Herpes simplex virus type 1 and Alzheimer’s disease

@article{Dobson1999HerpesSV,
  title={Herpes simplex virus type 1 and Alzheimer’s disease},
  author={Curtis B Dobson and Ruth F. Itzhaki},
  journal={Neurobiology of Aging},
  year={1999},
  volume={20},
  pages={457-465}
}
[Herpes simplex virus type 1 as risk factor associated to Alzheimer disease].
TLDR
Studies regarding the routes of dissemination of HSV-1 from the peripheral ganglions to the CNS, as well as the possible cellular and molecular mechanisms implied in generating neuronal damage during latent and productive infection, are of much relevance.
Herpes simplex encephalitis: involvement of apolipoprotein E genotype.
TLDR
It seems that apoE ε2 is a risk factor for HSE, based on the allele frequencies obtained from specimens from the brain or spleen of patients with HSE.
Effect of Apolipoprotein E on the Cerebral Load of Latent Herpes Simplex Virus Type 1 DNA
TLDR
It is shown that viral neuroinvasiveness depends directly on the overall ApoE dosage and especially on the presence of isoform apolipoprotein E4, which seems to facilitate HSV-1 latency in the brain much more so than apoE3.
Alzheimer ' s disease and the role of infectious Agents : A review
TLDR
It is suggested that some infectious agents, may contribute to the pathogenesis of AD and with the prevention and treatment of such infectious agents the sanitation authorities can decrease the risk of AD.
Association of HSV1 and apolipoprotein E-ε4 in Alzheimer’s disease
The results of Marques et al (2001) are very surprising in that only one brain specimen was found to be positive for herpes simplex virus type 1 (HSV1) in a group of 15 Alzheimer’s disease (AD)
Alzheimer's Disease: A Pathogenetic Autoimmune Disorder Caused by Herpes Simplex in a Gene-Dependent Manner
  • C. Carter
  • Biology
    International journal of Alzheimer's disease
  • 2010
TLDR
Alzheimer's disease is classified as an autoimmune disorder created by pathogen mimicry of key Alzheimer's disease-related proteins, which may well be prevented by vaccination and regular pathogen detection and elimination, and perhaps stemmed by immunosuppression or antibody adsorption-related therapies.
Herpes Viruses Increase the Risk of Alzheimer's Disease: A Meta-Analysis.
TLDR
A meta-analysis of published data found an increased risk for AD when herpesviridae is present in the brain compared to controls and HSV1 together with the presence of the APOE ɛ4 allele increases the risk of developing AD.
Vaccination prevents latent HSV1 infection of mouse brain
Involvement of apolipoprotein E in herpes simplex encephalitis
TLDR
It is concluded that apoE is involved in the response to damage associated with HSE, as in other forms of brain injury, however, APOE genotype does not appear to influence either the risk of developing HSE or subsequent mortality.
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References

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Latent herpes simplex virus type 1 in normal and Alzheimer's disease brains
TLDR
It is postulated that factors such as number or expression of viral genes and host susceptibility might be related to incidence of AD.
Herpes simplex virus type 1 DNA is present in specific regions of brain from aged people with and without senile dementia of the Alzheimer type
TLDR
The highly sensitive polymerase chain reaction has detected the viral thymidine kinase gene in post‐mortem brain from 14/21 cases of senile dementia of the Alzheimer type and 9/15 elderly normals, indicating the presence of Herpes simplex virus type 1 DNA is a region‐dependent feature of the aged brain.
Prevalence of Alzheimer plaques in AIDS
TLDR
The findings support the view that a stimulus to an inflammatory response in the brain favours argyrophilic plaque formation in the brains of patients with AIDS.
Herpes simplex virus genomes in human nervous system tissue analyzed by polymerase chain reaction
TLDR
The study has confirmed the previous demonstration of latent HSV in trigeminal ganglia in normal humans and assessed the frequency and distribution of HSV genomes in the nervous system tissues of patients dying of nonneurological causes.
Isolation of virus from brain after immunosuppression of mice with latent herpes simplex
TLDR
It is shown experimentally that mice carrying latent HSV in their trigeminal ganglia may, following massive immunosuppression, express infectious virus in the central nervous system (CNS).
Inflammatory infiltration of the trigeminal ganglion after herpes simplex virus type 1 corneal infection
TLDR
The data are consistent with the notion that gamma interferon produced by natural killer cells and/or gamma delta T cells may play an important role in limiting HSV-1 replication in the trigeminal ganglion during the acute stage of infection.
“Limbic Predilection in Alzheimer Dementia: Is Reactivated Herpesvirus Involved?”
  • M. Ball
  • Biology, Medicine
    Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques
  • 1982
SUMMARY: In the brains of patients with senile dementia of the Alzheimer type (SDA T), the quantitatively pathognomonic neuronal lesions (tangles, plaques, granulovacuolar degeneration, Hirano
Gamma interferon expression during acute and latent nervous system infection by herpes simplex virus type 1
TLDR
It is hypothesized that the persistence of T cells and the sustained IFN-gamma expression occur in response to an HSV-1 antigen in the nervous system and that prolonged secretion of IFN -gamma during latency may modulate a reactivated HSV -1 infection.
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