We therefore investigated whether the intranasal or intramuscular infection with NY-ESO-1 S-FLU virus differentially induced the expression of the molecules (VLA-1 [CD49a], CXCR6, CD103, CD44, CD49d, CCR5 and CXCR3) implicated in retention or trafficking of effector CD8+ T cells in lung. This evidence concerns the gene CXCR3 and infection.