Yuta Ishizuka
   Department   Kawasaki Medical School  Kawasaki Medical School, Department of Pathophysiology and Metabolism,
   Position   Assistant Professor
Article types 原著
Language English
Peer review Peer reviewed
Title Herpes Simplex Virus Type 1 Neuronal Infection Triggers the Disassembly of Key Structural Components of Dendritic Spines.
Journal Formal name：Frontiers in cellular neuroscience
Abbreviation：Front Cell Neurosci
ISSN code：16625102/16625102
Domestic / ForeginForegin
Publisher Frontiers
Volume, Issue, Page 15,pp.580717
Author and coauthor Francisca Acuña-Hinrichsen, Adriana Covarrubias-Pinto, Yuta Ishizuka, María Francisca Stolzenbach, Carolina Martin, Paula Salazar, Maite A. Castro, Clive R. Bramham, Carola Otth
Publication date 2021/02
Summary Herpes simplex virus type 1 (HSV-1) is a widespread neurotropic virus. Primary infection of HSV-1 in facial epithelium leads to retrograde axonal transport to the central nervous system (CNS) where it establishes latency. Under stressful conditions, the virus reactivates, and new progeny are transported anterogradely to the primary site of infection. During the late stages of neuronal infection, axonal damage can occur, however, the impact of HSV-1 infection on the morphology and functional integrity of neuronal dendrites during the early stages of infection is unknown. We previously demonstrated that acute HSV-1 infection in neuronal cell lines selectively enhances Arc protein expression - a major regulator of long-term synaptic plasticity and memory consolidation, known for being a protein-interaction hub in the postsynaptic dendritic compartment. Thus, HSV-1 induced Arc expression may alter the functionality of infected neurons and negatively impact dendritic spine dynamics. In this study we demonstrated that HSV-1 infection induces structural disassembly and functional deregulation in cultured cortical neurons, an altered glutamate response, Arc accumulation within the somata, and decreased expression of spine scaffolding-like proteins such as PSD-95, Drebrin and CaMKIIβ. However, whether these alterations are specific to the HSV-1 infection mechanism or reflect a secondary neurodegenerative process remains to be determined.
DOI 10.3389/fncel.2021.580717
PMID 33708072