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PubMed2006

A serological survey of pigs, horses, and ducks in Nepal for evidence of infection with Japanese encephalitis virus.

Japanese encephalitis (JE) is an emerging disease of animals and humans in Nepal. A serological study for antibody to JE virus was conducted in Nepal from September 2003 to August 2004 by collecting 280 sera from pigs, ducks, and horses covering 10 districts of the country. These sera were tested by performing competitive enzyme-linked immunosorbent assay for the detection of antibodies against JE virus. The total number of tested sera was 280, of which 43.92% were found positive for the presence of antibodies against JE virus infection in Nepal. Sero-prevalence of JE in pigs, ducks, and horses was 48.11%, 26.79%, and 50.0%, respectively.

Animals↗
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↗
PubMed2002

Role for mucosal immune responses and cell-mediated immune functions in protection from airborne challenge with Venezuelan equine encephalitis virus.

Venezuelan equine encephalitis virus (VEEV) replicates in lymphoid tissues following peripheral inoculation and a high titre viraemia develops. Encephalitis develops after the virus enters the central nervous system from the blood, with the earliest neuronal involvement being via the olfactory nerve. Following aerosol challenge with virulent VEEV, the virus is thought to replicate in the nasal mucosa and there could be direct entry into the olfactory nerve via infected neuroepithelial cells. Protection from VEEV infection is believed to be primarily mediated by virus specific antibody. The correlation between protection and neutralising serum antibody titres is, however, inconsistent when the virulent virus is administered by the airborne route. This study demonstrates a link between antibody in serum and the nasal mucosa and protection by means of passive immunisation studies. Intra-nasal administration of antibody increased protection against airborne virus in Balb/c mice. Vaccination of mu MT strain mice that do not have functional B cells and cannot produce antibody revealed normal proliferation of spleen cells in vitro and robust cytokine production. Aerosol challenge of mu MT mice demonstrated that complete protection was only achieved when passive immunisation with antibody was supplemented with active immunisation with the TC-83 vaccine strain of the virus. This implies that cell-mediated immune functions are required for protection against airborne challenge with virulent VEEV.

Administration, Intranasal↗
PubMed2000

Persistent preceding focal neurologic deficits in children with chronic Epstein-Barr virus encephalitis.

Epstein-Barr virus encephalitis is a self-limiting disease with few sequelae. Persistence of neurologic deficits prior to and after the acute illness has yet to be described in children. We describe five children with persistent cognitive and focal neurologic deficits due to chronic Epstein-Barr virus encephalitis with various T2-weighted magnetic resonance imaging abnormalities. Clinical features were a 9-year-old boy with aphasia and apraxia, an 11-year-old girl with impulsivity and inappropriate behavior, a 17-year-old boy with deterioration of cognitive skills and judgment, a 5-year-old boy with complex-partial seizures, and a 6-year-old girl with obsessive-compulsive behavior. All patients had elevated serum Epstein-Barr virus titers for acute infection, with cerebrospinal fluid polymerase chain reaction positive for Epstein-Barr virus in four patients. Three children were treated with methylprednisolone with minimal improvement without changes on magnetic resonance imaging. Epstein-Barr virus encephalitis can present with chronic and insidious neurologic symptoms and should be considered in the differential diagnosis of children with acute or chronic neurologic illness of unknown etiology.

Adolescent↗
PubMed1980

Interferon in biopsy and autopsy specimens of brain. Its presence in herpes simplex virus encephalitis.

Quantitative virus and interferon titers were assayed in temporal lobe brain biopsy specimens (six patients); in various regions of the brain at autopsy (five of the six patients); and in serums and CSF during courses of herpes simplex virus, type 1 (HSV-1) encephalitis. Until the tenth day of neurologic disease, interferon (geometric mean titer, 25 units/mL) was present in each virus-positive brain biopsy specimen. The geometric mean HSV-1 titer at brain biopsy was 328 tissue culture dose (TCD)50/g. On the sixth day of disease, CSF from the sole survivor contained 160 units/mL, but five other samples of CSF contained no detectable interferon. No serums from any of the six patients contained interferon. At autopsies performed on the sixth to 19th day of neurologic disease, 13 of 35 of the regional areas of the brain retained HSV, but only a single specimen from a temporal lobe had measurable interferon. Early in the course of HSV-1 encephalitis, substantial interferon titers are present in areas of virus multiplication. This local brain interferon is insufficient alone to inhibit progression of a disease but could possibly be important in combination with antiviral chemotherapy.

