HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Johnston, I. C. D. Articles by Brown, T. D. K. Search for Related Content PubMed PubMed Citation Articles by Johnston, I. C. D. Articles by Brown, T. D. K. Agricola Articles by Johnston, I. C. D. Articles by Brown, T. D. K.

Theiler's murine encephalomyelitis virus 3D RNA polymerase: its expression in the CNS and the specific immune response generated in persistently infected mice

¹ Department of Pathology, University of Cambridge, Cambridge, CB2 1QP
and² Department of Veterinary Pathology, University of Edinburgh, Summerhall, Edinburgh, EH9 1QH, UK

Intracerebral inoculation of the neurotropic murine picornavirus, Theiler's murine encephalomyelitis virus (TMEV), results either in an acute encephalitis (GDVII strain) or in the establishment of a persistent infection with the development of demyelinating lesions (BeAn strain). In this article, the expression of the viral RNA polymerase was studied in the central nervous system of both acutely and persistently infected mice and in infected cells in tissue culture. Similar numbers of acutely infected glial cells (80–85%) expressed both viral polymerase and structural proteins in vitro while a much smaller proportion of persistently infected glial cells (0·6–0·9%) expressed these proteins. Following infection of mice with GDVII, many cells in the brain were found to express polymerase. However, in the spinal cord of mice persistently infected with BeAn, very few cells were found to express the polymerase while many more cells showed the presence of viral structural proteins. This suggests that a restriction in viral replication, possibly at the level of polymerase expression, may be a feature of the persistent infection. However, enough polymerase was expressed to maintain a polymerase-specific antibody response in a number of infected animals as late as 21 months post-infection. Mechanisms that may be involved in the establishment and maintainance of TMEV persistence are discussed with reference to these findings.

^* Author for correspondence. Present address: Institut für Virologie und Immunbiologie der Universität Würzburg, Versbacher Strasse 7, D-97078 Würzburg, Germany. Fax +49 931 201 3934. e-mail ian.johnston@vax.rz.uni-wuerzburg.d400.de

Received 26 October 1994; accepted 30 June 1995.