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At least 19 recordsLinked to original sources
PubMed2003

Antibody and interleukin-12 treatment in murine models of encephalitogenic flavivirus (St. Louis encephalitis, tick-borne encephalitis) and alphavirus (Venezuelan equine encephalitis) infection.

Early and sustained treatment with interleukin-12 (IL-12) ameliorated disease in a mouse model of infection with the encephalitogenic flavivirus, St. Louis encephalitis virus (SLEV, Japanese encephalitis serogroup). However, this effect was not reproduced in murine infections with either the flavivirus tick-bore encephalitis virus (TBEV) or the alphavirus Venezuelan equine encephalitis virus (VEEV). IL-12 exacerbated TBEV disease when used in conjunction with monoclonal antibody (mAb), suggesting an enhancement of immunopathology, and was without clinical effects in VEEV infection. These data confirm the need to fully understand the pathogenesis of viral infection before cytokine intervention may be employed as a broad-spectrum antiviral therapy.

Animals↗
PubMed1986

Comparison of proteins specified by Murray Valley encephalitis, West Nile, Japanese encephalitis and St. Louis encephalitis viruses.

The relationships among proteins specified by Murray Valley encephalitis (MVE), West Nile (WN), Japanese encephalitis (JE) and St. Louis encephalitis (SLE) viruses were examined by peptide mapping. [3H]methionine-labelled tryptic peptides of viral proteins were separated by reverse phase high performance liquid chromatography (HPLC) and the separation profiles for a given protein specified by the different viruses were compared. Analyses of the non-structural protein NV5 (P98 or NS5) suggested that WN and SLE were the most closely related pair of viruses, and that JE was the virus most distant from the other three. Analyses of the structural proteins C and E failed to show the close relationship between WN and SLE indicated by the NV5 results, but did suggest that NV5 was the most conserved and E the least conserved of the three proteins.

Encephalitis Viruses↗
PubMed2000

Immunisation with gamma globulin to murray valley encephalitis virus and with an inactivated Japanese encephalitis virus vaccine as prophylaxis against australian encephalitis: evaluation in a mouse model.

In northwestern Australia, the flavivirus Murray Valley encephalitis (MVE) poses a significant health risk to infants in some aboriginal communities, particularly during each wet season. While there are too few cases to warrant the development of a vaccine against MVE, a safe, effective prophylaxis for these children is still urgently required. The use of passive transfer of human gamma globulin to MVE or immunisation with a vaccine to the closely related Japanese encephalitis (JE) virus were investigated as potential strategies. When 40 microg of IgG was purified from MVE-immune human sera and transferred to 3-week-old mice, the animals were protected from lethal IP inoculation with MVE virus while still producing a detectable immune response to the virus. Similarly, sera from adult mice infected sublethally with MVE or JE virus provided significant protection against MVE infection. However, sera from mice sublethally infected with the related Kunjin or immunised with the inactivated JE vaccine (Biken) provided no protection against MVE challenge. In fact, mice immunised passively with the latter appeared to succumb to MVE challenge more rapidly than mice that received serum from unimmunised animals, suggesting that antibody to the vaccine had accelerated the progression of disease. These preliminary trials in mice indicate that passive immunisation with human gamma globulin has the greatest potential as a strategy for MVE prophylaxis, whilst the apparent enhancement of MVE by antibodies to the JE vaccine requires further investigation, with particular reference to current vaccination programs in areas of Australia and Papua New Guinea, where both JE and MVE occur.

Animals↗
PubMed2003

Clinical, radiological and neurophysiological spectrum of JEV encephalitis and other non-specific encephalitis during post-monsoon period in India.

