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At least 109 records · Page 6Linked to original sources
PubMed1986

Serological surveillance for maedi-visna virus and caprine arthritis-encephalitis virus in Northern Ireland.

The results of serological testing for maedi-visna virus infection in indigenous and non-indigenous sheep in Northern Ireland, over a five year period (1980 to 1984) are presented. In tests carried out in 1980 and 1981 on pedigree breeds, 10 reactors were identified on seven farms and maedi-visna virus was isolated on three occasions from leucocyte cultures. None of the animals showed clinical signs of maedi-visna and all the reactors were subsequently destroyed. Nine of the reactors were imports from Scotland or the Republic of Ireland and the other was the progeny of an imported ewe. In subsequent tests (1982 to 1984) of exotic and indigenous flocks no further reactors were identified. A survey of goat herds for evidence of caprine arthritis-encephalitis virus infection was also negative.

Animals↗
PubMed1996

Inhibition of nitric oxide synthesis increases mortality in Sindbis virus encephalitis.

Sindbis virus (SV) is an alphavirus that causes acute encephalomyelitis in mice. The outcome is determined by the strain of virus and by the age and genetic background of the host. The mortality rates after infection with NSV, a neurovirulent strain of SV, were as follows v: 81% (17 of 21) in BALB/cJ mice; 20% (4 of 20) in BALB/cByJ mice (P < 0.001); 100% in A/J, C57BL/6J, SJL, and DBA mice; and 79% (11 of 14) in immunodeficient scid/CB17 mice. Treatment with Nomega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthetase (NOS) inhibitor, increased mortality to 100% (P < 0.05) in NSV-infected BALB/cJ mice, to 95% (P < 0.001) in BALB/cByJ mice, and to 100% in scid/CB17 mice. BALB/cJ and BALB/cByJ mice had similar levels of inducible NOS mRNA in their brains, which were not affected by L-NAME or NSV infection. Brain NOS activity was similar in BALB/cJ and BALB/cByJ mice before and after infection and was markedly inhibited by L-NAME. NSV replication in the brains of BALB/cJ mice, BALB/cByJ mice, and mice treated with L-NAME was similar. Treatment of N18 neuroblastoma cells with NO donors S-nitroso-N-acetylpenicillamine or sodium nitroprusside in vitro before infection increased cell viability at 42 to 48 h compared with untreated NSV-infected N18 cells with little effect on virus replication. These data suggest that NO protects mice from fatal encephalitis by a mechanism that does not directly involve the immune response or inhibition of virus growth but rather may enhance survival of the infected neuron until the immune response can control virus replication.

Alphavirus Infections↗
PubMed2006

Tunicamycin enhances neuroinvasion and encephalitis in mice infected with Venezuelan equine encephalitis virus.

Venezuelan equine encephalitis (VEE) viruses cause natural outbreaks in humans and horses and represent a significant biothreat agent. The effect of tunicamycin on the course of the disease in mice with VEE was investigated, and the combined effects of these agents was characterized. CD-1 mice given 2.5 microg of tunicamycin had >1,000-fold more virus in the brain 48 hours after infection with the virulent VEE strain V3000 and > or =100-fold of the attenuated strain V3034 at all tested times than did untreated mice, indicating enhanced neuroinvasion. Tunicamycin did not alter the viremia profiles of these viruses nor the replication of V3000 in the brain itself. Tunicamycin alone caused ultrastructural blood-brain barrier damage, yet neuroinvasion by V3000 in treated mice appeared to occur via the olfactory system rather than the blood-brain barrier. Tunicamycin-treated, V3000-infected mice also exhibited earlier and more severe weight loss, neurological signs, neuronal infection, neuronal necrosis and apoptosis, and inflammation than untreated, V3000-infected mice. The mean survival time of tunicamycin-treated, V3000-infected mice was 7.3 days versus 9.9 days for untreated, V3000-infected mice. These studies imply that animals that ingest toxins similar to tunicamycin, including the agent of annual ryegrass toxicity in livestock, are conceivably at greater risk from infections by encephalitis viruses and that humans and horses exposed to agents acting similar to tunicamycin may be more susceptible to encephalitis caused by VEE viruses. The exact mechanism of tunicamycin-enhanced neuroinvasion by VEE viruses requires further study.

