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PubMed1970

Experimental encephalitis following peripheral inoculation of West Nile virus in mice of different ages.

Experimental arbovirus infections of mice provide a convenient model to study factors which determine the occurrence or severity of encephalitis following extraneural infection with certain neurotropic viruses. Varying doses of West Nile or Powassan viruses were inoculated by intraperitoneal or intramuscular routes into mice of varing ages; individual variables were manipulated to influence the outcome of infection. Three patterns of pathogenesis were delineated: (1) Fatal encephalitis, preceded by early viraemia, and invasion of the central nervous system. (2) Inapparent infection, with no detectable viraemia and no evidence of central nervous system invasion. (3) Subclinical encephalitis, usually preceded by trace viraemia, with minimal transient levels of virus in the brain. In this latter type of subclinical infection with a potentially lethal virus, the immune response probably plays an important role in recovery.

Animals↗
PubMed2001

Acute encephalitis from 1967 to 1991.

We studied all the adult patients with acute encephalitis, 322 in all, in the Helsinki area, Finland, during the years 1967--1991. The average incidence was 1.4/100000 adults/year. The proportion of known and suggested etiologies in 5-year periods has risen from 36 (1967--71) to 59% (1987--91). Herpes simplex virus was identified most often (16%), followed by varicella-zoster (5%), mumps (4%), and influenza A viruses (4%). In addition, 20 other agents were identified. The leading cause of encephalitis in patients aged 65 years or more was varicella-zoster virus. Eighteen patients (5.6%) died. It appears that the etiology of encephalitis changes with age and with time. It is important to establish the etiological pattern, as this assists in prompt diagnosis, which is a prerequisite for successful therapy.

Adolescent↗
PubMed2003

Cross-protective and infection-enhancing immunity in mice vaccinated against flaviviruses belonging to the Japanese encephalitis virus serocomplex.

The Japanese encephalitis virus serocomplex is a group of mosquito-borne flaviviruses that cause severe encephalitic disease in humans. The recent emergence of several members of this serocomplex in geographic regions where other closely related flaviviruses are endemic has raised urgent human health issues. Thus, the impact of vaccination against one of these neurotropic virus on the outcome of infection with a second, serologically related virus is unknown. We show here that immunity against Murray Valley encephalitis virus in vaccinated mice can cross-protect but also augment disease severity following challenge with Japanese encephalitis virus. Immunepotentiation of heterologous flavivirus disease was apparent in animals immunized with a 'killed' virus preparation when humoral antiviral immunity of low magnitude was elicited.

Adjuvants, Immunologic↗
PubMed2003

Development of a recombinant vaccine against Japanese encephalitis.

Japanese encephalitis (JE) is the major form of viral encephalitis in much of the South-East Asia, India, and China. The disease is caused by a mosquito-borne virus known as Japanese encephalitis virus (JEV). The virus spreads in the form of epidemics, although several endemic areas for JEV activity are known. In recent years, JEV has spread to newer geographic locations such as Australia and Pakistan, and thus has become an important emerging virus infection in these areas. A mouse brain-derived, formalin-inactivated vaccine is available for immunization against JE. Because the formalin-inactivated JEV vaccine has limitations in terms of safety, availability, and cost, attempts are being made to develop improved vaccine using the recombinant DNA technology. This article reviews various attempts in this direction and summarizes the latest developments such as the recombinant yellow fever virus- or the plasmid DNA-based JEV vaccine.

Encephalitis Virus, Japanese↗
PubMed1964

THE PATHOGENESIS OF HERPES VIRUS ENCEPHALITIS. II. A CELLULAR BASIS FOR THE DEVELOPMENT OF RESISTANCE WITH AGE.

The resistance to herpes virus encephalitis which develops with age was studied in mice using fluorescent antibody staining. Adult mice remained susceptible to intracerebral inoculation, and the infection of the central nervous system was identical with that found in immature mice. A "barrier" to the spread of virus inoculated extraneurally developed with maturation, and the limitation of spread appeared to coincide with the infection of peritoneal and tissue macrophages. In vitro, suckling and adult mouse macrophages were infected with equal ease. However, suckling mouse macrophages infected other cells in contact with them, while infected adult mouse macrophages did not. Studies failed to reveal the nature of this change in macrophages which developed with age. The role of macrophages in the pathogenesis of herpes virus encephalitis is discussed. The hypothesis is made that an alteration in the macrophages of the maturing mouse plays an important role in its development of resistance to herpes virus encephalitis.

