Abstract
Herpes simplex virus (HSV) is known to replicate within the limbic system and to alter behavior in both humans and experimental animals. However, the reason why the virus selectively damages this anatomical, developmental, and functional neural unit remains a mystery. Nor is it known why herpes simplex encephalitis fails to respect these neuroanatomical boundaries in newborns. In the present study, the authors determined the spatiotemporal changes in the distribution of the major neural entry receptor for HSV (nectin-1) in postnatal mouse and rat brains. Discrete nectin-1 immunopositivity was observed in regions susceptible to HSV infection in specific developmental phases of central nervous system. The authors also describe nectin-1–related pathways controlling neuronal cell migration/brain morphogenesis, the disruption of which might lead to the emergence of mental disorders with a rapid cognitive decline. Journal of NeuroVirology (2006) 12, 161–170.
Szatmár Horváth, and Emese Prandovszky contributed equally to this work.
Rat monoclonal anti-nectin-1 was supplied by Y. Takai, Osaka University, Osaka, Japan. S.H. was a János Bolyai scholar during part of this project. This research was supported by grants from the Hungarian National Research Foundation (OTKA T046687, M36213) and GVOP-3.2.1.-2004-04-0357/3.0. R.J.E. and G.H.C. are supported by Public Health Service Grant NS-36731 from the National Institute of Neurological Diseases and Stroke. C.K. is supported by a grant from the University of Pennsylvania Research Foundation.