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Infection01:20

Infection

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When a pathogen enters the body and reproduces, it can cause an infection, damage body cells, and cause illness symptoms that eventually lead to disease. Therefore, its prevention requires breaking the chain of infection.
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Stages of Infection01:26

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Basic Science and Pathogenesis.

Giovanna De Chiara1, Virginia Protto2, Mariya Timotey Miteva1

  • 1Institute of Translational Pharmacology, CNR, Rome, Rome, Italy.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 23, 2025
PubMed
Summary
This summary is machine-generated.

Herpes simplex virus type-1 (HSV-1) infection promotes Alzheimer's disease (AD) by spreading tau protein via extracellular vesicles and activating the complement system, leading to synaptic damage. This study reveals key mechanisms linking HSV-1 to neurodegeneration.

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Area of Science:

  • Neuroscience
  • Immunology
  • Virology

Background:

  • Recurrent herpes simplex virus type-1 (HSV-1) infection is a proposed risk factor for Alzheimer's disease (AD).
  • Previous studies linked HSV-1 to AD biomarkers, neuroinflammation, and cognitive decline.
  • Novel mechanisms in AD pathogenesis include extracellular vesicles (EVs) for toxic protein spread and complement cascade activation for synaptic elimination.

Purpose of the Study:

  • To investigate if HSV-1 infection/reactivation activates EV-mediated ptau dissemination and complement cascade pathways.
  • To explore the role of these pathways in HSV-1-induced neurodegeneration in various models.

Main Methods:

  • Utilized in vitro (murine neurons, BV2 microglia), in vivo (BALB/c mice), and ex vivo (hippocampal slices) models of HSV-1 infection.
  • Performed molecular, biochemical, virological, and functional analyses.
  • Investigated EV-mediated ptau spread, complement protein expression, microglial phagocytosis, and synaptic density.

Main Results:

  • HSV-1 utilizes EVs to spread hyperphosphorylated tau (ptau) in vitro and in vivo, with recipient neurons internalizing EV-ptau.
  • HSV-1 infection significantly increases complement proteins (e.g., C1q, C4) and microglial phagocytosis of synaptic material.
  • Complement inhibition and blockade partially prevented HSV-1-induced synaptic damage and rescued decreased spine density.

Conclusions:

  • HSV-1 infection activates EV-mediated ptau spread and complement cascade activation.
  • These pathways contribute to synaptic damage and neurodegeneration in HSV-1 infection.
  • The findings highlight novel mechanisms linking HSV-1 to Alzheimer's disease pathogenesis.