AIMS: To study the spectrum of encephalitis during the post-monsoon period in a tertiary care centre of India. METHODS: Clinical, neurophysiological and radiological features of patients with encephalitis are reported in this communication. The patients were subjected to clinical examination, CT or MRI scan, EEG, motor and somatosensory evoked potentials in both upper and lower limbs bilaterally and concentric needle electromyography. The laboratory studies for Japanese encephalitis (JE) comprised virus isolated, IgM capture ELISA, mercaptoethanol test and hemagglutination inhibition titre in paired sera against JE virus. Patients were classified into JEV encephalitis and non-specific encephalitis. On the basis of radiological features, they were classified into group I (thalamic or basal ganglia involvement), group II (brainstem involvement only) and group III (normal MRI). The outcome was defined into poor (bedridden), partial (dependent for daily activities) and complete (independent) recovery at the end of 3 months. RESULTS: Out of 26 patients (Age 7-70 years, mean 24.8 years), laboratory evidences of JEV infection was present in 14 patients and one patient had herpes simplex encephalitis. The patients with JEV encephalitis had more severe illness as evidenced by lower GCS score, higher frequency of anterior horn cell involvement, movement disorders and more extensive MRI changes. The EEG and MEP changes were also more frequently abnormal in the JEV group. On radiology, 15 patients had thalamic or basal ganglia involvement (group I), 3 isolated midbrain involvement (group II) and 8 had normal MRI (group III). Laboratory evidence consistent with JE were present in 11 out of 12 patients in group I and 3 out of 8 in group III, however, there was no laboratory evidence of JE virus infection in patients with isolated brainstem involvement. There was overlap in the neurologic and systemic manifestations in all the 3 radiological groups as well as in the groups with and without laboratory evidences of JEV infection. CONCLUSION: The observed overlap in neurological and systemic involvement in different subgroups of encephalitis may be due to JE or JE-like viral infection. The possibility of strain variation, change in virulence of organism or immunity of host needs further studies.

Adolescent↗
PubMed1983

Primary viraemia responses of herons to experimental infection with Murray Valley encephalitis, Kunjin and Japanese encephalitis viruses.

Rufous night herons, Pacific herons, little egrets and intermediate egrets were experimentally infected with Murray Valley encephalitis, Kunjin or Japanese encephalitis viruses. Viraemias of at least one day's duration were detected in all birds except two intermediate egrets inoculated with a very low dose of Kunjin virus and one rufous night heron inoculated with Japanese encephalitis virus. there was usually a viraemia of 3 to 5 days' duration commencing on the first or second day and continuing until day 5 or 6 and rarely until day 7. Maximum titres tended to be higher in young birds, up to 2-5 months of age (10(4)-10(5) mouse LD50/ml), than in older birds more than 8 months of age (10(3)-10(4) mouse LD50/ml). Significant differences in maximum viraemia titres were not observed in the different species or between Murray Valley encephalitis and Kunjin viruses. Japanese encephalitis viraemias were significantly lower, but this was probably due to the high mouse brain passage level of the strain used. The onset of viraemia was earlier in intermediate egrets than in rufous night herons inoculated with similar doses of Murray Valley encephalitis virus, but no difference in the susceptibility to infection was observed. With Kunjin virus there was a significant difference in the susceptibility of intermediate egrets and rufous night herons, with rufous night herons being more susceptible to infection with low doses of virus. This difference in threshold of infection, if it extends to other species with both Kunjin and Murray Valley encephalitis viruses, may, in part, be an explanation for the greater incidence of natural infections observed in rufous night herons compared with other species and orders of water birds.

Animals↗
PubMed1995

Chronic encephalitis and epilepsy (Rasmussen's encephalitis): detection of cytomegalovirus and herpes simplex virus 1 by the polymerase chain reaction and in situ hybridization.

We made a pathologic diagnosis of chronic encephalitis on surgical resections or autopsy material in 10 patients with intractable seizures and studied the specimens by immunohistochemistry for herpes simplex virus (HSV) 1 and 2 and cytomegalovirus (CMV) as well as by the polymerase chain reaction (PCR) for viral DNA sequences (HSV1, HSV2, and CMV). We also assessed eight patients (nonepileptic) with pathologically documented or clinically suspected encephalitis and five resections from epileptics without encephalitis. Immunohistochemistry for viral antigens was negative in all cases. Using PCR assay, CMV was present in six and HSV1 in two of 10 epilepsy patients with chronic encephalitis. We demonstrated CMV by in situ hybridization in two of the six patients positive for CMV by PCR. We found no viral sequences by PCR in five epileptics without encephalitis. Of the eight patients (nonepileptic) with clinically suspected or pathologically confirmed encephalitis, two cases showed CMV sequences by PCR. These observations suggest that PCR allows detection of viral sequences in some cases of chronic encephalitis associated with epilepsy that may be missed by in situ hybridization.

