frame that encodes the structural proteins followed by the non-structural proteins. Amino acid sequence homology between the Murray Valley encephalitis and yellow fever (Rice et al., 1985) polyproteins is 42% over the region sequenced. The start points of the various Murray Valley encephalitis virus-coded proteins have been assigned on the basis of this homology and a consistent set of potential proteolytic cleavage sites identified, the sequences of which are similar in Murray Valley encephalitis and yellow fever. The deduced Murray Valley encephalitis gene order is 5'-C-prM (M)-E-NS1-ns2a-ns2b-NS3-3'. The genome organization of Murray Valley encephalitis and yellow fever appears to be identical and the sizes of the predicted virus-coded proteins similar between the two viruses. Both viruses encode a basic capsid protein followed by three glycoproteins; the glycoproteins appear to have the conventional topology of N terminus outside with a C-terminal membrane-spanning domain. There are conserved glycosylation sites in prM, the precursor to the M protein of the virion, and in NS1, a non-structural protein of uncertain function. The glycosylation sites in E, the major envelope protein of the virion, are not conserved as to position. We predict the existence, in flavivirus-infected cells, of two small, hydrophobic peptides, ns2a and ns2b, which show only limited amino acid sequence homology. Finally, about half of the amino acid sequence of NS3 has been obtained; NS3 is a hydrophilic non-structural protein that shows 55% amino acid sequence similarity between Murray Valley encephalitis and yellow fever over the region sequenced and is probably involved in RNA replication.

Amino Acid Sequence↗
PubMedDate not supplied

Difference between herpes simplex virus type 1 and type 2 neonatal encephalitis in neurological outcome.

24 infants consecutively treated with acyclovir or vidarabine for neonatal herpes simplex virus (HSV) encephalitis were followed up for 6 months to 3 years to assess neurological and developmental outcome. 15 patients had HSV-2 and 9 had HSV-1 encephalitis. Infants with HSV-2 encephalitis presented with a higher frequency of seizures, greater pleocytosis and protein concentrations in the cerebrospinal fluid, and more frequent evidence of structural damage on computerised tomographic scans of the brain than did those with HSV-1 encephalitis. 1 patient died. All 9 HSV-1 patients were normal at follow-up (mean 19.4 months) compared with only 4 (23%) of the 14 surviving HSV-2 infected infants (p = 0.003). Among infants with HSV-2 encephalitis, 50% became microcephalic; 57% had seizure disorders; 64% had ophthalmological defects; 64% had cerebral palsy; and 57% had mental retardation. Infants with neonatal HSV-1 encephalitis treated with systemic antiviral chemotherapy have excellent neurological outcomes; the neurological morbidity of those with HSV-2 encephalitis is still high.

Acyclovir↗
PubMed2004

On the evolutionary significance of encephalization in some eutherian mammals: effects of adaptive radiation, domestication, and feralization.

Allometries of the brain to body size relationship in eutherian mammals are examined in this study as they can be used for comparative analyses concerning encephalization. In contrast with some modern presentations of this issue, an older concept is revived and expanded through this author's current study. Three allometries with clearly different slopes are valid and lead to reliable results: interspecific, intraspecific, and ontogenetic allometries. Interspecific allometries follow lines with slope values of 0.56 or 0.63 for larger and smaller species, respectively, and characterize different average encephalization plateaus with rodents and lagomorphs generally more strongly encephalized compared to basal insectivores. Artiodactyls, perissodactyls and carnivores as a whole are again on a higher but rather similar plateau. Several species of carnivores have reached different encephalization levels with respect to their average plateau indicating diverse radiations. A phylogenetic brain size increase from fossil to recent radiations is also evident. Intraspecific allometries have slope values of about 0.25. These are of help in comparing brain sizes of ancestral species with their domesticated relatives. Domestication has generally led to a brain size decrease, but species on higher encephalization plateaus show this trend more strongly than species on a lower level of encephalization. Several brain parts and the sense organs also decrease in size during the domestication process, but vary arbitrarily and to different degrees. Ontogenetic growth allometries are species-specific, but are especially different between altricial and precocial mammals. A very steep 1st phase slope of highly encephalized species is particularly useful for understanding evolutionary and adaptive phenomena. Domesticated mammals that have become feral do not show an increase in brain size despite living many generations in wild habitats.

Adaptation, Physiological↗
PubMed1989

Encephalization in tropical teleost fishes and comparison with their mode of life.

