This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tsutsui, Y. Articles by Kosugi, I. Search for Related Content PubMed PubMed Citation Articles by Tsutsui, Y. Articles by Kosugi, I.

 Previous Article  |  Next Article 

Journal of Virology, July 2002, p. 7247-7254, Vol. 76, No. 14
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.14.7247-7254.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Reactivation of Latent Cytomegalovirus Infection in Mouse Brain Cells Detected after Transfer to Brain Slice Cultures

Second Department of Pathology, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan

Received 15 April 2002/ Accepted 23 April 2002

Cytomegalovirus (CMV) is the most significant infectious cause of brain disorders in humans involving the developing brain. It is hypothesized that the brain disorders occur after recurrent reactivation of the latent infection in some kinds of cells in the brains. In order to test this hypothesis, we examined the reactivation of latent murine CMV (MCMV) infection in the mouse brain by transfer to brain slice culture. We infected neonatal and young adult mice intracerebrally with recombinant MCMV in which the lacZ gene was inserted into a late gene. The brains were removed 6 months after infection and used to prepare brain slices that were then cultured for up to 4 weeks. Reactivation of latent infection in the brains was detected by ß-galactosidase (ß-Gal) staining to assess ß-galactosidase expression. Viral replication was also confirmed by the plaque assay. Reactivation was observed in about 75% of the mice infected during the neonatal period 6 months after infection. Unexpectedly, reactivation was also observed in 75% of mice infected as young adults, although the infection ratio in the brain slices was significantly lower than that in neonatally infected mice. ß-Gal-positive cells were observed in marginal regions of the brains or immature neural cells in the ventricular walls. Immunohistochemical staining showed that the ß-Gal-positive reactivated cells were neural stem or progenitor cells. These results suggest that brain disorders may occur long after infection by reactivation of latent infection in the immature neural cells in the brain.

This article has been cited by other articles:

• Kawasaki, H., Mocarski, E. S., Kosugi, I., Tsutsui, Y. (2007). Cyclosporine Inhibits Mouse Cytomegalovirus Infection via a Cyclophilin-Dependent Pathway Specifically in Neural Stem/Progenitor Cells. J. Virol. 81: 9013-9023 [Abstract] [Full Text]  
• Keller, M. J., Wu, A. W., Andrews, J. I., McGonagill, P. W., Tibesar, E. E., Meier, J. L. (2007). Reversal of Human Cytomegalovirus Major Immediate-Early Enhancer/Promoter Silencing in Quiescently Infected Cells via the Cyclic AMP Signaling Pathway. J. Virol. 81: 6669-6681 [Abstract] [Full Text]