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Cited by 60Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsInflammasome and immune disorders

Herpes simplex virus 1 accelerates the progression of Alzheimer’s disease by modulating microglial phagocytosis and activating NLRP3 pathway

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Wang, Zhimeng, Liu, Jing, Han, Jing, Zhang, Tianyi, Li, Shangjin, Hou, Yanfei, Su, Huili, Han, Fangping +1 more·2024·Journal of Neuroinflammation
DOI 10.1186/s12974-024-03166-9PMC PMC11264637
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Abstract

Accumulating evidence implicates that herpes simplex virus type 1 (HSV-1) has been linked to the development and progression of Alzheimer’s disease (AD). HSV-1 infection induces β-amyloid (Aβ) deposition in vitro and in vivo, but the effect and precise mechanism remain elusive. Here, we show that HSV-1 infection of the brains of transgenic 5xFAD mice resulted in accelerated Aβ deposition, gliosis, and cognitive dysfunction. We demonstrate that HSV-1 infection induced the recruitment of microglia to the viral core to trigger microglial phagocytosis of HSV-GFP-positive neuronal cells. In addition, we reveal that the NLRP3 inflammasome pathway induced by HSV-1 infection played a crucial role in Aβ deposition and the progression of AD caused by HSV-1 infection. Blockade of the NLRP3 inflammasome signaling reduces Aβ deposition and alleviates cognitive decline in 5xFAD mice after HSV-1 infection. Our findings support the notion that HSV-1 infection is a key factor in the etiology of AD, demonstrating that NLRP3 inflammasome activation functions in the interface of HSV-1 infection and Aβ deposition in AD.

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  • HSV-1 and bacterial amyloids can activate the NLRP3 inflammasome in glial cells, leading to the activation of caspase 1 and production of interleukin 1β (IL-1β).

    “HSV-1 and bacterial amyloids can activate the NLRP3 inflammasome in glial cells, leading to the activation of caspase 1 and production of interleukin 1β (IL-1β) [95].”

    From What would it take to prove that a chronic infection is a causal agent in Alzheimer’s disease? (2025) · cites this paper as [95]

    The Results section (‘NLRP3 inflammasome is activated after HSV-1 infection in 5xFAD mice’; page unavailable) reports NLRP3 activation after HSV-1 infection, predominantly in microglia, alongside increased cleaved caspase-1 and IL-1β. The paper does not address bacterial amyloids activating this pathway, so that part of the attributed claim is unsupported. (LLM, conf=0.89)

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Cited by

Sorted by citations

Authors
Wang, Z., Liu, J., Han, J., Zhang, T., Li, S., Hou, Y., Su, H., Han, F., & Zhang, C.
Affiliations
  • Center for Life Sciences (CN)
  • Chinese Academy of Sciences (CN)
  • Tsinghua University (CN)
Corresponding author
Zhang, Conggang
ORCID
Venue
Journal of Neuroinflammation
Publisher
Springer Science and Business Media LLC
Published
2024-07-18
Volume
21
Issue
1
Pages
176-176
ISSN
1742-2094 (ISSN-L)
DOI
10.1186/s12974-024-03166-9
PMC
PMC11264637
OpenAlex
W4400772417
Cited by
60
References
22
Citations by year
2026: 30 · 2025: 28 · 2024: 2
FWCI
16.97
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Neuroinflammation (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Natural Science Foundation of China (32070875)
  • Tsinghua-Peking Center for Life Sciences
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords
herpes simplex virus type 1, Alzheimer's disease, NLRP3 inflammasome, microglial phagocytosis, amyloid-beta deposition, 5xFAD mice, cognitive decline, gliosis, viral infection, neuroinflammation, neurodegeneration
MeSH terms
NLR Family, Pyrin Domain-Containing 3 Protein, Alzheimer Disease, Animals, Disease Models, Animal, Herpes Simplex, Humans, Mice, Transgenic, Phagocytosis, Signal Transduction, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Microglia, Herpesvirus 1, Human, Disease Progression, Mice, Presenilin-1

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