Bovine herpesvirus 5 (BHV-5) Us9 is essential for BHV-5 neuropathogenesis.
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Bovine herpesvirus 5 (BHV-5) is a neurovirulent alphaherpesvirus that causes fatal encephalitis in calves. In a rabbit model, the virus invades the central nervous system (CNS) anterogradely from the olfactory mucosa following intranasal infection. In addition to glycoproteins E and I (gE and gI, respectively), Us9 and its homologue in alphaherpesviruses are necessary for the viral anterograde spread from the presynaptic to postsynaptic neurons. The BHV-5 Us9 gene sequence was determined, and the predicted amino acid sequence of BHV-5 Us9 was compared with the corresponding Us9 sequences of BHV-1.1. Alignment results showed that they share 77% identity and 83% similarity. BHV-5 Us9 peptide-specific antibody recognized a doublet of 17- and 19-kDa protein bands in BHV-5-infected cell lysates and in purified virions. To determine the role of the BHV-5 Us9 gene in BHV-5 neuropathogenesis, a BHV-5 Us9 deletion recombinant was generated and its neurovirulence and neuroinvasive properties were compared with those of a Us9 rescue mutant of BHV-5 in a rabbit model. Following intranasal infection, the Us9 rescue mutant of BHV-5 displayed a wild-type level of neurovirulence and neural spread in the olfactory pathway, but the Us9 deletion mutant of BHV-5 was virtually avirulent and failed to invade the CNS. In the olfactory mucosa containing the olfactory receptor neurons, the Us9 deletion mutant virus replicated with an efficiency similar to that of the Us9 rescue mutant of BHV-5. However, the Us9 deletion mutant virus was not transported to the bulb. Confocal microscopy of the olfactory epithelium detected similar amounts of virus-specific antigens in the cell bodies of olfactory receptor neuron for both the viruses, but only the Us9 rescue mutant viral proteins were detected in the processes of the olfactory receptor neurons. When injected directly into the bulb, both viruses were equally neurovirulent, and they were transported retrogradely to areas connected to the bulb. Taken together, these results indicate that Us9 is essential for the anterograde spread of the virus from the olfactory mucosa to the bulb. (+info)
Cognitive rehabilitation of naming deficits following viral meningo-encephalitis.
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OBJECTIVE: This case study describes the neuropsychological assessment and cognitive rehabilitation of a patient who developed word retrieval deficits for objects and people's names, following an episode of viral meningo-encephalitits. It shows the implementation and outcome of two techniques adapted to the patient's individual characteristics and context providing a more ecologically valid approach. METHODS: In the first technique, "verbal semantic association", the patient was required to describe what she knew about an object as a strategy to help her retrieve its name. In the second one, "face-name association" she was taught to apply a visual-imagery technique in order to retrieve relevant people's names. RESULTS: Following the implementation of these procedures there was a decrease in the number of episodes of failure to retrieve objects and people's names in her everyday life context. CONCLUSION: The improvement found in the patient's ability to retrieve words is discussed in terms of the utility of cognitive rehabilitation programmes and cognitive models of language processing (+info)
A novel nonsuppurative meningoencephalitis in young greyhounds in Ireland.
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Fourteen 4- to 18-month-old vaccinated Greyhounds (10 males, 4 females) from three kennels in southern Ireland presented over a 2-year period with acute or insidious onset neurological signs. Head tilting, ataxia, recumbency, circling, and blindness were commonly observed, and animals were dull, dehydrated, and had lost weight. Hematologic and biochemical parameters reflected dehydration but were otherwise unremarkable. Microscopic examination revealed severe diffuse and focal gliosis and gemistocytosis accompanied by mononuclear cell perivascular cuffing in caudate nucleus and cortical gray matter of the cerebrum and in the periventricular gray matter of the anterior brainstem. Milder lesions were noted in the caudal brainstem, cranial spinal cord, and in the molecular layer of the cerebellum. This was accompanied by a lymphocyte and plasma cell infiltration of the cerebral and cerebellar meninges. Demyelination, neuropil necrosis, neuronophagia, and vasculitis were not observed. No inclusion bodies, fungi, or protozoal cysts were seen. Additional serologic and molecular pathology tests also failed to determine a cause, suggesting that these cases may represent a previously undiagnosed condition in the dog. (+info)
Primary infection, latency, and reactivation of bovine herpesvirus type 5 in the bovine nervous system.
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Bovine herpesvirus type 5 (BHV-5) infection in calves causes meningoencephalitis, a fatal disease highly prevalent in South America. To study the pathogenesis of BHV-5 infection in cattle, 12 calves (group 1: acute infection) and 11 calves (group 2: latent infection) were intranasally inoculated with an Argentinean BHV-5 isolate at 10(8) and 10(4.7) tissue culture infective doses, respectively; six calves (control group) were mock infected. At 3 months postinoculation, all of the calves in group 2 and three calves in group 3 were given dexamethasone to reactivate the virus. The animals were euthanatized between days 6 and 17 postinoculation (group 1) and between days 6 and 16 postreactivation (group 2). Seventy-five percent and 91% of animals in groups 1 and 2, respectively, excreted BHV-5 in nasal and ocular discharges. Following dexamethasone administration, 45% of calves shed virus in both types of secretions. Spontaneous virus reactivation and shedding was observed in one calf. Neurologic signs consisting of circling, teeth grinding, ptyalism, jaw chomping, tongue protrusion, and apathy were observed in two animals in group 1 and, during the reactivation period, in four animals in group 2. Macroscopic findings consisted of softening of the cerebral tissue, meningeal hemorrhages and swelling, and edema and hemorrhages of prescapular, retropharyngeal and submandibular lymph nodes. Histologic lesions consisted of meningitis, mononuclear perivascular cuffing, neuronophagia, satellitosis, gliosis, hemorrhage, and necrosis and edema. Lesions in anterior cerebral cortex, medulla, and pons were consistently seen in all the animals of group 1. In the acutely infected animals, lesions in the diencephalon appeared at day 10 postinoculation, whereas in the latently infected calves these lesions were observed as early as at day 6 postreactivation. Latently infected animals developed lesions simultaneously in anterior cortex, medulla, pons, and diencephalon, showing a remarkable difference from the acutely infected group. Trigeminal ganglionitis appeared relatively early in animals of both groups (day 7 postinoculation in group 1 and day 8 postreactivation in group 2). (+info)
Critical role of complement and viral evasion of complement in acute, persistent, and latent gamma-herpesvirus infection.
