Neuronal Function Impairment in Rabies-infected Rat Brain

Tsiang, H

doi:10.1099/0022-1317-61-2-277

Cited by 69 publications

(28 citation statements)

References 11 publications

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“…These findings have given support to the concept that neuronal dysfunction must play an important role in producing the disease. 24 A variety of experimental studies in rabies virus infection have investigated potential abnormalities in neurotransmission involving acetylcholine, [25][26][27] serotonin, 28,29 and γ-amino-n-butyric acid. 30 Abnormalities of uncertain significance were found, but no fundamental defects were demonstrated that explain neuronal dysfunction in rabies.…”

Section: Mechanisms For Neuronal Dysfunction and Deathmentioning

confidence: 99%

Update on rabies

Jackson¹

2011

RRTM

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Human rabies is almost invariably fatal, and globally it remains an important public health problem. Our knowledge of rabies pathogenesis has been learned mainly from studies performed in experimental animal models, and a number of unresolved issues remain. In contrast with the neural pathway of spread, there is still no credible evidence that hematogenous spread of rabies virus to the central nervous system plays a significant role in rabies pathogenesis. Although neuronal dysfunction has been thought to explain the neurological disease in rabies, recent evidence indicates that structural changes involving neuronal processes may explain the severe clinical disease and fatal outcome. Endemic dog rabies results in an ongoing risk to humans in many resource-limited and resource-poor countries, whereas rabies in wildlife is important in North America and Europe. In human cases in North America, transmission from bats is most common, but there is usually no history of a bat bite and there may be no history of contact with bats. Physicians may not recognize typical features of rabies in North America and Europe. Laboratory diagnostic evaluation for rabies includes rabies serology plus skin biopsy, cerebrospinal fluid, and saliva specimens for rabies virus antigen and/or RNA detection. Methods of postexposure rabies prophylaxis, including wound cleansing and administration of rabies vaccine and human rabies immune globulin, are highly effective after recognized exposure. Although there have been rare survivors of human rabies, no effective therapy is presently available. Therapeutic coma (midazolam and phenobarbital), ketamine, and antiviral therapies (known as the "Milwaukee protocol") were given to a rabies survivor, but this therapy was likely not directly responsible for the favorable outcome. New therapeutic approaches for human rabies need to be developed. A better understanding of basic mechanisms involved in rabies pathogenesis may be helpful in the development of potential new therapies for the future.

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Section: Mechanisms For Neuronal Dysfunction and Deathmentioning

confidence: 99%

Update on rabies

Jackson¹

2011

RRTM

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“…White Wistar rats (70 to 90 g) were inoculated into the footpad and after the onset of paralysis, the rats were killed and the brains were dissected (KSnig & Klippel, 1967;Tsiang, 1982). The infectivity of rabies virus in tissue extracts of the different brain regions was titrated in mice as described in World Health Organization Monograph number 23 (1973).…”

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confidence: 99%

Distribution of Rabies Virus, Interferon an dInterferon-mediated Enzymes in the Brains of Virus-infected Rats

Marcovistz

Tsiang

1984

Journal of General Virology

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SUMMARYThe distribution of rabies virus, interferon and interferon-mediated enzymes, pppA(2'p5'A)n synthetase (2-5A synthetase) and poly(rI).poly(rC)-Sepharose-bound protein kinase, was studied in different regions of the brains of rabies virus-infected rats. A broad range of virus infectivity was found in the brain stem, cerebellum, cortex, hippocampus and striatum. Similarly, the levels of interferon were variable (2500 to 60000 units/mg protein in tissue extracts) in the different brain regions studied but were unrelated to the corresponding infectivities. The level of 2-5A synthetase and protein kinase was enhanced several-fold in the individual brain regions and the degree of such enhancement was correlated with the level of interferon.

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“…Fu et al [96] proposed that neuronal dysfunction rather than morphological changes plays a role. Others have demonstrated dysfunction of ion channels in infected cell culture [97], and defective cholinergic neurotransmission [98]. Induction of inducible nitric oxide synthase mRNA and increased levels of nitric oxide have been demonstrated in rodents inoculated with the virus [96,97,99,100].…”

Section: Bat Rabiesmentioning

confidence: 99%

Perspectives in Diagnosis and Treatment of Rabies Viral Encephalitis: Insights from Pathogenesis

et al. 2016

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Rabies viral encephalitis, though one of the oldest recognized infectious disease of humans, remains an incurable, fatal encephalomyelitis, despite advances in understanding of its pathobiology. Advances in science have led us on the trail of the virus in the host, but the sanctuaries in which the virus remains hidden for its survival are unknown. Insights into host-pathogen interactions have facilitated evolving immunologic therapeutic strategies, though we are far from a cure. Most of the present-day knowledge has evolved from in vitro studies using fixed (attenuated) laboratory strains that may not be applicable in the clinical setting. Much remains to be unraveled about this elusive virus. This review attempts to re-examine the current advances in understanding of the pathobiology of the rabies virus that modulate the diagnosis, treatment, and prevention of this fatal disease.

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Neuronal Function Impairment in Rabies-infected Rat Brain

Cited by 69 publications

References 11 publications

Update on rabies

Update on rabies

Distribution of Rabies Virus, Interferon an dInterferon-mediated Enzymes in the Brains of Virus-infected Rats

Perspectives in Diagnosis and Treatment of Rabies Viral Encephalitis: Insights from Pathogenesis

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