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U.S.A."],"published-print":{"date-parts":[[1999,8,3]]},"abstract":"<jats:p>\n                    Cytotoxic T cell (CTL) memory was analyzed after infection with lymphocytic choriomeningitis virus (LCMV) and recombinant\n                    <jats:italic>Listeria monocytogenes<\/jats:italic>\n                    (rLM) expressing the complete nucleoprotein of LCMV (rLM-NP\n                    <jats:sub>actA<\/jats:sub>\n                    ) or only the immunodominant epitope of H-2\n                    <jats:sup>d<\/jats:sup>\n                    mice (rLM-NP\n                    <jats:sub>118\u2013126<\/jats:sub>\n                    ). Immunization with LCMV and rLM induced a long-lived increased CTL precursor (CTLp) frequency specific for the viral (NP\n                    <jats:sub>118\u2013126<\/jats:sub>\n                    ) and for the bacterial (LLO\n                    <jats:sub>91\u201399<\/jats:sub>\n                    ) epitope, respectively. However, after infection with rLM memory, CTLs were less protective against an intravenous LCMV challenge infection than a comparable number of LCMV-induced memory T cells. LCMV, but not recombinant\n                    <jats:italic>Listeria<\/jats:italic>\n                    -induced memory T cells were able to protect against lethal choriomeningitis by LCMV or a subsequent peripheral infection with recombinant vaccinia virus expressing LCMV-NP. The protective memory after viral and after rLM immunization was paralleled by evidence of LCMV but not rLM antigen persistence on day 15 and 30 after vaccination. 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