This finding contrasts with previous data showing that the peak of anti-VNHRFTLV cytotoxic and IFNγ-secreting CD8+ T-cells occurred after the peak of parasitemia (between 14 and 24 dpi in the studied strains), implying that there is a requirement for rounds of parasite multiplication to trigger CD8+ T-cell effector activities [29]. The gene discussed is CD8A; the disease is parasitic infectious disease.