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Journal of Virology, April 1999, p. 3080-3086, Vol. 73, No. 4
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

T Cells Contribute to Disease Severity during Coxsackievirus B4 Infection

Arlene I. Ramsingh,1,2,* William T. Lee,1,2 Doris N. Collins,1 and Lori E. Armstrong1

Wadsworth Center, New York State Department of Health, Albany, New York 12201-2002,1 and Department of Biomedical Sciences, School of Public Health, State University of New York at Albany, Albany, New York 122372

Received 22 October 1998/Accepted 16 December 1998

By using a model of coxsackievirus B4-induced disease, the question of whether tissue damage is due to the virus or to immune-mediated mechanisms was addressed. Both viral replication and T-cell function were implicated in contributing to the severity of disease. Three stages (I to III) of disease, which correspond to periods of high viral titers, low viral titers, and no infectious virus, have been identified. Stage I disease is considered to be primarily the result of viral replication. Immunopathological mechanisms appear to contribute to the severity of stage II and III disease. To investigate the role of T cells in contributing to the severity of disease, viral infection in CD8 knockout (ko) mice and CD4 ko mice was analyzed. CD8 T-cell responses appear to be beneficial during early, viral disease but detrimental in later disease when viral titers are diminishing. CD4 ko mice, unlike the parental strain, survived infection. Viral replication was lower in the CD4 ko mice. Was survival due to decreased viral replication or to the lack of T-helper-cell function? To investigate further the role of T helper cells in contributing to tissue damage, viral infection in two additional ko strains (interleukin-4 [IL-4] ko and gamma interferon ko strains) was examined. A clear correlation between viral replication and the outcome of infection was not observed. The absence of IL-4, which may influence T-helper-cell subset development, was advantageous during early viral disease but deleterious in later disease. The results suggest that T-cell-mediated immunity is both beneficial and detrimental during coxsackievirus B4 infection.

* Corresponding author. Mailing address: Wadsworth Center, New York State Department of Health, 120 New Scotland Ave., Albany, NY 12201-2002. Phone: (518) 474-8634. Fax: (518) 474-3181. E-mail: arlene.ramsingh{at}wadsworth.org.

Journal of Virology, April 1999, p. 3080-3086, Vol. 73, No. 4
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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