Adolescent↗
PubMed2001

St. Louis Encephalitis and West Nile Virus Encephalitis.

St. Louis encephalitis virus is a major cause of epidemic arboviral encephalitis in the US. Transmitted by a mosquito vector, this virus is an annual public health concern during the late summer and early fall in much of the midwest and southeast. The characteristic epidemic features of this viral encephalitis coupled with public health surveillance and vector monitoring programs have made the diagnosis readily accessible during the past decade. Recently, however, the arboviral landscape in the US changed dramatically with the emergence and persistence of West Nile virus and associated human neurologic illness in New York and the Northeast. In its New York presentation, West Nile virus encephalitis exhibited clinical and laboratory similarities to St. Louis encephalitis. Not surprisingly, this led to initial confusion in establishing the diagnosis. In anticipation of the potential geographic spread of West Nile virus beyond the northeastern US, neurologists must now consider West Nile virus along with St. Louis encephalitis when diagnosing patients with suspected epidemic mosquito-borne viral encephalitis or meningoencephalitis. Although no specific antiviral agents are yet available, patients will benefit from close monitoring during the initial phase of illness, supportive critical care, and appropriate rehabilitation.

Journal Article↗
PubMed2000

Difference in pathogenesis between herpes simplex virus type 1 encephalitis and tick-borne encephalitis demonstrated by means of cerebrospinal fluid markers of glial and neuronal destruction.

We determined the extent of neuronal and glial cell destruction in 13 patients with herpes simplex type 1 (HSV-1) encephalitis, 15 patients with tick-borne encephalitis (TBE), and 20 noninfectious controls by analyzing the cerebrospinal fluid (CSF) concentrations of neurofilament protein (a marker of neurons, mainly axons), neuron-specific enolase (a marker of neurons, mainly somas), glial fibrillary acidic protein, and S-100 protein (markers of astrocytes). In addition, in patients with HSV-1 encephalitis CSF samples were collected serially before 7, 8-14, and 18-49 days and 3-10 months after the onset of neurological symptoms. In the acute stage of HSV-1 encephalitis we found markedly higher CSF levels of the cell damage markers than in patients with TBE. The concentration of cell damage markers in HSV-1 encephalitis decreased within 45 days after acute infection, except for neurofilament protein. The CSF concentrations of neurofilament protein increased during the second week, remained extremely high throughout the next month, and decrease thereafter. The changes in these markers of neuronal and glial destruction demonstrate the neuronal and astroglial cell damage during the first month after HSV-1 encephalitis. In contrast, most patients with TBE had signs only of slight astrogliosis, except for two patients with paresis.

Adult↗
PubMed1974

Cross-protection between group B arboviruses: resistance in mice to Japanese B encephalitis and St. Louis encephalitis viruses induced by Dengue virus immunization.

Albino Swiss mice, immunized with any of several types and strains of dengue viruses, were afforded substantial protection against peripheral Japanese B encephalitis or St. Louis encephalitis virus challenge. Dengue-2 (New Guinea "C")-immunized mice showed, 10 and 20 weeks after immunization, undiminished resistance with concomitant cyclophosphamide treatment and virus challenge. Examination of the effects of immunization on Japanese B encephalitis virus pathogenesis, after virus challenge with concomitant cyclophosphamide treatment, indicated that protection was associated with decreased viremia and virtually no virus replication in the brain as compared with controls. These effects could be demonstrated before detection of any neutralizing antibody to the challenge virus. From the applied aspect, the data support the hypothesis, based on epidemiological evidence and experiments in hamsters, that prior exposure of man to dengue viruses can confer some degree of protection against Japanese B encephalitis or St. Louis encephalitis disease.