Adult↗
PubMed1988

Hyaluronidase enhances cell fusion and synthesis of viral DNA during infection with caprine arthritis encephalitis virus.

Caprine arthritis encephalitis virus (CAEV) is a lentivirus which infects goats and causes chronic progressive arthritis after a prolonged incubation period. CAEV replicates productively in cultures of goat synovial membrane cells and causes cytopathic effects characterized by multinucleated giant cell formation. The enzyme hyaluronidase was found to accelerate this virus induced fusion of GSM cells. Hyaluronidase treatment also resulted in synthesis of increased levels of unintegrated viral DNA early after infection. However, there was no significant increase in viral RNA in the infected cells or in the amount of virus produced. These studies suggest that hyaluronidase facilitates the interaction of CAEV with the target cells. Further it suggests that only a few copies of viral DNA are required to achieve maximal levels of virus replication. Additional copies of viral DNA appear to be redundant not contributing to viral specific transcription or increased production of virus.

Animal Diseases↗
PubMed2003

Structure of isolated nucleocapsids from venezuelan equine encephalitis virus and implications for assembly and disassembly of enveloped virus.

Venezuelan equine encephalitis virus (VEEV) is an important human and equine pathogen in the Americas, with widespread reoccurring epidemics extending from South America to the southern United States. Most troubling, VEEV has been made into a weapon by several countries and is currently restricted by the Centers for Disease Control and Prevention as a potential biological warfare and terrorism agent. To facilitate the development of antiviral compounds, the structure of the nucleocapsid isolated from VEEV has been determined by electron cryomicroscopy and image reconstruction and represents the first three-dimensional structure of a nucleocapsid isolated from a single-stranded enveloped RNA virus. The isolated VEEV nucleocapsid undergoes significant reorganization relative to its structure within VEEV. However, the isolated nucleocapsid clearly exhibits T=4 icosahedral symmetry, and its characteristic nucleocapsid hexons and pentons are preserved. The diameter of the isolated nucleocapsid is approximately 11.5% larger than that of the nucleocapsid within VEEV, with radial expansion being greatest near the hexons. Significantly, this is the first direct structural evidence showing that a simple enveloped virus undergoes large conformational changes during maturation, suggesting that the lipid bilayer and the transmembrane proteins of simple enveloped viruses provide the energy necessary to reorganize the nucleocapsid during maturation.

Encephalitis Virus, Venezuelan Equine↗
PubMed1999

Astrocytes as targets for Venezuelan equine encephalitis virus infection.

Venezuelan equine encephalitis virus (VEE) produces an acute infection in humans and induces a well-characterized cytopathic effect in neurons of the central nervous system (CNS). However, little is known about the role of glial cells in response to VEE infection of the CNS. Our results demonstrate that VEE is capable of a productive infection in primary astrocyte cultures and that this infection is cytotoxic. Further, there were significant differences in the growth kinetics comparing virulent and attenuated strains of VEE. Additionally, VEE infection of astrocyte cultures induced gene expression of two neuro-immune modulators, tumor necrosis factor-alpha (TNF-alpha) and inducible nitric oxide synthase (iNOS). Assays for TNF-alpha protein and nitric oxide (NO) demonstrated high levels of TNF-alpha protein and low levels of NO in response to VEE infection of astrocytes. These observations suggest an important role of astrocytes in this virus-induced encephalitis, and that interactions between astrocytes, other glial cells, and neurons may be important in VEE pathogenesis. Such interactions, which could impact neuronal survival, may include loss of functional changes in astrocytes or, alternatively, their production of neurotoxic molecules.

Animals↗
PubMed2004

Generation and characterization of closely related epizootic and enzootic infectious cDNA clones for studying interferon sensitivity and emergence mechanisms of Venezuelan equine encephalitis virus.

Venezuelan equine encephalitis virus (VEEV) is a reemerging pathogen and a continuing threat to humans and equines in the Americas. Identification of the genetic determinants that enable epizootic VEEV strains to arise and exploit equines as amplification hosts to cause widespread human disease is pivotal to understanding VEE emergence. The sensitivity to murine alpha/beta interferon-mediated antiviral activity was previously correlated to the epizootic phenotype of several VEEV strains. Infectious cDNA clones were generated from an epizootic subtype IC VEEV strain (SH3) isolated during the 1992 Venezuelan outbreak and a closely related enzootic, sympatric subtype ID strain (ZPC738). These VEEV strains had low-cell-culture-passage histories and differed by only 12 amino acids in the nonstructural and structural proteins. Rescued viruses showed similar growth kinetics to their parent viruses in several cell lines, and murine infections resulted in comparable viremia and disease. Unlike what was found in other studies of epizootic and enzootic VEEV strains, the sensitivities to murine alpha/beta interferon did not differ appreciably between these epizootic versus enzootic strains, calling into question the reliability of interferon sensitivity as a marker of epizootic potential.