Animals↗
PubMed1989

Analysis of regulatory elements of the equine infectious anemia virus and caprine arthritis-encephalitis virus long terminal repeats.

We analyzed the equine infectious anemia virus (EIAV) long terminal repeat (LTR) for sequences that influence its promoter activity and ability to be trans-activated by the EIAV tat gene product. A series of LTR deletion mutants and recombinants between LTR and simian virus 40 (SV40) regulatory sequences were used for these studies. We were able to identify the EIAV promoter region and showed that sequences within the U3 region significantly inhibited LTR-directed transcription. However, when placed in a heterologous context (SV40 promoter) these U3 sequences functioned as an enhancer. trans-activation of the EIAV LTR was found to depend upon sequences downstream of the transcription initiation site and also within U3. Deletion mutagenesis experiments showed that the major downstream element was present in a 46-nucleotide stretch (+4 to +50). An SV40 promoter construct containing these sequences could be trans-activated in cells expressing the EIAV tat gene product. For comparative purposes we also examined the LTR of another animal lentivirus, caprine arthritis-encephalitis virus (CAEV), for positive and negative transcriptional regulatory elements and demonstrated the presence of an enhancer within its U3 sequence. There is evidence that trans-activation of the CAEV LTR requires U3 sequences. When the EIAV U3 region was replaced by the CAEV U3 sequence, the promoter activity of the EIAV LTR was markedly elevated, but the responsiveness to the EIAV trans-activator could not be restored.

Animals↗
PubMed2002

Expression and self-assembly of norwalk virus capsid protein from venezuelan equine encephalitis virus replicons.

The Norwalk virus (NV) capsid protein was expressed using Venezuelan equine encephalitis virus replicon particles (VRP-NV1). VRP-NV1 infection resulted in large numbers of recombinant NV-like particles that were primarily cell associated and were indistinguishable from NV particles produced from baculoviruses. Mutations located in the N-terminal and P1 domains of the NV capsid protein ablated capsid self-assembly in mammalian cells.

Animals↗
PubMed2004

Increased presence of matrix metalloproteinases 2 and 9 in short- and long-term experimental herpes simplex virus encephalitis.

Herpes simplex virus encephalitis (HSVE) causes elevated morbidity and mortality despite antiviral treatment. Virus-independent mechanisms may perpetuate brain damage. Matrix metalloproteinases (MMPs) target extracellular matrix components. This study describes the protein and mRNA expression of MMP2 and MMP9 in experimental HSVE in the short and long term. Ten SJL-NBOM mice were infected with neurovirulent HSV-1 and compared with nine controls. The presence of MMP2 and MMP9 in brain tissue was analyzed with sodium-dodecyl-sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) gelatin zymography and mRNA expression of MMP2 and MMP9 with quantitative real-time PCR at days 7, 21 and 180 post-inoculation. Infected animals had a significantly elevated gelatinolytic activity of MMP2 at all time points, and of MMP9 at days 21 and 180. Increased presence of MMP2 and MMP9 in chronic HSVE may contribute to ongoing damage. Inhibition of MMP2 and MMP9 might be a suitable target for therapeutic intervention.

Animals↗
PubMed2003

Enhancing biosynthesis and secretion of premembrane and envelope proteins by the chimeric plasmid of dengue virus type 2 and Japanese encephalitis virus.

We have constructed a series of plasmids encoding premembrane (prM) and envelope (E) protein genes of dengue virus type 2 (DEN-2). These plasmids included an authentic DEN-2 prM-E construct (pCBD2-14-6), and two chimeric constructs, 90% DEN-2 E-10% Japanese encephalitis (JE) virus E (pCB9D2-1J-4-3) and 80% DEN-2 E-20% JE E (pCB8D2-2J-2-9-1). Monoclonal antibody (MAb) reactivity indicated that all three plasmids expressed authentic DEN-2 virus E protein epitopes representative of flavivirus domains 1, 2, and 3. However, only the pCB8D2-2J-2-9-1 construct secreted high levels of prM, M (membrane), and E proteins into the culture fluid of plasmid-transformed COS-1 cells. The major portion of the prM and E proteins expressed by COS-1 cells transformed by pCBD2-14-6 or pCB9D2-4-3 plasmids remained membrane-bound. The results supported the notion that an unidentified membrane retention sequence is located between E-397 and E-436 of DEN-2 virus E protein. Replacing the carboxyl-terminal 20% of DEN-2 E (397-450) with the corresponding JE sequence had no effect on anti-DEN-2 MAb reactivity, indicating that this region is antigenically inert, although it is required for antigen secretion. Plasmid pCBD2-2J-2-9-1, which expressed secreted forms of prM/M and E that have the potential to form subviral particles, was superior to other constructs in stimulating an antibody response. Ninety percent neutralization titers ranging from 1:40 to >1:1000 were observed in seven of nine serum specimens from pCB8D2-2J-2-9-1-immunized mice. Eleven of twelve 2-day-old neonatal mice, derived from a pCB8D2-2J-2-9-1 immunized female mouse, survived intraperitoneal challenge of DEN-2 New Guinea C virus.

