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Journal of Virology, July 2002, p. 6618-6635, Vol. 76, No. 13
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.13.6618-6635.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Critical Role for Glial Cells in the Propagation and Spread of Lymphocytic Choriomeningitis Virus in the Developing Rat Brain

Daniel J. Bonthius,1,2,3* Jolonda Mahoney,1 Michael J. Buchmeier,4 Bahri Karacay,1 and Derek Taggard5

Departments of Pediatrics,1 Neurology,2 Anatomy & Cell Biology,3 Neurosurgery, University of Iowa College of Medicine, Iowa City, Iowa 52242,5 Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California 920374

Received 19 December 2001/ Accepted 4 April 2002

Inoculation of the neonatal rat with lymphocytic choriomeningitis virus (LCMV) results in the selective infection of several neuronal populations and in focal pathological changes. However, the pathway by which LCMV reaches the susceptible neurons has not been described, and the nature and time course of the pathological changes induced by the infection are largely unknown. This study examined the sequential migration of LCMV in the developing rat brain and compared the pathological changes among infected brain regions. The results demonstrate that astrocytes and Bergmann glia cells are the first cells of the brain parenchyma infected with LCMV and that the virus spreads across the brain principally via contiguous glial cells. The virus then spreads from glial cells into neurons. However, not all neurons are susceptible to infection. LCMV infects neurons in only four specific brain regions: the cerebellum, olfactory bulb, dentate gyrus, and periventricular region. The virus is then cleared from glial cells but persists in neurons. LCMV induces markedly different pathological changes in each of the four infected regions. The cerebellum undergoes an acute and permanent destruction, while the olfactory bulb is acutely hypoplastic but recovers fully with age. Neurons of the dentate gyrus are unaffected in the acute phase but undergo a delayed-onset mortality. In contrast, the periventricular region has neither acute nor late-onset cell loss. Thus, LCMV infects four specific brain regions in the developing brain by spreading from glial cells to neurons and then induces substantially different pathological changes with diverse time courses in each of the four infected regions.

* Corresponding author. Mailing address: Department of Pediatrics, Division of Child Neurology, 2504 JCP, University of Iowa Hospital and Clinics, 200 Hawkins Dr., Iowa City, IA 52242. Phone: (319) 356-7727. Fax: (319) 356-4855. E-mail: daniel-bonthius{at}uiowa.edu.

Journal of Virology, July 2002, p. 6618-6635, Vol. 76, No. 13
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.13.6618-6635.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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