Animals↗
PubMed2006

Viral load, organ distribution, histopathological lesions, and cytokine mRNA expression in goats infected with a molecular clone of the caprine arthritis encephalitis virus.

Caprine arthritis encephalitis virus (CAEV) is a lentivirus of goats that causes persistent infection characterized by the appearance of inflammatory lesions in various organs. To define the sites of persistence, 5 goats were infected with a molecular clone of CAEV, and the viral load was monitored by real-time-PCR and RT-PCR in different sites 8 years after infection. The lymph nodes proved to be an important virus reservoir, with moderate virus replication relative to what is reported for lentiviruses of primates. Mammary gland and milk cells were preferred sites of viral replication. The viral load varied significantly between animals, which points to an important role of the genetic background. We found a clear association between occurrence of histopathological lesions and viral load in specific sites. The mRNA expression analysis of several cytokines did not reveal differences between animals that could explain the considerable individual variations in viral load observed.

Animals↗
PubMed1981

Development of age-dependent resistance to sindbis virus encephalitis: correlation with inactivation of virus within the blood stream.

The clearance of Sindbis virus from the blood stream and its localization in the reticuloendothelial system (RES) was studied in mice susceptible (2 weeks old) and resistant (6 weeks old) to fatal Sindbis virus encephalitis. No significant differences in the relative capacity of 2-week-old and 6-week-old mice to remove 125I-labelled virus from the blood stream and to localize virus within the liver were observed. However, the decline of infectious virus was more rapid in the blood of adult mice. These studies suggest that, in addition to physical removal of virus by the RES, inactivation of virus in the blood serum stream plays an important role in limiting viremia during infections with Sindbis virus.

Aging↗
PubMed2005

Emerging zoonotic encephalitis viruses: lessons from Southeast Asia and Oceania.

The last decade of the 20th Century saw the introduction of an unprecedented number of encephalitic viruses emerge or spread in the Southeast Asian and Western Pacific regions (Mackenzie et al, 2001; Solomon, 2003a). Most of these viruses are zoonotic, either being arthropod-borne viruses or bat-borne viruses. Thus Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, has spread through the Indonesian archipelago to Papua New Guinea (PNG) and to the islands of the Torres Strait of northern Australia, to Pakistan, and to new areas in the Indian subcontinent; a strain of tick-borne encephalitis virus (TBEV) was described for the first time in Hokkaido, Japan; and a novel mosquito-borne alphavirus, Me Tri virus, was described from Vietnam. Three novel bat-borne viruses emerged in Australia and Malaysia; two, Hendra and Nipah viruses, represent the first examples of a new genus in the family Paramyxoviridae, the genus Henipaviruses, and the third, Australian bat lyssavirus (ABLV) is new lyssavirus closely related to classical rabies virus. These viruses will form the body of this brief review.

Alphavirus↗
PubMed1992

Breakdown of blood-brain barrier by virus-induced cytokine during Japanese encephalitis virus infection.

In this study we have shown, for the first time, that Japanese encephalitis virus (JEV) and a low molecular weight (10 kDa) macrophage-derived neutrophil chemotactic factor (MDF) produced following JEV infection in mice could cause an alteration in the permeability of the blood-brain barrier resulting in leakage of plasma protein bound Evans blue dye and radiolabelled erythrocytes in brain. The maximum leakage occurred at day 6 after intracerebral (i.c.) JEV infection and was sensitive to anti-JEV antisera. Further, MDF caused peak leakage of dye and radiolabelled erythrocytes at 1 h post inoculation with a decline thereafter. Complete restoration of the integrity of the blood-brain barrier occurred by the 4th hour. The extent of leakage was dose dependent and showed a direct correlation between the level of MDF, clinical sickness and virus titre in brain. Anti-MDF antisera protected the mice against the effects of MDF. These findings show that JEV-induced cytokine, MDF, alters the integrity of the blood-brain barrier and thus controls the cellular and plasma leakage into the CNS.

Animals↗
PubMed2001

Self-replicative RNA vaccines elicit protection against influenza A virus, respiratory syncytial virus, and a tickborne encephalitis virus.

