Pathology

Rossiter, John P.; Jackson, Alan C.

doi:10.1016/b978-0-12-396547-9.00009-2

Cited by 9 publications

(7 citation statements)

References 119 publications

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“…RABV not only impacts on innate immune signaling within infected cells, but also has developed mechanisms to suppress broader adaptive inflammatory responses. In the CNS, despite high levels of viral replication in naturally infected humans and animals, a lack of significant infiltration by inflammatory immune cells is a hallmark of pathogenic infection [ 59 ]. Several lines of evidence indicate key roles in pathogenesis [ 2 , 74 ].…”

Section: Evasion Of Inflammatory Responses In the Cnsmentioning

confidence: 99%

“…Pathogenesis is dependent on virus reaching the CNS (reviewed in [ 26 ]) where replication and neural network-dependent spread induce severe neurological symptoms including agitation, spasms and paralysis, preceding a lethal outcome [ 25 ]. Despite this, it has been long appreciated that pathological changes in the CNS are generally mild, with infected humans/animals lacking significant inflammation or neural cell death [ 59 ]. Thus, RABV appears to have evolved neuro-protective capacity involving mechanisms to evade host immunity, thereby replicating in neurons without inducing strong immune responses.…”

mentioning

confidence: 99%

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The importance of immune evasion in the pathogenesis of rabies virus

Ito

Moseley

Sugiyama

2016

The Journal of Veterinary Medical Science

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Rabies is a zoonotic disease caused by the Lyssavirus rabies virus (RABV) that can infect most mammals, including humans, where it has a case-fatality rate of almost 100%. Although preventable by vaccination, rabies causes c. 59,000 human fatalities every year worldwide. Thus, there exists an urgent need to establish an effective therapy and/or improve dissemination of vaccines for humans and animals. These outcomes require greater understanding of the mechanisms of RABV pathogenesis to identify new molecular targets for the development of therapeutics and/or live vaccines with high levels of safety. Importantly, a number of studies in recent years have indicated that RABV specifically suppresses host immunity through diverse mechanisms and that this is a key process in pathogenicity. Here, we review current understanding of immune modulation by RABV, with an emphasis on its significance to pathogenicity and the potential exploitation of this knowledge to develop new vaccines and antivirals.

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Section: Evasion Of Inflammatory Responses In the Cnsmentioning

confidence: 99%

mentioning

confidence: 99%

The importance of immune evasion in the pathogenesis of rabies virus

Ito

Moseley

Sugiyama

2016

The Journal of Veterinary Medical Science

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“…Rabies is an illness caused by a virus that primarily affects the central nervous system. The virus almost exclusively affects neurons, resulting in notable neurological changes without any apparent morphological changes in the affected nervous tissue [ 6 ]. Even neuronal death from apoptosis is not considered important in the pathology.…”

Section: Introductionmentioning

confidence: 99%

“…In addition to its exclusive neurotropic feature, rabies differs from other viruses because it does not induce viremia and has the highest mortality of any known infectious disease (more than Ebola, for example) [ 6 ]. Another characteristic of rabies is its apparently late effect on different pathophysiological parameters; the electroencephalogram pattern is preserved unchanged for almost the entire duration of the disease and collapses only a few hours before the disease in both humans and animal models.…”

Section: Introductionmentioning

confidence: 99%

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Overexpression of MAP2 and NF-H Associated with Dendritic Pathology in the Spinal Cord of Mice Infected with Rabies Virus

Monroy-Gómez

Santamaría

Torres‐Fernández

2018

Viruses

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Rabies is a viral infection that targets the nervous system, specifically neurons. The clinical manifestations of the disease are dramatic and their outcome fatal; paradoxically, conventional histopathological descriptions reveal only subtle changes in the affected nervous tissue. Some researchers have considered that the pathophysiology of rabies is based more on biochemical changes than on structural alterations, as is the case with some psychiatric diseases. However, we believe that it has been necessary to resort to other methods that allow us to analyze the effect of the infection on neurons. The Golgi technique is the gold standard for studying the morphology of all the components of a neuron and the cytoskeletal proteins are the structural support of dendrites and axons. We have previously shown, in the mouse cerebral cortex and now with this work in spinal cord, that rabies virus generates remarkable alterations in the morphological pattern of the neurons and that this effect is associated with the increase in the expression of two cytoskeletal proteins (MAP2 and NF-H). It is necessary to deepen the investigation of the pathogenesis of rabies in order to find therapeutic alternatives to a disease to which the World Health Organization classifies as a neglected disease.

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