Aging↗
PubMed2000

Construction and characterization of monoclonal antibodies against western equine encephalitis virus.

A repertoire of mouse monoclonal antibodies (MAbs) against western equine encephalitis virus (WEE) was constructed and characterized. Anti-WEE antibodies were expressed from hybridomas and purified by protein G chromatography. Each of the antibodies was functionally assessed by indirect enzyme-linked immunosorbent assays (ELISAs), Western blotting, and immunoprecipitations. All antibodies bound to WEE antigen in ELISAs, whereas only a subgroup of antibodies was found to be active in Western blotting and immunoprecipitations. A subset of antibodies was found to cross-react with other alphaviruses, such as Sindbis virus (SIN), Venezuelan equine encephalitis (VEE), and eastern equine encephalitis (EEE). Because many of the antibodies were highly reactive to WEE antigen in one or more of the assays, these antibodies are excellent candidates for immunodetection and immunotherapy studies.

Animals↗
PubMed1976

California arbovirus (La Crosse) infections. III. Epidemiology of California encephalitis in Minnesota.

Mosquitoes (eggs, larvae, and adults), small woodland animals, and residents of an area where California encephalitis is endemic were studied to elucidate the host-vector cycle of La Crosse virus. Elementary schoolchildren from surrounding communities and gray squirrels from another area were tested to compare the prevelence of serum antibodies to La Crosse virus in areas where the disease is endemic with the prevalence of these antibodies in areas where the disease is not endemic. From 1971 to 1974, eight isolations of La Crosse virus were made. Three of the isolates were from adult mosquitoes, one from Aedes triseriatus eggs, and four from A. triseriatus larvae. The isolation of virus from field-collected eggs and larvae confirms previous studies from Wisconsin that suggest that La Crosse virus overwinters in eggs of the mosquite A. triseriatus. In an area where California encephalitis is endemic, 10 of 19 small woodland animals (53%), which are the natural hosts of A. triseriatus, had hemagglutination-inhibiting and neutralizing antibodies to La Crosse virus. In contrast, none of 10 squirrels from an area where the disease is not endemic had such antibodies. Fourteen of 79 residents of this area (17.7%) had both types of antibody. Eleven of the 14 seropositive residents lived in one small sector of the community studied, an indication that foci of La Crosse virus activity may be very localized. Elementary schoolchildren from surrounding communitites had a significantly lower prevalence of hemagglutination-inhibiting antibody to La Crosse virus than did the residents of the area where California encephalitis was endemic.

Adult↗
PubMed1975

Arbovirus vector ecology studies in Mexico during the 1972 Venezuelan equine encephalitis outbreak.

Virus vector studies were conducted in the States of Durango, Chihuahua, and Tamaulipas, Mexico, in June and July 1972. Apparently only a low level of Venzuelan equine encephalitis (VEE) virus transmission to equines occured at the time of the study, and the infection was restricted to areas which had not experienced overt activity during the preceding year. The low level of infection was associated with a scarcity of mosquitoes. The IB (epidemic) strain of VEE virus was isolated from two pools of Anopheles pseudopunctipennis (Theo.) and the blood of one symptomatic equine. The low mosquito population, the relatively few equine cases observed, and the absence of reports of VEE human disease from the outbreak area suggested VEE virus persistence through a low-level mosquito-equine transmission cycle. Other studies have already indicated that wild vertebrates play no more than a minor role in outbreaks of epidemic VEE. Mosquito collections made in areas of the states of Durango, Chihuahua, and Tamaulipas, where considerable epidemic activity of VEE had occurred in 1971, failed to reveal evidence of VEE virus persistence. Twenty-nine ioslations of other arboviruses were also made in these studies: including 22 of St. Louis encephalitis virus (SLE), 2 of Flanders virus, 1 of Turlock virus, 1 of Trivittatus virus of the California Group, 1 of western equine encephalitis virus (VEE), and 2 (from Santa Rose) which possibly represent a hitherto unknown virus in the Bunyamwera Group. These are the first reports of SLE virus isolations from mosquitoes in Mexico, and the first demonstration of Trivittatus, VEE Turlock and Flanders viruses in Mexico from any source.

