Evidence map›Paper›PMID 40251168›Full record

ArticleNature communications2025

A microengineered 3D human neurovascular unit model to probe the neuropathogenesis of herpes simplex encephalitis.

Min Zhang, Peng Wang, Yunsong Wu, Lin Jin, Jiayue Liu, Pengwei Deng, Rongcan Luo, Xiyue Chen, Mengqian Zhao, Xu Zhang and 4 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. HSV-1 as a Potential Driver of Alzheimer's Disease.Pathogens (Basel, Switzerland) · 2025
    Review
  10. Review
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Min Zhang *Division of Biotechnology, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Peng Wang *University of Science and Technology of China, Hefei, China.
Yunsong WuDivision of Biotechnology, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Lin JinCollege of Veterinary Medicine, Shanxi Agricultural University, Jinzhong, China.ORCID http://orcid.org/0000-0001-6273-9140
Jiayue LiuUniversity of Science and Technology of China, Hefei, China.
Pengwei DengUniversity of Science and Technology of China, Hefei, China.
Rongcan LuoKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences & Yunnan Province, and KIZ-CUHK Joint Laboratory of Bioresources and Molecular Research in Common Diseases, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China.ORCID http://orcid.org/0000-0003-4472-7079
Xiyue ChenDivision of Biotechnology, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Mengqian ZhaoDivision of Biotechnology, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Xu ZhangDivision of Biotechnology, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Yaqiong GuoDivision of Biotechnology, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China.
Ying YanState Key Laboratory of Functions and Applications of Medicinal Plants & College of Pharmacy, Guizhou Provincial Engineering Technology Research Center for Chemical Drug R&D, Guizhou Medical University, Guiyang, China.
Yingtong DiState Key Laboratory of Phytochemistry and Plant Resources in West China, Kunming Institute of Botany, Chinese Academy of Sciences, Kunming, China.ORCID http://orcid.org/0000-0001-5766-0198
Jianhua QinDivision of Biotechnology, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China. jhqin@dicp.ac.cn.ORCID http://orcid.org/0000-0001-5735-6436

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31971373
6 · The paper itself

Abstract

Herpes simplex encephalitis (HSE) caused by HSV-1 is the most common non-epidemic viral encephalitis, and the neuropathogenesis of HSE remains elusive. This work describes a 3D human neurovascular unit (NVU) model that allows to explore the neuropathogenesis of HSE in vitro. This model is established by co-culturing human microvascular endothelial cells, astrocytes, microglia and neurons on a multi-compartment chip. Upon HSV-1 infection, this NVU model exhibited HSE-associated pathological changes, including cytopathic effects, blood-brain barrier dysfunction and pro-inflammatory cytokines release. Besides, significant innate immune responses were observed with the infiltration of peripheral immune cells and microglial activation. Transcriptomic analysis revealed broadly inflammatory and chemotactic responses in host cells. Mechanistically, we found HSV-1 could induce severe suppression of autophagic flux in glial cells, especially in microglia. Autophagy activators could effectively inhibit HSV-1 replication and rescue neurovascular injuries, indicating the utility of this unique platform for studying neurological diseases and new therapeutics.

Indexed as

Encephalitis, Herpes SimplexAstrocytesAutophagyBlood-Brain BarrierCoculture TechniquesCytokinesEndothelial CellsHerpesvirus 1, HumanHumansImmunity, InnateMicrogliaNeuronsVirus ReplicationCytokines

Identifiers

PMID40251168
PMCPMC12008363

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.