How an increase in the copy number of HSV-1 during latency can cause Alzheimer’s disease: the viral and cellular dynamics according to the microcompetition model

Polansky, Hanan; Goral, Benjamin

doi:10.1007/s13365-021-01012-9

Cited by 4 publications

(4 citation statements)

References 182 publications

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“…Post-mortem human HSE brains show a high reduction in mitochondrial transcripts compared to controls, demonstrating that mitochondrial damage underlies the HSE phenotype, and this is confirmed in a primary human astrocyte HSV-1 infection model [18]. It is noteworthy that the same decrease in the expression of many genes important for mitochondrial function, observed with HSV infection, can also result in oxidative stress and neuronal damage leading to Alzheimer's disease [19].…”

Section: Herpes Virusmentioning

confidence: 65%

Exogenous Players in Mitochondria-Related CNS Disorders: Viral Pathogens and Unbalanced Microbiota in the Gut-Brain Axis

et al. 2023

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Billions of years of co-evolution has made mitochondria central to the eukaryotic cell and organism life playing the role of cellular power plants, as indeed they are involved in most, if not all, important regulatory pathways. Neurological disorders depending on impaired mitochondrial function or homeostasis can be caused by the misregulation of “endogenous players”, such as nuclear or cytoplasmic regulators, which have been treated elsewhere. In this review, we focus on how exogenous agents, i.e., viral pathogens, or unbalanced microbiota in the gut-brain axis can also endanger mitochondrial dynamics in the central nervous system (CNS). Neurotropic viruses such as Herpes, Rabies, West-Nile, and Polioviruses seem to hijack neuronal transport networks, commandeering the proteins that mitochondria typically use to move along neurites. However, several neurological complications are also associated to infections by pandemic viruses, such as Influenza A virus and SARS-CoV-2 coronavirus, representing a relevant risk associated to seasonal flu, coronavirus disease-19 (COVID-19) and “Long-COVID”. Emerging evidence is depicting the gut microbiota as a source of signals, transmitted via sensory neurons innervating the gut, able to influence brain structure and function, including cognitive functions. Therefore, the direct connection between intestinal microbiota and mitochondrial functions might concur with the onset, progression, and severity of CNS diseases.

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Section: Herpes Virusmentioning

confidence: 65%

Exogenous Players in Mitochondria-Related CNS Disorders: Viral Pathogens and Unbalanced Microbiota in the Gut-Brain Axis

et al. 2023

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“…In the case of HSV-1, few studies have been performed regarding the long-term sequels after affecting NT signaling. Interestingly, it has been reported that an increase in the number of HSV-1 viral copies can decrease the BDNF levels [ 159 ]. Together with a reduction in NMDA receptors, this phenomenon induces problems in synaptic plasticity and the accumulation of Aβ protein that can lead to Alzheimer’s disease [ 159 ].…”

Section: Effect Of Cns Viral Infections On Neurotrophin Signalingmentioning

confidence: 99%

“…Interestingly, it has been reported that an increase in the number of HSV-1 viral copies can decrease the BDNF levels [ 159 ]. Together with a reduction in NMDA receptors, this phenomenon induces problems in synaptic plasticity and the accumulation of Aβ protein that can lead to Alzheimer’s disease [ 159 ]. Even though there is no information regarding the association between the infection with EBV and its effect in the long term, it can be suggested that EBV can promote similar phenomena since they both belong to the same family.…”

Section: Effect Of Cns Viral Infections On Neurotrophin Signalingmentioning

confidence: 99%

Neurotrophin Signaling Impairment by Viral Infections in the Central Nervous System

Böhmwald

Andrade

Mora

et al. 2022

IJMS

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Neurotrophins, such as nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin 3 (NT-3), NT-4, and NT-5, are proteins involved in several important functions of the central nervous system. The activation of the signaling pathways of these neurotrophins, or even by their immature form, pro-neurotrophins, starts with their recognition by cellular receptors, such as tropomyosin receptor kinase (Trk) and 75 kD NT receptors (p75NTR). The Trk receptor is considered to have a high affinity for attachment to specific neurotrophins, while the p75NTR receptor has less affinity for attachment with neurotrophins. The correct functioning of these signaling pathways contributes to proper brain development, neuronal survival, and synaptic plasticity. Unbalanced levels of neurotrophins and pro-neurotrophins have been associated with neurological disorders, illustrating the importance of these molecules in the central nervous system. Furthermore, reports have indicated that viruses can alter the normal levels of neurotrophins by interfering with their signaling pathways. This work discusses the importance of neurotrophins in the central nervous system, their signaling pathways, and how viruses can affect them.

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“…Currently, ~70% of the world's population under the age of 50 harbors an infection with HSV-1 [9]. While the infection is typically mild, its access to the nervous system can allow for it to spread to nearby organs, causing encephalitis in the brain [10], keratitis in the eye [11], and possibly progressive neurodegenerative disorders like Alzheimer's Disease [12][13][14][15][16][17][18][19]. The risk of developing serious neurodegenerative diseases associated with HSV-1 infection is significant in both immunocompetent and immunocompromised individuals [10,13,20].…”

Section: Introductionmentioning

confidence: 99%

Non-Thermal Plasma Reduces HSV-1 Infection of and Replication in HaCaT Keratinocytes In Vitro

Sutter,

Brettschneider,

Wigdahl

et al. 2024

IJMS

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Herpes simplex virus type 1 (HSV-1) is a lifelong pathogen characterized by asymptomatic latent infection in the trigeminal ganglia (TG), with periodic outbreaks of cold sores caused by virus reactivation in the TG and subsequent replication in the oral mucosa. While antiviral therapies can provide relief from cold sores, they are unable to eliminate HSV-1. We provide experimental results that highlight non-thermal plasma (NTP) as a new alternative therapy for HSV-1 infection that would resolve cold sores faster and reduce the establishment of latent infection in the TG. Additionally, this study is the first to explore the use of NTP as a therapy that can both treat and prevent human viral infections. The antiviral effect of NTP was investigated using an in vitro model of HSV-1 epithelial infection that involved the application of NTP from two separate devices to cell-free HSV-1, HSV-1-infected cells, and uninfected cells. It was found that NTP reduced the infectivity of cell-free HSV-1, reduced viral replication in HSV-1-infected cells, and diminished the susceptibility of uninfected cells to HSV-1 infection. This triad of antiviral mechanisms of action suggests the potential of NTP as a therapeutic agent effective against HSV-1 infection.

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How an increase in the copy number of HSV-1 during latency can cause Alzheimer’s disease: the viral and cellular dynamics according to the microcompetition model

Cited by 4 publications

References 182 publications

Exogenous Players in Mitochondria-Related CNS Disorders: Viral Pathogens and Unbalanced Microbiota in the Gut-Brain Axis

Exogenous Players in Mitochondria-Related CNS Disorders: Viral Pathogens and Unbalanced Microbiota in the Gut-Brain Axis

Neurotrophin Signaling Impairment by Viral Infections in the Central Nervous System

Non-Thermal Plasma Reduces HSV-1 Infection of and Replication in HaCaT Keratinocytes In Vitro

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