Beschreibung:
<jats:p>To determine whether established CD8<jats:sup>+</jats:sup>T cell memory to an epitope prominent during the replicative phase of a γ-herpesvirus infection protects against subsequent challenge, mice were primed with a recombinant vaccinia virus expressing the p56 peptide and then boosted by intranasal exposure to an influenza A virus incorporating p56 in the neuraminidase protein. Clonally expanded populations of functional, p56-specific CD8<jats:sup>+</jats:sup>T cells were present at high frequency in both the lung and the lymphoid tissue 1 month later, immediately before respiratory challenge with γHV-68. This prime-and-boost regime led to a massive reduction of productive γHV-68 infection in the respiratory tract and, initially, to much lower levels of latency in both the regional lymph nodes and the spleen. The CD8<jats:sup>+</jats:sup>T cell response to another epitope (p79) was diminished, there was less evidence of B cell activation, and the onset of the CD4<jats:sup>+</jats:sup>T cell-dependent splenomegaly was delayed. Within 3–4 weeks of the γHV-68 challenge, however, the extent of latent infection in the lymph nodes and spleen was equivalent, and both groups developed the prominent infectious mononucleosis-like syndrome that is characteristic of this infection. The reverse protocol (influenza then vaccinia) seemed to be slightly less effective. Even though immune CD8<jats:sup>+</jats:sup>T cells may be present at the time and site of virus challenge, establishing a high level of CD8<jats:sup>+</jats:sup>T cell memory to lytic-phase epitopes alone does not protect against the longer-term consequences of this γHV infection.</jats:p>