Animals↗
PubMed1995

Japanese encephalitis virus is an important cause of encephalitis among children in Penang.

This study was carried out to determine if Japanese encephalitis virus is an important causative agent of viral encephalitis among pediatric admissions in Penang, Malaysia. 195 children with CNS symptoms and 482 children with non-specific febrile illness admitted into the Pediatric Ward of Penang Hospital during a 16 month period were entered into the study. The presence in serum of cerebrospinal fluid (csf) of Japanese encephalitis virus (JEV) specific IgM was determined by an IgM capture ELISA and cytomegalovirus (CMV) specific IgM was determined using a commercially available kit (Behringwerke AG). It was determined that 5 of 13 children with a discharge diagnosis of viral encephalitis had JEV specific IgM in csf, indicating that 38.5% of the viral encephalitis cases was due to JEV. One of the non-JEV cases was found to have mumps virus specific IgM in csf, while no etiology was determined for the other cases. It was also determined that 4 of the 195 (2.1%) cases with CNS symptoms had IgM to CMV, suggesting CMV may be an agent of encephalopathy in children in Penang. Other viruses found to be associated with CNS symptoms in children admitted into our study were measles and herpes simplex virus. A viral etiology was confirmed for 13 or the 195 cases (6.7%). We also screened 482 non-specific febrile cases for IgM to JEV and to dengue viruses and found that 2 (0.4%) had IgM specific for JEV and 9 (1.9%) had IgM specific for dengue virus.

Antibodies, Viral↗
PubMedDate not supplied

Computed tomographic findings in acute viral encephalitis in adults with emphasis on herpes simplex encephalitis.

Nine patients with acute viral encephalitis were diagnosed by CT. Seven had herpes simplex and two had nonherpetic acute viral encephalitis. All patients with herpes simplex encephalitis initially were febrile. They developed confusion and seizures. Five had focal neurological deficit and two had papilledema. The CT scan showed an abnormality on the initial CT in 6 of 7 cases. In one case initial CT study was normal; however follow-up scan (performed 5 days later) showed a definite abnormality. CT showed the characteristic pattern of herpes simplex encephalitis in all cases. This is a temporal lobe hypodense lesion (unilateral, 5 cases; bilateral, 2 cases) with a small interspersed hyperdense region. The hyperdense component represents hemorrhage. Mass effect was seen in all cases. Two patients showed enhancement which was diffuse or patchy in one case and cisternal-gyral in the other; however enhancement was absent in 5 cases. One patient showed progression of the size of the hypodense lesion despite antiviral treatment. Follow-up CT showed hypodense lesion(s) in the temporal lobe region with enlargement of the temporal horns and contiguous basal cisterns in 4 cases. In 2 other cases of acute viral encephalitis the patients initially developed fever, confusion and seizures. CT showed basal ganglia calcification or hypodense lesions.

Acute Disease↗
PubMedDate not supplied

Diffusion MRI in Rasmussen's encephalitis, herpes simplex encephalitis, and bacterial meningoencephalitis.

Three patients with Rasmussen's encephalitis, herpes simplex type 1 encephalitis, and bacterial meningoencephalitis are included in this study. Echo-planar diffusion MRI was acquired with the trace protocol at 1.5 T. b= 1000 s/mm(2) images, and apparent diffusion coefficient (ADC) maps were studied with respect to lesion identification. ADC values were also studied, and compared to those of 25 normals. In Rasmussen's encephalitis b= 1000 s/mm(2) images were uninformative while ADC maps had superior information. In herpes simplex type 1 encephalitis both b= 1000 s/mm(2) images, and ADC maps had diagnostic information. In meningoencephalitis b= 1000 s/mm(2) images had superior information, especially with respect to early cerebritis while ADC maps were negative. In conclusion, diffusion MRI provided useful imaging data on different types of encephalitis, either on b= 1000 s/mm(2) images or on ADC maps, or on both.

Adolescent↗