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Journal of Virology, July 2004, p. 6827-6835, Vol. 78, No. 13
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.13.6827-6835.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

An Optimized CD4 T-Cell Response Can Control Productive and Latent Gammaherpesvirus Infection

Rebecca L. Sparks-Thissen, Douglas C. Braaten, Scott Kreher, Samuel H. Speck,{dagger} and Herbert W. Virgin IV*

Department of Pathology and Immunology and Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 63110

Received 20 October 2003/ Accepted 4 March 2004

CD4 T cells are important for control of infection with murine gammaherpesvirus 68 ({gamma}HV68), but it is not known whether CD4 T cells function via provision of help to other lymphocyte subsets, such as B cells and CD8 T cells, or have an independent antiviral function. Moreover, under conditions of natural infection, the CD4 T-cell response is not sufficient to eliminate infection. To determine the functional capacities of CD4 T cells under optimal or near-optimal conditions and to determine whether CD4 T cells can control {gamma}HV68 infection in the absence of CD8 T cells or B cells, we studied the effect of ovalbumin (OVA)-specific CD4 T cells on infection with a recombinant {gamma}HV68 that expresses OVA. OVA-specific CD4 T cells limited acute {gamma}HV68 replication and prolonged the life of infected T-cell receptor-transgenic RAG (DO.11.10/RAG) mice, demonstrating CD4 T-cell antiviral activity, independent of CD8 T cells and B cells. Despite CD4 T-cell-mediated control of acute infection, latent infection was established in DO.11.10/RAG mice. However, OVA-specific CD4 T cells reduced the frequency of latently infected cells both early (16 days postinfection) and late (42 days postinfection) after infection of mice containing CD8 T cells and B cells (DO.11.10 mice). These results show that OVA-specific CD4 T cells have B-cell and CD8 T-cell-independent antiviral functions in the control of acute infection and can, in the absence of preexisting CD8 T-cell or B-cell immunity, inhibit the establishment of gammaherpesvirus latency.

* Corresponding author. Mailing address: Department of Pathology and Immunology, Washington University School of Medicine, 660 S. Euclid Ave., Box 8118, St. Louis, MO 63110. Phone: (314) 362-9223. Fax: (314) 362-4096. E-mail: virgin{at}wustl.edu.

{dagger} Present address: Division of Microbiology and Immunology, Yerkes National Primate Research Center, Emory University, Atlanta, GA 30329.

Journal of Virology, July 2004, p. 6827-6835, Vol. 78, No. 13
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.13.6827-6835.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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