HHV-6A infection dysregulates autophagy/UPR interplay increasing beta amyloid production and tau phosphorylation in astrocytoma cells as well as in primary neurons, possible molecular mechanisms linking viral infection to Alzheimer's disease

Maria Anele Romeo, Maria Saveria Gilardini Montani, Aurelia Gaeta, Gabriella D'Orazi, Alberto Faggioni, Mara Cirone

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HHV-6A and HHV-6B are neurotropic viruses able to dysregulate autophagy and activate ER stress/UPR in several cell types. The appropriate functioning of these processes is required for cell homeostasis, particularly in post-mitotic cells such as neuronal cells. Interestingly, neurodegenerative diseases such as Alzheimer's disease (AD) are often accompanied by autophagy dysregulation and abnormal UPR activation. This study demonstrated for the first time that HHV-6A infection of astrocytoma cells and primary neurons reduces autophagy, increases Aβ production and activates ER stress/UPR promoting tau protein hyper-phosphorylation. Our results support previous studies suggesting that HHV-6A infection may play a role in AD and unveil the possible underlying molecular mechanisms involved.

Original languageEnglish
Article number165647
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Issue number3
Publication statusPublished - Mar 1 2020



  • Alzheimer's disease
  • Autophagy/UPR
  • HHV-6A
  • Neurons
  • Tau phosphorylation

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology

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