Animals↗
PubMed1986

Antigenic comparison of envelope protein E between Japanese encephalitis virus and some other flaviviruses using monoclonal antibodies.

The antigenic relationships between Japanese encephalitis (JE) virus and several other flaviviruses have been investigated using anti-JE virus monoclonal antibodies (MAbs). Seventeen MAbs directed against envelope protein E of JE virus were characterized and divided into eight MAb groups based on reactivity patterns in haemagglutination inhibition test, neutralization (N) test, ELISA and competitive binding assay with JE virus. The results suggest the existence of at least eight epitopes on the E protein of JE viruses. Analysis of cross-reactivity of the antibodies with several other flaviviruses indicated these findings JE virus, belonging to West Nile (WN) subgroup, is antigenically closely related to viruses in the same subgroup, i.e. Murray Valley encephalitis (MVE), WN and St. Louis encephalitis (SLE) viruses. Of these three viruses, JE virus has the closest relationship with MVE virus. WN virus is relatively close to JE virus, whereas SLE virus is the least closely related. Dengue viruses types 1 and 2, which belong to another subgroup of flaviviruses, show markedly less antigenic homology to JE virus. One of the critical N sites on the E protein showed JE virus specificity. Some cross-reactive antibodies which did not neutralize JE virus showed low but significant N activity against several other flaviviruses. Mixtures of several MAbs, which showed different reactivity patterns, potentiated the N activity against not only JE virus but also other members of the WN subgroup of flaviviruses, namely MVE, WN and SLE viruses.

Antibodies, Monoclonal↗
PubMed1980

Carbon dioxide sensitivity of mosquitoes infected with California encephalitis virus.

Four species of mosquitoes became sensitive to carbon dioxide approximately 3 to 4 days after they received intrathoracic injectins of California encephalitis virus. Aedes melanimon and Aedes dorsalis infected orally with California encephalitis virus also became carbon dioxide-sensitive, but mosquitoes infected transovarially did not. Sensitivity to carbon dioxide was inhibited by antiserum to California encephalitis virus. To our knowledge this is the first report of carbon dioxide sensitivity induced in arthropods by a bunyavirus and the first demonstration of this phenomenon by an arbovirus in its proven vector.

Aedes↗
PubMed2001

Molecular basis for attenuation of neurovirulence of a yellow fever Virus/Japanese encephalitis virus chimera vaccine (ChimeriVax-JE).

A yellow fever virus (YFV)/Japanese encephalitis virus (JEV) chimera in which the structural proteins prM and E of YFV 17D are replaced with those of the JEV SA14-14-2 vaccine strain is under evaluation as a candidate vaccine against Japanese encephalitis. The chimera (YFV/JEV SA14-14-2, or ChimeriVax-JE) is less neurovirulent than is YFV 17D vaccine in mouse and nonhuman primate models (F. Guirakhoo et al., Virology 257:363-372, 1999; T. P. Monath et al., Vaccine 17:1869-1882, 1999). Attenuation depends on the presence of the JEV SA14-14-2 E protein, as shown by the high neurovirulence of an analogous YFV/JEV Nakayama chimera derived from the wild JEV Nakayama strain (T. J. Chambers, A. Nestorowicz, P. W. Mason, and C. M. Rice, J. Virol. 73:3095-3101, 1999). Ten amino acid differences exist between the E proteins of ChimeriVax-JE and the YFV/JEV Nakayama virus, four of which are predicted to be neurovirulence determinants based on various sequence comparisons. To identify residues that are involved in attenuation, a series of intratypic YFV/JEV chimeras containing either single or multiple amino acid substitutions were engineered and tested for mouse neurovirulence. Reversions in at least three distinct clusters were required to restore the neurovirulence typical of the YFV/JEV Nakayama virus. Different combinations of cluster-specific reversions could confer neurovirulence; however, residue 138 of the E protein (E(138)) exhibited a dominant effect. No single amino acid reversion produced a phenotype significantly different from that of the ChimeriVax-JE parent. Together with the known genetic stability of the virus during prolonged cell culture and mouse brain passage, these findings support the candidacy of this experimental vaccine as a novel live-attenuated viral vaccine against Japanese encephalitis.