Animals↗
PubMed2002

Neuropathogenesis of Japanese encephalitis virus.

In the central nervous system, the Japanese encephalitis virus can replicate only in neurons. The mechanism of the type of neurotropism was analyzed. The susceptibility to Japanese encephalitis virus infection in the rat brain was closely associated with neuronal immaturity. The initial specific binding of the virus to cells is one of the reasons for neurotropism of the Japanese encephalitis virus. The treatment of Japanese encephalitis virus infection with the neutralizing monoclonal antibody against the E protein did not inhibit the virus from binding to the cell surfaces, but strongly inhibited Japanese encephalitis virus-induced cell fusion and internalization of the virus into the host cells. One of the genome regions responsible for neuropathogenesis of the Japanese encephalitis virus was located on the E protein-coding region. The 138th amino acid of the E protein was important for neuropathogenesis expression of the Japanese encephalitis virus. The cell fusion activity of the E protein was closely correlated with neuropathogenesis of the virus.

Animals↗
PubMed2004

Neuronal apoptosis pathways in Sindbis virus encephalitis.

Sindbis virus infects neurons of the brain and spinal cord leading to neuronal apoptosis and encephalitis in mice. During postnatal development, neurons of mice remain susceptible to infection but become refractory to SV-induced programmed cell death. Failure to undergo programmed cell death results in a persistent infection. However, some neurovirulent strains of Sindbis virus overcome the age-dependent protective function in neurons, leading to enhanced apoptotic cell death in the central nervous system and higher mortality rates. Sindbis virus infections can also cause hind-limb paralysis due to the death of infected spinal cord motor neurons. However, spinal cord neuron death in older mice appears to occur by mechanisms that differ from classical apoptosis observed in newborn mice based on the morphology of dying neurons at these two sites. Sindbis virus infections of mosquitoes and some mosquito cell lines, on the other hand, do not induce cell death but persistent infections, a phenomenon also observed occasionally in cultured mammalian cells as well as in brains of infected mice surviving lethal infections. Thus, both viral and cellular factors contribute to the varied outcomes of infection. The molecular mechanisms that govern the susceptibility or resistance of particular cell types to SV-induced cell death are not well understood. Furthermore, the cellular execution machinery that produces the characteristic morphological distinctions between brain and spinal cord (i.e. apoptotic versus non-apoptotic) remain to be discovered.

Age Factors↗
PubMed1977

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

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

Animals↗
PubMed2006

A dynamic transmission model of eastern equine encephalitis virus.

Eastern equine encephalitis virus (EEEV) is one of several arthropod-borne viruses (arboviruses) endemic to the United States. Interactions between arthropod (mosquito) vectors and avian amplification host populations play a significant role in the dynamics of arboviral transmission. Recent data have suggested the hypothesis that an increased rate of successful feeding on young-of-the-year (YOY) birds might play a role in the dynamics of EEEV transmission. To test this hypothesis, we developed a model to explore the effect of the interactions of the vectors and avian host populations on EEEV transmission. Sensitivity analyses conducted using this model revealed eleven parameters that were capable of disproportionately affecting the predicted level of EEEV infection in the vertebrate reservoir and vector populations. Of these, four parameters were related to the interaction of the vector with young-of-the-year birds. Furthermore, adult birds could not substitute for young-of-the-year in initiating and maintaining a predicted enzootic outbreak of EEEV. Taken together, the model predicted that young-of-the-year birds play a key role in establishing and maintaining enzootic outbreaks of EEEV.

Journal Article↗
PubMed2005

A synthetic peptide based on the NS1 non-structural protein of tick-borne encephalitis virus induces a protective immune response against fatal encephalitis in an experimental animal model.

