Experimentally, it has been described that a senescence prone SAM-P1 mouse strain (H-2 K), which shares the genetic background of AKR/J mice, is more susceptible to infection by hRSV, and shows a deficient CD8+ T cell response, as well as a lower gamma-interferon (INF-γ) production, which contrasts to high interleukin (IL)-4 production (Liu and Kimura, 2007). This evidence concerns the gene CD8A and infection.