Amino Acid Sequence↗
PubMed2006

Japanese encephalitis: development of new candidate vaccines.

Japanese encephalitis (JE) is the most common form of viral encephalitis that appears in the form of frequent epidemics of brain fever throughout Southeast Asia, China and India. The disease is caused by a Flavivirus named Japanese encephalitis virus that is spread to humans by mosquitoes. An internationally approved mouse brain-derived inactivated vaccine has been available that is relatively expensive, gives immunity of uncertain duration and is not completely safe. Cell culture-derived inactivated and attenuated JE vaccines are in use in China, but these are not produced as per the norms acceptable in most countries. Several new promising JE vaccine candidates have been developed, some of which are under different stages of clinical evaluation. These new candidate JE vaccines have the potential to generate long-lasting immunity at low cost.

Animals↗
PubMed2026

Protein Profiling Identifies Biomarkers for Predicting Disease Severity in Anti-NMDAR Encephalitis.

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe autoimmune neurological disorder characterized by pathogenic antibodies against the NMDAR. A systematic protein profiling approach is warranted to identify biomarkers capable of predicting disease status. An Olink proximity extension assay (PEA) profiled 91 inflammation-related proteins from anti-NMDAR encephalitis patients. Disease severity or prognosis were assessed by CASE score or mRS score at 6-month follow-up. Patients were stratified into distinct molecular clusters using unsupervised clustering. Logistic regression models incorporating selected biomarkers were developed to predict disease severity and prognosis, followed by absolute quantification using ELISA. Patients were classified into four consensus clusters. Clusters 1 and 2 corresponded to the mild group, while Cluster 3 represented the severe group, consistent with CASE score above 6. Cluster 4 showed heterogeneous clinical features. Elevated serum levels of IL-10, IL-6, and SIRT2, as well as increased CSF levels of CXCL10, CXCL11, and MMP10, were positively associated with severe disease. Conversely, several proteins including LTA and CCL11, CCL8, TGFB1, CXCL6 were associated with severe disease or unfavorable 6-month outcomes. A logistic regression model combining serum CXCL6 and CCL11 with CSF MMP10 achieved an area under the curve (AUC) of 0.95 for predicting disease severity. Serum CCL11 alone showed predictive value for 6-month prognosis, with an AUC of 0.79. These findings delineate distinct protein signatures associated with clinical heterogeneity of anti-NMDAR encephalitis. Prediction models incorporating multiple biomarkers may provide an approach for disease severity stratification and prognosis forecast.

Humans↗
PubMed1987

Arbovirus isolations from mosquitoes collected during and after the 1982-1983 epizootic of western equine encephalitis in Argentina.

Mosquitoes were collected in Santa Fe and Rio Negro provinces, Argentina, in 1982-1983 during a western equine encephalitis (WEE) epizootic. Totals of 153,084 mosquitoes from Santa Fe Province and 484 from Rio Negro Province were tested for virus in 2,351 pools. Seventeen virus strains were isolated, all from Santa Fe collections, as follows: 4 WEE, 6 Venezuelan equine encephalitis, 1 St. Louis encephalitis, 2 Antequera, 1 Maguari, 1 Melao, 1 new vesiculovirus (Calchaqui), and 1 Gamboa. The WEE virus isolates were from Aedes albifasciatus, Anopheles albitarsis, Mansonia species, and Psorophora pallescens. Collections during the spring and summer (1983-1984) following the epizootic yielded 49,707 mosquitoes from Santa Fe, 15,961 from Rio Negro, and 2,019 from Chubut provinces. Twenty-two virus strains were isolated, all from Santa Fe mosquitoes, as follows: 3 strains of SLE virus and 19 strains of Turlock (TUR) virus. All but one of the TUR virus isolates appear to have come from mosquitoes that engorged on a viremic chicken following entry into a bait trap. The vector relationships of each virus isolated during and after the WEE epizootic are discussed.

Aedes↗
PubMed1988

A rapid dot immunoassay for the detection of serum antibodies to eastern equine encephalomyelitis and St. Louis encephalitis viruses in sentinel chickens.