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Several gamma-herpesviruses encode homologs of host regulators of complement activation (RCA) proteins, suggesting that they have evolved immune evasion strategies targeting complement. We evaluated the role of complement factor C3 (C3) and the murine gamma-herpesvirus 68 (gammaHV68) RCA protein in viral pathogenesis. Deletion of the gammaHV68 RCA protein decreased virulence during acute CNS infection, and this attenuation was specifically reversed by deletion of host C3. The gammaHV68 RCA protein was also important for persistent viral replication and virulence in IFNgammaR(-/-) mice. In addition, C3 played a role in regulating latency, but this was not counteracted by the gammaHV68 RCA protein. We conclude that complement is a key host defense against gamma-herpesvirus infection and that gamma-herpesviruses have evolved an immune evasion strategy that is effective against complement-mediated antiviral responses during acute but not latent infection. (+info)
Japanese spotted fever involving the central nervous system: two case reports and a literature review.
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Japanese spotted fever (JSF), first reported in 1984, is a rickettsial disease caused by Rickettsia japonica. Until now, affliction of the central nervous system has been rarely reported. Here we report two cases of JSF associated with a central nervous system disorder such as meningoencephalitis. (+info)
A clinical study of eosinophilic meningoencephalitis caused by angiostrongyliasis.
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OBJECTIVE: To improve the clinician's awareness of angiostrongyliasis. METHODS: The clinical and laboratory data as well as the epidemiological information concerning 18 patients with eosinophilic meningoencephalitis caused by Angiostrongylus cantonensis were analyzed. RESULTS: All patients had a history of eating raw fresh water snail (Ampularium canaliculatus) before the onset of the disease. Incubation period ranged from 1 to 25 days. The major symptoms of the patients had severe headache and pain in the trunk and limbs. Increased eosinophlic count in peripheral blood and cerebrospinal fluid was noted. Tested by enzyme-linked immunoadsorbent assay (ELISA), sera were specifically IgG-antibody positive against Angiostrougylus cantonensis antigen, but were negative against other parasitic antigens such as Paragonimus westermani, Cysticerus, Cellulosae hominis, Echinococcus granulosus and Trichinella spiralis. Abnormal spotty signals were found in 2 cases with brain magnetic resonance imaging. Electroencephalogram (EEG) showed slow alpha rhythm. All the patients were effectively treated with combined administration of albendazole and dexamethazone. CONCLUSIONS: Angiostrongyliasis is one of the common causes leading to eosinophilic meningoencephalitis. To our knowledge, Wenzhou is the first small outbreak site of angiostrongyliasis discovered in Chinese mainland. (+info)
Evidence for the role of demyelination, HLA-DR alleles, and cytokines in the pathogenesis of parvovirus B19 meningoencephalitis and its sequelae.
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OBJECTIVE: To review the clinical and pathological features of parvovirus B19 meningoencephalitis and its sequelae in 12 previously published cases, and to perform additional tests to determine the pathogenesis of the disease. METHODS: Cases were reviewed and available serum and cerebrospinal fluid (CSF) tested for antiganglioside antibodies and a range of cytokines. In situ hybridisation for parvovirus B19 DNA was performed on postmortem brain tissue in two cases. HLA-DRB1 typing was undertaken on genomic DNA extracted from peripheral blood leucocytes. RESULTS: Cerebellar involvement was suggested either clinically or pathologically in four cases. In the two cases with postmortem histology, there was marked atrophy of the molecular and granular layers of the cerebellum with focal loss of Purkinje cells. Brain scanning by MRI or CT was done in six cases during the acute phase. Three were abnormal with evidence of demyelination. Three had markedly enlarged ventricles, in two of which there was high signal intensity from the white matter on both T1 and T2 weighted images. The three cases with abnormal brain scans had long term neurological sequelae (mental retardation, personality change, altered affect). In situ hybridisation on available postmortem brain tissue was negative in the two cases tested. All cases in which HLA-DR alleles were determined carried at least one of the following alleles: HLA-DRB1*01, *04, *07, *09, *15, *16. Available serum and CSF was tested for antiganglioside antibodies (all negative) and for a panel of cytokines, which had a similar profile in both serum (n = 5) and CSF (n = 1) during the acute phase. Cytokines that were consistently detectable were IL-6 (mean 726.20 pg/ml), TNFalpha (50.64 pg/ml), IFNgamma (39.64 pg/ml), GM-CSF (216.12 pg/ml), and MCP-1 (154.43 pg/ml); IL-1beta, IL-5, and IL-13 were undetectable. CONCLUSIONS: HLA-DR associations, an increased cytokine response, and benefit from immunomodulatory treatment (in one case) support a role for the immune response in the pathogenesis of parvovirus B19 meningoencephalitis. (+info)