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-Herpesvirus: Role for a
Viral Superantigen?
By
From the * Department of Immunology, The murine Department of Pathology, St. Jude Children's Research
Hospital, Memphis, Tennessee 38105; and the § Department of Pediatrics, Department of Pathology,
University of Tennessee, Memphis, Tennessee 38163
-herpesvirus 68 has many similarities to EBV, and induces a syndrome comparable to infectious mononucleosis (IM). The frequency of activated CD8+ T cells (CD62Llo) in
the peripheral blood increased greater than fourfold by 21 d after infection of C57BL/6J (H-2b)
mice, and remained high for at least a further month. The spectrum of T cell receptor usage
was greatly skewed, with as many as 75% of the CD8+ T cells in the blood expressing a V
4+
phenotype. Interestingly, the V4 dominance was also seen, to varying extents, in H-2k, H-2d,
H-2u, and H-2q strains of mice. In addition, although CD4 depletion from day 11 had no effect
on the V4 bias of the T cells, the V4+CD8+ expansion was absent in H-2IAb-deficient congenic mice. However, the numbers of cycling cells in the CD4 antibody-depleted mice and
mice that are CD4 deficient as a consequence of the deletion of MHC class II, were generally lower. The findings suggest that the IM-like disease is driven both by cytokines provided by
CD4+ T cells and by a viral superantigen presented by MHC class II glycoproteins to
V4+CD8+ T cells.
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