The brains were dissected from a total of 1225 fishes representing 737 species, 310 genera and 113 families of tropical and subtropical teleosts. Each fish was weighed before brain dissection, and each brain weighed after its removal. The encephalization coefficient k was determined for each fish from a quadratic formula; to conveniently compare brain size of one species with that of another, we used an encephalization index so that an encephalization index of 100 is the average for all the species investigated. The encephalization indices for the families of fishes studied varied from 7 for the Moringuidae to 233 for the Coryphaenidae. There is no strong correlation in relative brain size with phylogenetic position. Although there is a general trend for the more highly evolved fishes to have larger brains, this is partially obscured by some high values in certain primitive groups and low ones in the more advanced. Elongate fishes have lower encephalization indices in general. This may in part be related to low phylogenetic position of most elongate species (anguilliform fishes, for example), in part to the greater relative body weight due to the longer vertebral column (and usually more numerous fin rays as as well), and to their usual mode of swimming by lateral undulations of the body (the most primitive type of aquatic locomotion--one in which the spinal cord plays a major role). No difference could be noted in the encephalization indices of herbivorous families of fishes compared to carnivorous ones. Within a genus, among medium to large-size fishes, those species of larger size tend to have lower encephalization indices. This may be related to larger fishes having less to fear of predators. Fishes which in some passive way avoid predation have low indices in general. This is particularly true of benthic species which conceal themselves by flattened form, fleshy protuberances or protective coloration, or which bury in the sediment or take refuge in burrows. Also correlated with low indices is some form of predator deterence such as production of skin toxins, presence of venomous spines or ability to enlarge the body by inflation. Fishes which have more than a single sense highly developed exhibit a larger relative brain size than those with only one well developed sense. Fishes which live in a complex community of high species diversity, such as a coral reef, have higher indices, in general, than those which dwell on mud and sand flat. Pelagic fishes, such as scombrids and carangids, are among those with the highest indices.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Viral encephalitis.

Acute viral encephalitis may be caused by a wide range of viruses but the most important is herpes simplex encephalitis (HSE) because of its severity, especially if untreated, and its good response to specific treatment with acyclovir. The outcome of any CNS viral infection is dependent on both the immune status of the host and the virulence of the infecting virus. In evaluating a patient with suspected viral encephalitis there are 3 essential steps, namely the identification of a true parenchymal virus infection of the brain rather than a non-infective encephalopathy, the distinction of an infectious viral encephalitis from an acute disseminated encephalomyelitis (ADEM), and then the determination, where possible, of the specific virus involved. In practice, the precise viral cause of the encephalitis may never be established. Analysis of the CSF for herpes simplex virus (HSV) DNA using the Polymerase Chain Reaction (PCR) has been a significant advance in the diagnosis of HSE as this test has a very high sensitivity and specificity especially with appropriate sample timing. It is essential to commence early treatment with intravenous acyclovir in patients suspected of having HSE because of the remarkable safety and efficacy of this drug and the dangers of delaying potentially effective treatment of life threatening disease. This review outlines the general management approach in patients suspected of having viral encephalitis.

Encephalitis, Herpes Simplex↗
PubMed2025

Diagnostic and phylogenetic perspectives of the 2023 Murray Valley encephalitis virus outbreak in Australia: an observational study.

BACKGROUND: An outbreak of Murray Valley encephalitis virus (MVEV), the largest since 1974, was observed in Australia between Jan 1 and July 31, 2023. This study aims to characterise the utility of diagnostic platforms, testing algorithms, and genomic characteristics of MVEV to facilitate a comprehensive framework for MVEV testing and surveillance in the outbreak setting. METHODS: In this observational study, we assessed flavivirus diagnostics for all patients with suspected Murray Valley encephalitis in Australia from Jan 1 to July 31, 2023. We included all patients with confirmed Murray Valley encephalitis, probable Murray Valley encephalitis, or acute unspecified flavivirus infection using the Communicable Diseases Network Australia case definition. Cases were excluded if an alternative diagnosis was identified. We collected blood, serum, cerebrospinal fluid, brain tissue, urine, or a combination of these samples, as appropriate and at the discretion of the treating clinician. We conducted multimodal diagnostic testing, which included flavivirus-specific serological and nucleic acid amplification testing. Metagenomic next-generation sequencing, including next-generation deep sequencing, target-enrichment, and targeted amplification, was conducted on human and representative mosquito-derived samples obtained from established mosquito population surveillance programmes for phylogenetic analysis. FINDINGS: 27 patients with encephalitis were assessed for MVEV between Jan 1, 2023, and July 31, 2023, 23 (85%) of whom fulfilled national case definitions for confirmed Murray Valley encephalitis. Patient ages ranged from 6 weeks to 83 years (median 62·0 years [IQR 31·0-67·5]) and patients were mostly male (21 [78%] male patients and six [22%] female patients). Incidence varied widely by geographical region and was highest in the Northern Territory (32·0 per 1 000 000 population). Diagnostic specimen collection generally occurred promptly (median 6·0 days [IQR 4·0-14·5] from symptom onset to diagnostic specimen collection). In seven patients, case assignation relied on convalescent serum samples to assess for seroconversion or an appropriate rise in antibody titre (to four times the initial value or greater), or both. MVEV-specific IgM was detectable in serum samples of 17 (81%) of 21 patients tested by day 7 and MVEV IgG or total antibody (TAb) were detected in 18 (100%) of 18 patients tested by day 30. MVEV-specific IgM (or TAb) and MVEV RNA were detected in cerebrospinal fluid collected within 14 days of symptom onset in nine (39%) of 23 patients and seven (28%) of 25 patients, respectively. Phylogenetic analysis revealed two circulating MVEV genotypes, G1A and G2, in mosquitoes and humans in 2023. In southeast Australia, only G1A was detected and probably introduced from enzootic foci in northern Australia. INTERPRETATION: This study provides a comprehensive overview of the diagnostic workflows and phylogenetic evaluations used during the 2023 MVEV outbreak in Australia, emphasising the importance of a multimodal approach for accurate and timely confirmation of flavivirus infection. Further One Health surveillance for MVEV and other zoonotic flaviviruses is key, given potential expanded ecological niches in the context of episodic climatic events. FUNDING: None.

