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Journal of Virology, December 2008, p. 11619-11627, Vol. 82, No. 23
0022-538X/08/$08.00+0     doi:10.1128/JVI.00375-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Role of T Cells in Virus Control and Disease after Infection with Pneumonia Virus of Mice{triangledown}

Stefanie Frey,1 Christine D. Krempl,2,3 Annette Schmitt-Gräff,4 and Stephan Ehl1*

Center for Pediatrics and Adolescent Medicine, University of Freiburg, Freiburg, Germany,1 Department of Virology, Institute for Medical Microbiology and Hygiene, University of Freiburg, Freiburg, Germany,2 Institute of Virology and Immunobiology, University of Würzburg, Würzburg, Germany,3 Institute of Pathology, University of Freiburg, Freiburg, Germany4

Received 21 February 2008/ Accepted 11 September 2008

Infection of mice with pneumonia virus of mice (PVM) is used as a natural host experimental model for studying the pathogenesis of infection with the closely related human respiratory syncytial virus. We analyzed the contribution of T cells to virus control and pathology after PVM infection. Control of a sublethal infection with PVM strain 15 in C57BL/6 mice was accompanied by a 100-fold increase in pulmonary cytotoxic T lymphocytes, 20% of which were specific for PVM. T-cell-deficient mice failed to eliminate PVM and became virus carriers in the absence of the clinical or histopathological signs of pneumonia that occurred after infection of control mice. Mice with limited T-cell numbers did not achieve virus control without weight loss, indicating that T-cell-mediated virus control was closely linked to immunopathology. Both CD4 and CD8 T cells independently contributed to virus elimination and disease. Virus control and disease were similar in the absence of perforin, gamma interferon, or tumor necrosis factor alpha. Interestingly, disease and mortality after lethal high-dose PVM infection were independent of T cells. These data illustrate a key role for T cells in control of PVM infection and demonstrate that both T-cell-dependent and -independent pathways contribute to disease in a viral dose-dependent fashion.

* Corresponding author. Mailing address: Center for Pediatrics and Adolescent Medicine, Mathildenstr. 1, D-79106 Freiburg, Germany. Phone: 49-761-270-4309. Fax: 49-761-270-4481. E-mail: stephan.ehl{at}uniklinik-freiburg.de

{triangledown} Published ahead of print on 24 September 2008.

Journal of Virology, December 2008, p. 11619-11627, Vol. 82, No. 23
0022-538X/08/$08.00+0     doi:10.1128/JVI.00375-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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