To determine how memory CD8<sup>+</sup> T cells generated during latency differ from those primed during acute or chronic viral infection, we adoptively transferred naive P14 CD8<sup>+</sup> T cells into uninfected recipients, and examined surface proteins, cytokines and transcription factors following infection with the Armstrong (acute) or Clone 13 (chronic) strains of lymphocytic choriomeningitis virus (LCMV), or murine gammaherpesvirus 68 (MHV68) expressing the LCMV epitope D<sup>b</sup>GP33-41.
Blockade of α<sub>4</sub> β<sub>7</sub> by monoclonal antibodies (mAbs) inhibited lymphocytic choriomeningitis virus-induced accumulation of P14 T<sub>RM</sub> cells in the intestine but not in SGs.