Herpes Simplex Virus Type 1 Induces AD-like Neurodegeneration Markers in Human Progenitor and Differentiated ReNcell VM Cells

被引:2
作者
Salgado, Blanca [1 ,2 ]
Sastre, Isabel [1 ,2 ]
Bullido, Maria J. [1 ,2 ,3 ]
Aldudo, Jesus [1 ,2 ,3 ]
机构
[1] Univ Autonoma Madrid, Ctr Biol Mol Severo Ochoa CSIC UAM, Madrid 28049, Spain
[2] Inst Salud Carlos III, Ctr Invest Biomed Red Enfermedades Neurodegenerat, Madrid 28031, Spain
[3] Inst Invest Sanitaria Hosp Univ La Paz IdiPAZ, Madrid 28046, Spain
关键词
Alzheimer's disease; HSV-1; ReNcell VM; differentiation; infection; neurodegeneration; lysosome alterations; neurons; glial cells; MODEL; ACCUMULATION; DYSFUNCTION; PYROPTOSIS; SYSTEM; BRAIN; TAU;
D O I
10.3390/microorganisms11051205
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
An increasing body of evidence strongly suggests that infections or reactivations of herpes simplex virus type 1 (HSV-1) may be closely linked to Alzheimer's disease (AD). Promising results have been obtained using cell and animal models of HSV-1 infection, contributing to the understanding of the molecular mechanisms linking HSV-1 infection and AD neurodegeneration. ReNcell VM is a human neural stem cell line that has been used as a model system to study the impact of various infectious agents on the central nervous system. In this study, we demonstrate the suitability of the ReNcell VM cell line for developing a new in vitro model of HSV-1 infection. By following standard differentiation protocols, we were able to derive various nervous cell types, including neurons, astrocytes, and oligodendrocytes, from neural precursors. Additionally, we demonstrated the susceptibility of ReNcell VM cells, including precursor and differentiated cells, to HSV-1 infection and subsequent viral-induced AD-like neurodegeneration. Our findings support the use of this cell line to generate a new research platform for investigating AD neuropathology and its most significant risk factors, which may lead to important discoveries in the context of this highly impactful disease.
引用
收藏
页数:18
相关论文
共 47 条
  • [41] Tau interactome analyses in CRISPR-Cas9 engineered neuronal cells reveal ATPase-dependent binding of wild-type but not P301L Tau to non-muscle myosins
    Wang, Xinzhu
    Williams, Declan
    Muller, Iris
    Lemieux, Mackenzie
    Dukart, Ramona
    Maia, Isabella B. L.
    Wang, Hansen
    Woerman, Amanda L.
    Schmitt-Ulms, Gerold
    [J]. SCIENTIFIC REPORTS, 2019, 9 (1)
  • [42] DNA Damage Increases Secreted Aβ40 and Aβ42 in Neuronal Progenitor Cells: Relevance to Alzheimer's Disease
    Welty, Starr
    Thathiah, Amantha
    Levine, Arthur Samuel
    [J]. JOURNAL OF ALZHEIMERS DISEASE, 2022, 88 (01) : 177 - 190
  • [43] Endo-lysosomal and autophagic dysfunction: a driving factor in Alzheimer's disease?
    Whyte, Lauren S.
    Lau, Adeline A.
    Hemsley, Kim M.
    Hopwood, John J.
    Sargeant, Timothy J.
    [J]. JOURNAL OF NEUROCHEMISTRY, 2017, 140 (05) : 703 - 717
  • [44] Zika virus causes supernumerary foci with centriolar proteins and impaired spindle positioning
    Wolf, Benita
    Diop, Fode
    Ferraris, Pauline
    Wichit, Sineewanlaya
    Busso, Coralie
    Misse, Dorothee
    Gonczy, Pierre
    [J]. OPEN BIOLOGY, 2017, 7 (01):
  • [45] Herpes simplex virus infection causes cellular β-amyloid accumulation and secretase upregulation
    Wozniak, Matthew A.
    Itzhaki, Ruth F.
    Shipley, Suzanne J.
    Dobson, Curtis B.
    [J]. NEUROSCIENCE LETTERS, 2007, 429 (2-3) : 95 - 100
  • [46] Advance of sporadic Alzheimer's disease animal models
    Zhang, Lili
    Chen, Chen
    Mak, Marvin S. H.
    Lu, Junfeng
    Wu, Zeqing
    Chen, Qiuhe
    Han, Yifan
    Li, Yuefeng
    Pi, Rongbiao
    [J]. MEDICINAL RESEARCH REVIEWS, 2020, 40 (01) : 431 - 458
  • [47] APOE ε4 modifies the relationship between infectious burden and poor cognition
    Zhao, Chen
    Strobino, Kevin
    Moon, Yeseon Park
    Cheung, Ying Kuen
    Sacco, Ralph L.
    Stern, Yaakov
    Elkind, Mitchell S. V.
    [J]. NEUROLOGY-GENETICS, 2020, 6 (04)