A dot enzyme-linked immunosorbent assay utilizing a novel membrane, polyvinylidene difluoride, is described. This assay was developed for the rapid detection of serum antibodies to eastern equine encephalomyelitis virus and St. Louis encephalitis virus in sentinel chickens. Antigens were spot-filtered through the membrane. Membranes were dipped into small vials of sera. Antigen-antibody complexes were detected with enzyme-conjugated antiglobulin which, when exposed to substrate, produced a colored insoluble product. The antibody detection protocol was completed within 50 min and was compared with a standard plate enzyme immunoassay. Chickens were experimentally infected with eastern equine encephalomyelitis and St. Louis encephalitis and bled on a daily basis. The dot immunoassay correctly identified 99% (123/124) of the eastern equine encephalomyelitis virus and 100% (67/67) of the St. Louis encephalitis virus antisera. Sera from sentinel chicken flocks in Maryland were also assayed. These data indicate that the dot immunoassay should be considered as an alternative to current assays for the screening of sera for antibodies to virus antigens. This assay could easily be performed in the field and allows for the screening of antibodies to several different viruses in one test.

Alphavirus↗
PubMed1990

[Incidence of zoonoses with their natural foci in the West Bohemia Region. II. Antibodies to the Tahyna and Tribec tick-borne encephalitis viruses].

The authors examined serum samples from 475 men from different districts of the West Bohemian region for the presence of antibodies against viruses of tick-borne encephalitis, Tahyna and Tribec, strain Lipovník. Antibodies against the virus of tick-borne encephalitis were found in 1.1% and antibodies against the Tahyna virus in 4.4% of the examined sera. Antibodies against the Tribec virus were not detected. In the prevalence of antibodies against both viruses no geographical differences were revealed. The ratio of subjects with antibodies against the virus of tick-borne encephalitis was consistent with the long-term follow-up of morbidity and the reported clinical manifestation of the infection.

Antibodies, Viral↗
PubMed1977

St. Louis encephalitis in southern Ontario: laboratory studies for arboviruses.

The first reported outbreak of St. Louis encephalitis in Canada occurred in the summer of 1975 in southern Ontario -- in the Windsor-Sarnia-Chatham area, the Niagara region and the city of Toronto. Hemmagglutination inhibition and complement fixation testing of serum samples collected during the outbreak confirmed that St. Louis encephalitis virus was the etiologic agent. Furthermore, this virus was isolated from brain tissue of a patient who died. This outbreak was probably an extension of the outbreak that occurred in the United States that summer. It was the first outbreak of arbovirus encephalitis in the province of Ontario.

Antibodies, Viral↗
PubMed1997

Ticks, Lyme disease spirochetes, trypanosomes, and antibody to encephalitis viruses in wild birds from coastal Georgia and South Carolina.

Ticks and blood samples were collected from wild birds mist-netted on St. Catherine's Island, Georgia, and at the Wedge Plantation in coastal South Carolina in 1994 and 1995. Immature stages of 5 species of ixodid ticks were recovered from 10 of 148 (7%) birds belonging to 6 species in Georgia, whereas 6 ixodid species were recovered from 45 of 259 (17%) birds representing 10 avian species in South Carolina. Borrelia burgdorferi sensu lato was isolated from 27 of 120 (23%) screened ticks (Ixodes scapularis and Ixodes minor) recovered from South Carolina birds, but from none of 16 screened ticks removed from Georgia birds. This spirochete was also isolated from 1 of 97 (1%) birds in South Carolina. In 1995, neither eastern equine encephalitis (EEE) virus nor St. Louis encephalitis (SLE) virus was isolated from any of 218 bird sera screened, but serum neutralizing antibodies were found to EEE virus in 4 of 121 (3%) sera and to SLE virus in 2 of 121 (2%) sera from South Carolina. No antibody to either virus was detected in 51 avian sera screened from Georgia. Trypanosomes (probably Trypanosoma avium) were isolated from 1 of 51 (2%) birds from Georgia and from 13 of 97 (13%) birds from South Carolina. Our data suggest that some wild birds may be reservoir hosts for the Lyme disease spirochete and for encephalitis viruses in coastal Georgia and South Carolina and that migrating birds can disperse immature ticks infected with B. burgdorferi.

Animals↗