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Synaptic Plasticity and Neurological Disorders in Neurotropic Viral Infections.

Atluri VS, Hidalgo M, Samikkannu T, Kurapati KR, Nair M - Neural Plast. (2015)

Bottom Line: While rabies and poliovirus are considered as strictly neurotropic, other neurotropic viruses involve nervous tissue only secondarily.Since the AIDS pandemic, the interest in neurotropic viral infections has become essential for all clinical neurologists.In this review, we have discussed the neurotropic viruses, which play a major role in altered synaptic plasticity and neurological disorders.

View Article: PubMed Central - PubMed

Affiliation: Department of Immunology, Institute of NeuroImmune Pharmacology, Herbert Wertheim College of Medicine, Florida International University, Miami, FL 33199, USA.

ABSTRACT
Based on the type of cells or tissues they tend to harbor or attack, many of the viruses are characterized. But, in case of neurotropic viruses, it is not possible to classify them based on their tropism because many of them are not primarily neurotropic. While rabies and poliovirus are considered as strictly neurotropic, other neurotropic viruses involve nervous tissue only secondarily. Since the AIDS pandemic, the interest in neurotropic viral infections has become essential for all clinical neurologists. Although these neurotropic viruses are able to be harbored in or infect the nervous system, not all the neurotropic viruses have been reported to cause disrupted synaptic plasticity and impaired cognitive functions. In this review, we have discussed the neurotropic viruses, which play a major role in altered synaptic plasticity and neurological disorders.

No MeSH data available.


Related in: MedlinePlus

A model of HIV-induced neurotoxicity. Infected microglia or macrophages release viral proteins, chemokines, and cytokines. This activates uninfected microglia and macrophages. Neuronal injury, synapse damage, and cell death occur because immune activated and HIV-infected brain microglia and macrophages release neurotoxic elements. Excessive influx of Ca2+ ions occurs because of the overactivation of NMDA receptor-coupled ion channels that mediate neuronal injury. As a consequence, potentially harmful enzymes, release of glutamate, and free-radical formation are triggered. Subsequently, glutamate overstimulates NMDA receptors on nearby neurons, which causes additional injury. Upregulation of HDAC2 expression and increased eIF2α-phosphorylation leads to the dysregulated synaptic plasticity gene and protein expression which results in impaired synaptic plasticity.
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fig3: A model of HIV-induced neurotoxicity. Infected microglia or macrophages release viral proteins, chemokines, and cytokines. This activates uninfected microglia and macrophages. Neuronal injury, synapse damage, and cell death occur because immune activated and HIV-infected brain microglia and macrophages release neurotoxic elements. Excessive influx of Ca2+ ions occurs because of the overactivation of NMDA receptor-coupled ion channels that mediate neuronal injury. As a consequence, potentially harmful enzymes, release of glutamate, and free-radical formation are triggered. Subsequently, glutamate overstimulates NMDA receptors on nearby neurons, which causes additional injury. Upregulation of HDAC2 expression and increased eIF2α-phosphorylation leads to the dysregulated synaptic plasticity gene and protein expression which results in impaired synaptic plasticity.

Mentions: Glycoprotein gp120 is another structural protein that has been reported to induce neuronal apoptosis. This gp120 has a significant function in the viral infection cycle and binds to chemokine coreceptors CCR5 and CXCR4, allowing conformational change and entering of the virus into cells [159]. Neuronal apoptosis can be induced by a short exposure of neurons to gp120 [160, 161]. It has also been reported to stimulate axonal degeneration [162] as well as dendritic injury [163, 164]. These two main effects are associated with the synaptodendritic atrophy seen in HAD [165]. Gp120 transgenic mice have been reported to show dendritic reduction and neuronal loss [166], which indicates that gp120 is capable of reducing and affecting synaptic plasticity. Figure 3 is showing the role of HIV infection, Tat, and gp120 in the HIV-induced neurotoxicity.


