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* Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892; and
Cancer Vaccine Unit, Ludwig Institute for Cancer Research, Austin and Repatriation Medical Center, Heidelberg, Victoria, Australia
The extent to which naive CD8+ CTLs (TCD8+) are primed by APCs presenting endogenous Ags (direct priming) or Ags acquired from other infected cells (cross-priming) is a critical topic in basic and applied immunology. To examine the contribution of direct priming in the induction of VV-specific TCD8+, we generated recombinant vaccinia viruses that express human CMV proteins (US2 and US11) that induce the destruction of newly synthesized MHC class I molecules. Expression of US2 or US11 was associated with a 24–63% decrease in numbers of primary or secondary VV-specific TCD8+ responding to i.p. infection. Using HPLC-isolated peptides from VV-infected cells, we show that US2 and US11 selectively inhibit TCD8+ responses to a subset of immunogenic VV determinants. Moreover, VV-US2 and lysates from VV-infected histoincompatible cells elicit TCD8+ specific for a similar subset of VV determinants. These findings indicate that US2 and US11 can function in vivo to interfere with the activation of virus-specific TCD8+. Furthermore, they suggest that 1) both cross-priming and direct priming contribute significantly to the generation of VV-specific TCD8+, 2) the sets of immunogenic vaccinia virus determinants generated by cross-priming and direct priming are not completely overlapping, and 3) cross-priming overrides the effects of cis-acting viral interference with the class I Ag presentation pathway.
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