Large study from UK Biobank finds that people seropositive for all of these four herpesviruses—HSV-1, HHV-6, HHV-7 and VZV—have greatly increased risk of developing dementia.
While MRV administered peripherally led to brain infection and neuroinflammation, it did not increase Aß deposition
Infection increases ROS, induces ER stress and activates STAT3, NF-κB and mTOR pathways.
HHV-6A was found to both enhance expression and inhibit degradation of amyloid precursor protein in vitro.
HHV-6, like some other herpesviruses, dysregulates autophagy in multiple cell types, with important biological consequences.
Three top experts on HHV-6A/B teamed up to write a comprehensive review and propose criteria for establishing HHV-6A/B to MS, epilepsy and Alzheimer’s disease.
Dysregulation of the microRNA miR155 is associated with pathophysiological progression of Alzheimer’s disease. HHV-6A has been shown to suppress miR155.
Researchers at the NIH used RNA-Seq cells from skin and blood to study the underlying mechanisms in DIHS/DRESS and identified both HHV-6 and JAK-STAT pathways as potential targets. Central memory CD4+T cells were enriched with HHV-6B.
A team led by Steven Jacobson, PhD at NINDS analyzed RNA-seq datasets from 901 brains, and found only 1.2% of Alzheimer’s patients and 0.4% of controls positive for HHV-6 RNA. They also found HHV-6 DNA in less than 4% of samples tested by ddPCR.
Two groups have challenged the widely-publicized 2018 study in 2018, that found increased HHV-6A & 7 abundance and an association with clinical and pathology scores in Alzheimer’s. The topic has become the focus vigorous debate.
Building on their prior work, an Italian team has shown that HHV-6A is able to induce dysregulation of autophagy in neurons and astrocytoma cells, increasing amyloid beta and tau production.
HHV-6A infection of microglia cells increases inflammatory markers and Aβ and tau expression dramatically, supporting the hypothesis that plaque development in Alzheimer’s disease may be an innate immune response to pathogens
Investigators propose that the induction of endoplasmic reticulum stress, likely exacerbated by autophagy inhibition, could contribute to the immune suppression induced by HHV-6B in exanthem subitem patients.
Researchers from GlaxoSmithKline found a significant overlap in differentially expressed genes shared by those with herpesvirus infections, Alzheimer’s and Parkinson’s. On the other hand, there was no significant overlap between herpesviruses and Type 2 diabetes or Huntington’s disease.
Swedish researchers report that viruses interact with proteins to form a coating or protein corona that facilitates the formation of amyloid plaque, supporting previous findings by Harvard’s Rudy Tanzi and Robert Moir.
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