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.
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页数:18
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