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Microbes Infect. 2008 Nov-Dec;10(14-15):1514-23. doi: 10.1016/j.micinf.2008.09.005. Epub 2008 Sep 25.

Primary target cells of herpes simplex virus type 1 in the hippocampus.

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Laboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, 53 Shogoin-kawara-cho, Sakyo-ku, Kyoto 606-8507, Japan.


Herpes simplex virus type 1 (HSV-1) causes fatal and sporadic encephalitis in human. The encephalitis-survivors frequently suffer from symptoms of memory deficits. It remains unclear how HSV-1 induces tissue damages in memory formation-associated brain tissues such as the hippocampus. In this study, we examined HSV-1 infection in the hippocampus using a rat HSV-1 infection model. We found profound pathological changes in the hippocampus and large numbers of HSV-1 antigen-positive cells in the dentate gyrus (DG) subfield of HSV-1-infected rats. To understand the precise mechanism of HSV-1-induced tissue damages in the hippocampus, we employed rat organotypic hippocampal slice cultures (OHC) as an in vitro HSV-1 infection model. In OHC, HSV-1 infection predominated in neuronal cells and the infected neuronal cells were severely damaged. Longitudinal analysis indicated that granule cells in DG subfield were extremely vulnerable to HSV-1 infection among neuronal cells in the hippocampus. Since DG granule cells play a crucial role in memory formation, disruption of these cells may be a primary step leading to memory deficits.

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