Pathogenesis

Jackson, Alan C.; Fu, Zhen F.

doi:10.1016/b978-0-12-396547-9.00008-0

Cited by 27 publications

(23 citation statements)

References 177 publications

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“…During development and adulthood, it interacts with different biochemical systems, including neurotransmission systems that can affect the assembly of the cytoskeleton (Johnson & Jope;Wilson & Keith, 1998;Kaufmann et al;Sánchez et al). In the etiology of the pathogenesis of rabies, there is evidence of effect of the infection on neurotransmitters (Jackson & Fu;Rengifo & Torres-Fernández, 2007;Santamaría et al, 2010). RESUMEN: La proteína asociada a microtúbulos MAP-2 es una parte integral del citoesqueleto y juega un papel importante en la morfogénesis neuronal.…”

Section: Discussionmentioning

confidence: 99%

“…Rabies is a zoonosis transmitted mainly by carnivore mammals or bats through the bite of an infected animal. When the virus comes into contact with specific cells of the muscle fibers of the infected individual, it enters through peripheral nerves, reaches the spinal cord and ascends to the brain through the motor tracts by retrograde axonal transport (Jackson & Fu, 2013). Although rabies symptoms are very dramatic, there are, paradoxically, very few morphological changes (macroscopic and microscopic) in the nervous system (Iwasaki & Tobita, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Immunohistochemical Overexpression of MAP-2 in the Cerebral Cortex of Rabies-Infected Mice

2015

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SUMMARY:The microtubule-associated protein MAP-2 is an integral part of the cytoskeleton and plays an important role in neural morphogenesis. This protein is an essential component of the dendritic cytoskeleton, especially in the adult brain, and its expression can be altered under experimental or pathological conditions. The purpose of this study was to evaluate the effect of infection with the rabies virus on MAP-2 immunoreactivity in the cerebral cortex of mice. The mice were inoculated with the rabies virus and the animals were sacrificed when the disease reached its advanced stage, together with uninfected animals of the same age. The brains were extracted after being previously perfusion-fixed with paraformaldehyde; coronal sections were obtained with a vibratome. The coronal sections were processed by immunohistochemistry to reveal the presence of the MAP-2 protein in neurons of the motor area of the cerebral cortex. Rabies-infected mice showed an increase in the immunoreactivity of the somata and apical dendrites in pyramidal neurons of the motor cortex. This is an unexpected result, as dendritic pathology has been previously demonstrated in rabies, and some studies on neurological disorders associate dendritic alterations with loss of expression of the MAP-2 protein. Therefore, whatever the alteration in the expression of this protein, decrease or increase, it could be causing a biochemical imbalance in the integrity and stability of the neuronal cytoskeleton.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Immunohistochemical Overexpression of MAP-2 in the Cerebral Cortex of Rabies-Infected Mice

2015

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“…Studies conducted on experimental animals have greatly improved our current understanding about rabies pathogenesis (Jackson et al, 2007).…”

Section: The Viral Pathogenesismentioning

confidence: 99%

Mitochondrial dysfunction in rabies virus infection of neurons

et al. 2013

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“…Despite its 32 small 12 Kb single-stranded negative sense RNA genome and limited five gene coding capacity 33 (Wunner, 2007), infection with this virus results in rabies, a feared neurological disease that is 34 universally fatal except in extremely rare circumstances (Jackson, 2007). These viruses can 35 infect any mammalian species but they are maintained in association with particular reservoir 36 hosts (Hanlon et al, 2007).…”

mentioning

confidence: 99%