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Journal of Virology, September 2000, p. 7903-7910, Vol. 74, No. 17
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Role of Viral Persistence in Retaining CD8+ T Cells within the Central Nervous System

Norman W. Marten,1 Stephen A. Stohlman,1,2 and Cornelia C. Bergmann1,2,*

Departments of Neurology1 and Molecular Microbiology and Immunology,2 Keck School of Medicine, University of Southern California, Los Angeles, California 90033

Received 6 April 2000/Accepted 8 June 2000

The continued presence of virus-specific CD8+ T cells within the central nervous system (CNS) following resolution of acute viral encephalomyelitis implicates organ-specific retention. The role of viral persistence in locally maintaining T cells was investigated by infecting mice with either a demyelinating, paralytic (V-1) or nonpathogenic (V-2) variant of a neurotropic mouse hepatitis virus, which differ in the ability to persist within the CNS. Class I tetramer technology revealed more infiltrating virus-specific CD8+ T cells during acute V-1 compared to V-2 infection. However, both total and virus-specific CD8+ T cells accumulated at similar peak levels in spinal cords by day 10 postinfection (p.i.). Decreasing viral RNA levels in both brains and spinal cords following initial virus clearance coincided with an overall progressive loss of both total and virus-specific CD8+ T cells. By 9 weeks p.i., T cells had largely disappeared from brains of both infected groups, consistent with the decline of viral RNA. T cells also completely disappeared from V-2-infected spinal cords coincident with the absence of viral RNA. By contrast, a significant number of CD8+ T cells which contained detectable viral RNA were recovered from spinal cords of V-1-infected mice. The data indicate that residual virus from a primary CNS infection is a vital component in mediating local retention of both CD8+ and CD4+ T cells and that once minimal thresholds of stimuli are lost, T cells within the CNS cannot survive in an autonomous fashion.

* Corresponding author. Mailing address: 1333 San Pablo St., MCH 142, Los Angeles, CA 90033. Phone: (323) 442-1062. Fax: (323) 225-2369. E-mail: cbergman{at}hsc.usc.edu.

Journal of Virology, September 2000, p. 7903-7910, Vol. 74, No. 17
0022-538X/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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