Synaptic Plasticity and Neurological Disorders in Neurotropic Viral Infections.

Atluri VS, Hidalgo M, Samikkannu T, Kurapati KR, Nair M - Neural Plast. (2015)

A model of HIV-induced neurotoxicity. Infected microglia or macrophages release viral proteins, chemokines, and cytokines. This activates uninfected microglia and macrophages. Neuronal injury, synapse damage, and cell death occur because immune activated and HIV-infected brain microglia and macrophages release neurotoxic elements. Excessive influx of Ca2+ ions occurs because of the overactivation of NMDA receptor-coupled ion channels that mediate neuronal injury. As a consequence, potentially harmful enzymes, release of glutamate, and free-radical formation are triggered. Subsequently, glutamate overstimulates NMDA receptors on nearby neurons, which causes additional injury. Upregulation of HDAC2 expression and increased eIF2α-phosphorylation leads to the dysregulated synaptic plasticity gene and protein expression which results in impaired synaptic plasticity.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4663354&req=5

fig3: A model of HIV-induced neurotoxicity. Infected microglia or macrophages release viral proteins, chemokines, and cytokines. This activates uninfected microglia and macrophages. Neuronal injury, synapse damage, and cell death occur because immune activated and HIV-infected brain microglia and macrophages release neurotoxic elements. Excessive influx of Ca2+ ions occurs because of the overactivation of NMDA receptor-coupled ion channels that mediate neuronal injury. As a consequence, potentially harmful enzymes, release of glutamate, and free-radical formation are triggered. Subsequently, glutamate overstimulates NMDA receptors on nearby neurons, which causes additional injury. Upregulation of HDAC2 expression and increased eIF2α-phosphorylation leads to the dysregulated synaptic plasticity gene and protein expression which results in impaired synaptic plasticity.
Mentions: Glycoprotein gp120 is another structural protein that has been reported to induce neuronal apoptosis. This gp120 has a significant function in the viral infection cycle and binds to chemokine coreceptors CCR5 and CXCR4, allowing conformational change and entering of the virus into cells [159]. Neuronal apoptosis can be induced by a short exposure of neurons to gp120 [160, 161]. It has also been reported to stimulate axonal degeneration [162] as well as dendritic injury [163, 164]. These two main effects are associated with the synaptodendritic atrophy seen in HAD [165]. Gp120 transgenic mice have been reported to show dendritic reduction and neuronal loss [166], which indicates that gp120 is capable of reducing and affecting synaptic plasticity. Figure 3 is showing the role of HIV infection, Tat, and gp120 in the HIV-induced neurotoxicity.

Bottom Line: While rabies and poliovirus are considered as strictly neurotropic, other neurotropic viruses involve nervous tissue only secondarily.Since the AIDS pandemic, the interest in neurotropic viral infections has become essential for all clinical neurologists.In this review, we have discussed the neurotropic viruses, which play a major role in altered synaptic plasticity and neurological disorders.

View Article: PubMed Central - PubMed

Affiliation: Department of Immunology, Institute of NeuroImmune Pharmacology, Herbert Wertheim College of Medicine, Florida International University, Miami, FL 33199, USA.

ABSTRACT
Based on the type of cells or tissues they tend to harbor or attack, many of the viruses are characterized. But, in case of neurotropic viruses, it is not possible to classify them based on their tropism because many of them are not primarily neurotropic. While rabies and poliovirus are considered as strictly neurotropic, other neurotropic viruses involve nervous tissue only secondarily. Since the AIDS pandemic, the interest in neurotropic viral infections has become essential for all clinical neurologists. Although these neurotropic viruses are able to be harbored in or infect the nervous system, not all the neurotropic viruses have been reported to cause disrupted synaptic plasticity and impaired cognitive functions. In this review, we have discussed the neurotropic viruses, which play a major role in altered synaptic plasticity and neurological disorders.

No MeSH data available.


Related in: MedlinePlus