Linear immunogenic peptides corresponding to amino acid sequences from the NS1 non-structural protein from tick-borne encephalitis virus (strain Sophyin) were predicted using established algorithms and synthesized. Of the 12 peptides predicted, 11 were able to induce peptide-specific antibodies in BALB/c mice but only 1 of these 11 was able to induce antibodies, which reacted with the native protein in a radio-immune precipitation assay. This peptide corresponds to amino acids 37--55, and forms one of the predicted structurally conserved alpha helices of the virus NS1 protein. It was able to protect 60% of animals against lethal challenge with the homologous highly pathogenic tick-borne encephalitis virus strain, and adoptive transfer experiments indicated the involvement of the antibodies induced by this peptide in its protective activity in mice.

Amino Acid Sequence↗
PubMed2003

Sensitivity of the VecTest antigen assay for eastern equine encephalitis and western equine encephalitis viruses.

VecTest assays for detecting eastern equine encephalitis virus (EEE) and western equine encephalitis virus (WEE) antigen in mosquito pools were evaluated to determine their sensitivity and specificity by using a range of EEE, WEE, St. Louis encephalitis virus (SLE), and West Nile virus (WN) dilutions as well as individual and pooled mosquitoes containing EEE or WEE. The EEE test produced reliable positive results with samples containing > or = 5.3 log10 plaque-forming units (PFU) of EEE/ml, and the WEE test produced reliable positive results with samples containing > or = 4.7 log10 PFU WEE/ml. Both assays detected the respective viral antigens in single virus-positive mosquitoes and in pools containing a single positive mosquito and 49 negative specimens. The SLE and WN assays also contained on the dipsticks accurately detected their respective viruses. No evidence was found of cross reaction or false positives in any of the tests. The VecTest assays were less sensitive than the EEE- and WEE-specific TaqMan reverse transcriptase polymerase chain reaction and Vero cell plaque assay, but appear to be useful for detecting arboviruses in mosquito-based arbovirus surveillance programs.

Animals↗
PubMed1997

Ilheus virus (Flaviviridae, Flavivirus) is closely related to Japanese encephalitis virus complex.

The Ilheus (ILH) virus has long been known to belong to group B of the arboviruses. Previous attempts to relate it to existing serogroups within the Flavivirus genus using conventional serological techniques such as hemagglutination inhibition, neutralization and complement fixation tests have been inconclusive. We have first used denaturing gel electrophoresis to estimate the molecular weight of immunoprecipitated radiolabeled viral proteins and the cross-reactivity among ILH proteins and hyperimmune sera to several flaviviruses only from the mosquito-borne encephalitis virus serogroups. The estimated molecular weight for the three proteins was in the same order of magnitude, as previously established, for mosquito-borne flaviviruses. Cross-immunoprecipitation tests showed that NS3 protein is the most cross-reactive. Partial nucleotide sequence analyses of the NS3 gene, corresponding to an area linking the helicase and the RNA triphosphatase domains, revealed that ILH virus is very closely related to the Japanese encephalitis virus complex confirming earlier serological data.

Animals↗
PubMed1983

Transmission and control of caprine arthritis-encephalitis virus.

Caprine arthritis-encephalitis virus was isolated from goat milk and transmitted most efficiently to kids through both milk and colostrum. In addition, it appeared that transmissions through other secretions of the doe occurred, but were less important than transmission in milk and colostrum. Intrauterine infection may have occurred in 2 of 32 cesarean-derived goats, but postpartum horizontal transmission could not be ruled out. Transmission by the aerosol route was not demonstrated, and even short-term direct contact between virus-infected bucks and virus-free does during breeding did not result in transmission. Prolonged direct contact for over 12 months between weaned cesarean-derived goats and virus-infected goats was necessary before horizontal transmission could be demonstrated under nondairy conditions. However, when uninfected does were milked with infected does, a high percentage became infected in less than 10 months. Heat inactivation (56 C) reduced approximately 10(5) median tissue culture infective doses of caprine arthritis-encephalitis virus to below titratable levels, and virus was not transmitted to kids fed virus-infected colostrum that had been heated at 56 C for 1 hour. A program of eradication is discussed in which kids are removed from their dams at birth, fed safe sources of colostrum and milk, and isolated from other goats until weaning.

Animals↗