Lethal Encephalitis in 14-Day-Old Mice Given Avirulent Semliki Forest Virus

Chew-Lim, May

doi:10.1177/030098587801500315

Cited by 4 publications

(2 citation statements)

References 13 publications

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“…Selective degeneration of the hippocampal cortex occurs in several experimental neurotropic infections [3,5,6,8,21,221. In Tacaribe virus infection in mice it was shown that hippocampal necrosis was related to local viral replication [3].…”

Section: Discussionmentioning

confidence: 99%

“…In Tacaribe virus infection in mice it was shown that hippocampal necrosis was related to local viral replication [3]. In murine Semliki Forest virus infection selective hippocampal involvement has been explained by the extremely rich blood supply to this area increasing the rate of entry of hematogenous virus into brain tissue [8]. Whether a similar mechanism exists in distemper infection is uncertain.…”

Section: Discussionmentioning

confidence: 99%

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Polioencephalomalacia Associated with Canine Distemper Virus Infection

Lisiak

Vandevelde

1979

Vet Pathol

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Abstract. Eight dogs with severe neurologic signs, including seizures, had polioencephalomalacia of the pyriform cortex, Ammon's horn and deep structures in the temporal lobe. The polioencephalomalacia was considered to be a consequence of canine distemper virus infection based on clinical signs, typical inclusions, the demonstration of viral antigens in the lesions and of characteristic paramyxovirus nucleocapsids by electron microscopy. Little evidence for neuronal destruction by direct viral activity was found. Selective nerve cell necrosis was attributed to ischemia (vascular lesions and seizure induced consumptive anoxia) and immune mechanisms. The selective involvement of the rhinencephalic structures was thought to be related to the mode of entry and spread of the virus.Cerebrocortical necrosis in dogs has been associated with cyanide poisoning [ 131, lead intoxication [32] and cardiac arrest [20]. Several reported cases, in which no cause could be established, were classified as idiopathic encephalomalacia [ 131. Selective necrosis of the rhinencephalon of unknown cause also has been described in the dog [ 111. In a dog [ 131 distemper inclusion bodies were associated with the lesions and in another report [ 1 I] polioencephalomalacia occurred together with demyelinating distemper encephalitis. Our report presents the clinical and pathological findings in dogs with polioencephalomalacia predominantly in the pyriform lobe and hippocampus as described [ 1 I]. All our dogs had canine distemper infection and an attempt was made to correlate directly the malacic lesions with the presence of canine distemper virus. Materials and MethodsEight dogs were referred to the Small Animal Clinic for neurologic disorders. Each dog was given a detailed general and neurologic examination.Fluorescent antibody conjugates were prepared by fractionation of globulins from rabbits hyperimmunized against canine distemper virus and conjugation of globulins with fluorescein isothiocyanate [7]. Fluorescent antibody tests were done by a direct technique on conjunctival smears in five dogs and on smears of cerebral spinal fluid sediment in three dogs.All dogs were killed. Brain, spinal cord and representative samples of extraneural tissues were collected at necropsy from all dogs and immersed in buffered neutral formalin. Tissues 650

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Polioencephalomalacia Associated with Canine Distemper Virus Infection

Lisiak

Vandevelde

1979

Vet Pathol

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The Effect of Defective-Interfering Semliki Forest Virus on the Histopathology of Infection with Virulent Semliki Forest Virus in Mice

Crouch¹,

Mackenzie²,

Dimmock³

1982

Journal of Infectious Diseases

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The majority of mice inoculated with a mixture of a lethal dose of virulent Semliki Forest virus (SFV) strain ts+ and defective-interfering (DI) SFV remained completely health, with virus infectivity levels in brain tissue reduced by 99.9%. The results of previous studies had suggested that these effects were primarily the result of the intrinsic interfering capacity of DI virus rather than of host defense responses. Because SFV strain ts+ and an avirulent strain of SFV have clearly distinguishable histopathologic effects in brain tissue, the capability of DI virus to change the virulent into the avirulent form of the disease was examined. Modulation of strain ts+ virus infection by DI virus was accompanied by a complete absence of histopathologic changes despite significant levels of infectious virus and thus differed qualitatively from infection with avirulent SFV. These results provide further evidence that the interference is not mediated through stimulation of an immune cell infiltration.

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The Gangliosidoses: Comparative Features and Research Applications

et al. 1979

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Abstract. Ganglioside storage diseases are inherited defects of lysosomal hydrolases that result in intralysosomal accumulation of gangliosides and other complex metabolites. Gangliosidoses occur in man, cats, cattle, dogs and swine. In all species, these diseases are characterized clinically by relentlessly progressive neurological deterioration. Lysosomal hypertrophy with characteristic ultrastructural inclusions occur in neurons, endothelial and other cells. Definitive diagnosis requires biochemical identification of the storage product and enzyme deficiency. Gangliosidoses in animals are important models of human lysosomal diseases and may be a significant complication in the maintenance of certain purebred stocks of domestic animals.According to current concepts, the lysosomal system is the principal site of intracellular digestion and consists of membrane-bound cytoplasmic organelles containing more than 40 acid hydrolases capable of degrading most biologically important macromolecules. Mutations that cause reduced hydrolytic activity of lysosomal hydrolases result in diseases characterized by incomplete catabolism and concomitant accumulation ("storage") of undergraded substrate within lysosomes [7, 9, 181. The gangliosidoses are lysosomal diseases resulting from incomplete catabolism and intralysosomal accumulation of gangliosides and related complex glycolipids and glycoproteins. These diseases have been recognized in five mammalian species including man, cats, cattle, dogs and swine (31. Regardless of species affected, the gangliosidoses are characterized by 1) progressive nervous system deterioration that usually begins early in life and ultimately leads to premature death; 2) autosomal recessive inheritance; 3) lysosomal hypertrophy in neurons, hepatocytes, macrophages and other cells resulting from deposition of glycoproteins or glycolipids; and 4) absence or marked reduction in activity of specific lysosomal enzymes required for hydrolysis of accumulated compounds.Most lysosomal storage diseases, including the gangliosidoses, are untreatable. Furthermore, the pathogenesis of cell injury and death resulting from lysosomal hypertrophy remains obscure. Therefore, animal models of these diseases are of critical importance for progress in basic and applied research. Also, it is becoming 635

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Lethal Encephalitis in 14-Day-Old Mice Given Avirulent Semliki Forest Virus

Cited by 4 publications

References 13 publications

Polioencephalomalacia Associated with Canine Distemper Virus Infection

Polioencephalomalacia Associated with Canine Distemper Virus Infection

The Effect of Defective-Interfering Semliki Forest Virus on the Histopathology of Infection with Virulent Semliki Forest Virus in Mice

The Gangliosidoses: Comparative Features and Research Applications

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