Long-term persistence and reactivation of T cell memory in the lung of mice infected with respiratory syncytial virus

In mice acutely infected with respiratory syncytial virus (RSV), more than 20% of pulmonary CD8(+) cells, but only 2-3% of CD8(+) T cells in the drain ing lymph node secreted interferon-gamma in response to a single peptide. S urprisingly, the percentage of virus-specific T cells in the lung remained at these high levels long after the acute infection. Pulmonary memory T cel ls were further studied in a sensitive adoptive transfer system, which allo ws visualizing polyclonal CD4(+) and CD8(+) virus-specific memory T cell re sponses. Fifty days after infection, persisting RSV-specific pulmonary T ce lls remained CD69(hi) CD62L(lo), but had returned to a resting memory state according to functional criteria. In the absence of neutralizing antibodie s reinfection first induced cell division among virus-specific memory T cel ls 3 days after infection predominantly in the local lymph node. However, d ivided cells then rapidly accumulated in the lung without significantly inc reasing in the lymph node. These results suggest rapid export of reactivate d cells from the lymph node to the target organ. Thus, although memory T ce lls can be maintained in the infected organ after a localized virus infecti on, amplification of a recall response appears to be most effective in orga nized lymphoid tissue.