Perturbations of hematopoiesis by bacterial [15] or viral infections [13], by social stress [12], or by transplantation [1,4], mediated by interferon-α [18] or interferon-γ [19], by poly-I:C dsRNA [15], or by G-CSF [20] have all been found to impact on steady-state multilineage hematopoiesis of HSC and favor differentiation-restricted HSC, leading, e.g., to emergency granulopoiesis [21]. The gene discussed is CSF3; the disease is viral infectious disease.