2. Academic Validation
  3. Herpes simplex virus 1 accelerates the progression of Alzheimer's disease by modulating microglial phagocytosis and activating NLRP3 pathway

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

  • J Neuroinflammation. 2024 Jul 18;21(1):176. doi: 10.1186/s12974-024-03166-9.
Zhimeng Wang # 1 2,  Jing Liu # 3,  Jing Han 1 2,  Tianyi Zhang 4,  Shangjin Li 4,  Yanfei Hou 1,  Huili Su 1,  Fangping Han 1,  Conggang Zhang 5 6
Affiliations

Affiliations

  • 1 School of Pharmaceutical Sciences, Tsinghua University, Beijing, 100084, China.
  • 2 State Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, Beijing Frontier Research Center of Biological Structure, SXMU-Tsinghua Collaborative Innovation Center for Frontier Medicine, Tsinghua University, Beijing, 100084, China.
  • 3 State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
  • 4 School of Pharmaceutical Sciences, IDG/McGovern Institute for Brain Research, Tsinghua-Peking Joint Center for Life Sciences, Tsinghua University, Beijing, 100084, China.
  • 5 School of Pharmaceutical Sciences, Tsinghua University, Beijing, 100084, China. cgzhang@tsinghua.edu.cn.
  • 6 State Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, Beijing Frontier Research Center of Biological Structure, SXMU-Tsinghua Collaborative Innovation Center for Frontier Medicine, Tsinghua University, Beijing, 100084, China. cgzhang@tsinghua.edu.cn.
  • # Contributed equally.
PMID: 39026249 DOI: 10.1186/s12974-024-03166-9
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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