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Apparent MHC-Independent Stimulation of CD8⁺ T Cells In Vivo During Latent Murine Gammaherpesvirus Infection¹

Michael A. Coppola^2,*, Emilio Flaño^*, Phuong Nguyen^*, Charles L. Hardy^*, Rhonda D. Cardin^3,*, Nilabh Shastri, David L. Woodland^*, and Marcia A. Blackman^4,*,

^* Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN 38105; Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720; and Department of Pathology, University of Tennessee, Memphis, TN 38163

Like EBV-infected humans with infectious mononucleosis, mice infected with the rodent gammaherpesvirus MHV-68 develop a profound increase in the number of CD8⁺ T cells in the circulation. In the mouse model, this lymphocytosis consists of highly activated CD8⁺ T cells strikingly biased toward V4 TCR expression. Moreover, this expansion of V4⁺CD8⁺ T cells does not depend on the MHC haplotype of the infected animal. Using a panel of lacZ-inducible T cell hybridomas, we have detected V4-specific T cell stimulatory activity in the spleens of MHV-68-infected mice. We show that the appearance and quantity of this activity correlate with the establishment and magnitude of latent viral infection. Furthermore, on the basis of Ab blocking studies as well as experiments with MHC class II, ₂-microglobulin (₂m) and TAP1 knockout mice, the V4-specific T cell stimulatory activity does not appear to depend on conventional presentation by classical MHC class I or class II molecules. Taken together, the data indicate that during latent infection, MHV-68 may express a T cell ligand that differs fundamentally from both conventional peptide Ags and classical viral superantigens.