Humans↗
PubMed2001

A recombinant particulate antigen of Japanese encephalitis virus produced in stably-transformed cells is an effective noninfectious antigen and subunit immunogen.

A COS-1 cell line, stably transformed by a plasmid encoding the premembrane and envelope glycoproteins of Japanese encephalitis virus, produced a noninfectious recombinant antigen expressed as extracellular particles. Extracellular particles purified by equilibrium density centrifugation in sucrose gradients followed by electron microscopy were characterized as spherical particles with an average diameter of approximately 30 nm and a buoyant density of 1.15 g/cc. Purified extracellular particles were shown by western blot to contain premembrane, membrane and envelope proteins. The gradient-purified particles exhibited hemagglutination activity at the same pH optimum (6.6) as Japanese encephalitis virus. Recombinant antigen from cell culture fluid was concentrated by precipitation with polyethylene glycol and evaluated for immunogenicity in 8-10-week-old ICR mice. Groups of five mice received only one immunization of recombinant antigen with or without Freund's incomplete adjuvant. Mice immunized with recombinant antigen plus Freund's incomplete adjuvant elicited the highest anti-viral titers as determined by both enzyme-linked immunosorbent assay (ELISA) and plaque-reduction neutralization tests. The polyethylene glycol-concentrated recombinant antigen was also evaluated for use in IgM antibody-capture ELISA and indirect IgG ELISA. The IgM-capture ELISA results using recombinant antigen correlated well with the results of a similar test using Japanese encephalitis virus-infected mouse brain antigen for the analysis of serum samples from patients with symptoms of acute encephalitis. Similar IgG titers were observed in an indirect ELISA comparing recombinant antigen and purified Japanese encephalitis virus as plate-bound antigens. Based on these studies, this entirely safe, easily produced antigen that expresses authentic Japanese encephalitis virus envelope glycoprotein would provide an excellent alternative to standard viral antigens used in various ELISA formats.

Animals↗
PubMed1998

Australian encephalitis in the Northern Territory: clinical and epidemiological features, 1987-1996.

BACKGROUND: The last epidemic of Australian encephalitis occurred in 1974. Since then, cases have been reported from the Kimberley of Western Australia (WA). AIMS: To describe the epidemiology and clinical features of Australian encephalitis in the Northern Territory (NT) of Australia. METHODS: Review of cases of Australian encephalitis presenting to Royal Darwin Hospital from 1987-1996 and review of sentinel chicken surveillance for Australian encephalitis viruses. RESULTS: Sixteen patients were identified; ten from the NT and six from WA. Cases occurred in the years 1987, 1988, 1991 and 1993. Infection was acquired throughout northern NT below latitude 20 degrees S in the months March to July. All infections were due to Murray Valley encephalitis (MVE) virus. Eleven of the patients were children. Distinguishing features were spinal cord and brainstem involvement and the absence of seizures in adults. CT scanning was normal and EEG showed no focal activity. Five died (31%) and four (25%) have residual neurological disability. Sentinel chicken surveillance since 1992 shows yearly seroconversion to MVE virus throughout northern NT; human cases occurred simultaneously with chicken seroconversion in 1993. CONCLUSIONS: Australian encephalitis is endemic in the NT; the areas at risk are north of Tennant Creek. Outbreaks are seasonal and occur every few years. Young children are most at risk. Mortality and morbidity are high. Prevention of disease is by avoidance of mosquito exposure and vector control measures.

Adult↗