In genetic vaccination, recipients are immunized with antigen-encoding nucleic acid, usually DNA. This study addressed the possibility of using the recombinant alpha virus RNA molecule, which replicates in the cytoplasm of transfected cells, as a novel approach for genetic vaccination. Mice were immunized with recombinant Semliki Forest virus RNA-encoding envelope proteins from one of 3 viruses: influenza A virus, a tickborne flavivirus (louping ill virus), or respiratory syncytial virus (RSV). Serologic analyses showed that antigen-specific antibody responses were elicited. IgG isotyping indicated that predominantly Th1 type immune responses were induced after immunization with RSV F protein-encoding RNA, which is relevant for protection against RSV infection. Challenge infection showed that RNA immunization had elicited significant levels of protection against the 3 model virus diseases.

Animals↗
PubMed2006

Replication and clearance of Venezuelan equine encephalitis virus from the brains of animals vaccinated with chimeric SIN/VEE viruses.

Venezuelan equine encephalitis virus (VEEV) is an important, naturally emerging zoonotic pathogen. Recent outbreaks in Venezuela and Colombia in 1995, involving an estimated 100,000 human cases, indicate that VEEV still poses a serious public health threat. To develop a safe, efficient vaccine that protects against disease resulting from VEEV infection, we generated chimeric Sindbis (SIN) viruses expressing structural proteins of different strains of VEEV and analyzed their replication in vitro and in vivo, as well as the characteristics of the induced immune responses. None of the chimeric SIN/VEE viruses caused any detectable disease in adult mice after either intracerebral (i.c.) or subcutaneous (s.c.) inoculation, and all chimeras were more attenuated than the vaccine strain, VEEV TC83, in 6-day-old mice after i.c. infection. All vaccinated mice were protected against lethal encephalitis following i.c., s.c., or intranasal (i.n.) challenge with the virulent VEEV ZPC738 strain (ZPC738). In spite of the absence of clinical encephalitis in vaccinated mice challenged with ZPC738 via i.n. or i.c. route, we regularly detected high levels of infectious challenge virus in the central nervous system (CNS). However, infectious virus was undetectable in the brains of all immunized animals at 28 days after challenge. Hamsters vaccinated with chimeric SIN/VEE viruses were also protected against s.c. challenge with ZPC738. Taken together, our findings suggest that these chimeric SIN/VEE viruses are safe and efficacious in adult mice and hamsters and are potentially useful as VEEV vaccines. In addition, immunized animals provide a useful model for studying the mechanisms of the anti-VEEV neuroinflammatory response, leading to the reduction of viral titers in the CNS and survival of animals.

Animals↗
PubMed2005

Antiviral effect of dehydroepiandrosterone on Japanese encephalitis virus infection.

Japanese encephalitis virus (JEV), which causes neurological disorders, completes its life cycle and triggers apoptotic cell death in infected cells. Dehydroepiandrosterone (DHEA), an adrenal-derived steroid, has been implicated in protection against neurotoxicity and protection of animals from viral-induced encephalitis, resulting in an increased survival rate of the animals. Currently, the mechanisms underlying the beneficial effects of DHEA against the virus are largely unknown. In this study, DHEA suppression of JEV replication and virus-induced apoptosis in murine neuroblastoma (N18) cells was investigated. It was found that DHEA suppressed JEV-induced cytopathic effects, JEV-induced apoptotic cell death and JEV propagation in a concentration-dependent manner. Antiviral activity was more efficient in cultures treated with DHEA immediately after viral adsorption compared with that in cultures receiving delayed administration after adsorption or transient exposure before adsorption. JEV-induced cytotoxicity was accompanied by the inactivation of extracellular signal-regulated protein kinase (ERK). Inactivation of ERK by JEV infection was reversed by DHEA. When cells were treated with the ERK inhibitor U0126, DHEA lost its antiviral effect. Activation of ERK by anisomycin mimicked the action of DHEA in suppressing JEV-induced cytotoxicity. DHEA-related compounds, such as its sulfate ester (DHEAS) and pregnenolone, were unable to suppress JEV-induced cytotoxicity and ERK inactivation. The hormone-receptor antagonists ICI 182780 and flutamide failed to abrogate the antiviral effect of DHEA. These findings suggest that the antiviral effect of DHEA is not linked directly to the genomic steroid-receptor pathways and suggest that the signalling pathways of ERK play a role in the antiviral action of DHEA.

Animals↗